start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240411
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Artificial intelligence to detect noise events in remote monitoring data
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background: Remote monitoring (RM) of cardiac implantable electrical devices (CIEDs) can detect various events early. However, the diagnostic ability of CIEDs has not been sufficient, especially for lead failure. The first notification of lead failure was almost noise events, which were detected as arrhythmia by the CIED. A human must analyze the intracardiac electrogram to accurately detect lead failure. However, the number of arrhythmic events is too large for human analysis. Artificial intelligence (AI) seems to be helpful in the early and accurate detection of lead failure before human analysis.<br>
Objective: To test whether a neural network can be trained to precisely identify noise events in the intracardiac electrogram of RM data.<br>
Methods: We analyzed 21?918 RM data consisting of 12?925 and 1884 Medtronic and Boston Scientific data, respectively. Among these, 153 and 52 Medtronic and Boston Scientific data, respectively, were diagnosed as noise events by human analysis. In Medtronic, 306 events, including 153 noise events and randomly selected 153 out of 12?692 nonnoise events, were analyzed in a five-fold cross-validation with a convolutional neural network. The Boston Scientific data were analyzed similarly.<br>
Results: The precision rate, recall rate, F1 score, accuracy rate, and the area under the curve were 85.8?±?4.0%, 91.6?±?6.7%, 88.4?±?2.0%, 88.0?±?2.0%, and 0.958?±?0.021 in Medtronic and 88.4?±?12.8%, 81.0?±?9.3%, 84.1?±?8.3%, 84.2?±?8.3% and 0.928?±?0.041 in Boston Scientific. Five-fold cross-validation with a weighted loss function could increase the recall rate.<br>
Conclusions: AI can accurately detect noise events. AI analysis may be helpful for detecting lead failure events early and accurately.
en-copyright=
kn-copyright=

en-aut-name=NishiiNobuhiro
en-aut-sei=Nishii
en-aut-mei=Nobuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=BabaKensuke
en-aut-sei=Baba
en-aut-mei=Kensuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=MorookaKen'Ichi
en-aut-sei=Morooka
en-aut-mei=Ken'Ichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=ShiraeHaruto
en-aut-sei=Shirae
en-aut-mei=Haruto
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=MizunoTomofumi
en-aut-sei=Mizuno
en-aut-mei=Tomofumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=MasudaTakuro
en-aut-sei=Masuda
en-aut-mei=Takuro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=UeokaAkira
en-aut-sei=Ueoka
en-aut-mei=Akira
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=AsadaSaori
en-aut-sei=Asada
en-aut-mei=Saori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=MiyamotoMasakazu
en-aut-sei=Miyamoto
en-aut-mei=Masakazu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=EjiriKentaro
en-aut-sei=Ejiri
en-aut-mei=Kentaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=KawadaSatoshi
en-aut-sei=Kawada
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=NakagawaKoji
en-aut-sei=Nakagawa
en-aut-mei=Koji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=NakamuraKazufumi
en-aut-sei=Nakamura
en-aut-mei=Kazufumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=MoritaHiroshi
en-aut-sei=Morita
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=YuasaShinsuke
en-aut-sei=Yuasa
en-aut-mei=Shinsuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

affil-num=1
en-affil=Department of Cardiovascular  Therapeutics, Okayama University  Graduate School of Medicine, Dentistry,  and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Cyber-Physical Engineering Informatics  Research Core, Okayama University
kn-affil=

affil-num=3
en-affil=Division of Industrial Innovation Sciences,  Graduate School of Natural Science  and Technology, Okayama University
kn-affil=

affil-num=4
en-affil=Division of Industrial Innovation Sciences,  Graduate School of Natural Science  and Technology, Okayama University
kn-affil=

affil-num=5
en-affil=Department of Cardiovascular Medicine,  Okayama University Graduate School of  Medicine, Dentistry, and Pharmaceutical  Sciences
kn-affil=

affil-num=6
en-affil=Department of Cardiovascular Medicine,  Okayama University Graduate School of  Medicine, Dentistry, and Pharmaceutical  Sciences
kn-affil=

affil-num=7
en-affil=Department of Cardiovascular Medicine,  Okayama University Graduate School of  Medicine, Dentistry, and Pharmaceutical  Sciences
kn-affil=

affil-num=8
en-affil=Department of Cardiovascular Medicine,  Okayama University Graduate School of  Medicine, Dentistry, and Pharmaceutical  Sciences
kn-affil=

affil-num=9
en-affil=Department of Cardiovascular Medicine,  Okayama University Graduate School of  Medicine, Dentistry, and Pharmaceutical  Sciences
kn-affil=

affil-num=10
en-affil=Department of Cardiovascular Medicine,  Okayama University Graduate School of  Medicine, Dentistry, and Pharmaceutical  Sciences
kn-affil=

affil-num=11
en-affil=Department of Cardiovascular Medicine,  Okayama University Graduate School of  Medicine, Dentistry, and Pharmaceutical  Sciences
kn-affil=

affil-num=12
en-affil=Department of Cardiovascular Medicine,  Okayama University Graduate School of  Medicine, Dentistry, and Pharmaceutical  Sciences
kn-affil=

affil-num=13
en-affil=Department of Cardiovascular Medicine,  Okayama University Graduate School of  Medicine, Dentistry, and Pharmaceutical  Sciences
kn-affil=

affil-num=14
en-affil=Department of Cardiovascular  Therapeutics, Okayama University  Graduate School of Medicine, Dentistry,  and Pharmaceutical Sciences
kn-affil=

affil-num=15
en-affil=Department of Cardiovascular Medicine,  Okayama University Graduate School of  Medicine, Dentistry, and Pharmaceutical  Sciences
kn-affil=
en-keyword=artificial intelligence
kn-keyword=artificial intelligence
en-keyword=five-fold cross-validation
kn-keyword=five-fold cross-validation
en-keyword=intracardiac electrogram
kn-keyword=intracardiac electrogram
en-keyword=noise event
kn-keyword=noise event
en-keyword=remote monitoring
kn-keyword=remote monitoring
END

start-ver=1.4
cd-journal=joma
no-vol=25
cd-vols=
no-issue=2
article-no=
start-page=987
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240112
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Induced Pluripotent Stem Cell-Derived Cardiomyocytes Therapy for Ischemic Heart Disease in Animal Model: A Meta-Analysis
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Ischemic heart disease (IHD) poses a significant challenge in cardiovascular health, with current treatments showing limited success. Induced pluripotent derived-cardiomyocyte (iPSC-CM) therapy within regenerative medicine offers potential for IHD patients, although its clinical impacts remain uncertain. This study utilizes meta-analysis to assess iPSC-CM outcomes in terms of efficacy and safety in IHD animal model studies. A meta-analysis encompassing PUBMED, ScienceDirect, Web of Science, and the Cochrane Library databases, from inception until October 2023, investigated iPSC therapy effects on cardiac function and safety outcomes. Among 51 eligible studies involving 1012 animals, despite substantial heterogeneity, the iPSC-CM transplantation improved left ventricular ejection fraction (LVEF) by 8.23% (95% CI, 7.15 to 9.32%; p < 0.001) compared to control groups. Additionally, cell-based treatment reduced the left ventricle fibrosis area and showed a tendency to reduce left ventricular end-systolic volume (LVESV) and end-diastolic volume (LVEDV). No significant differences emerged in mortality and arrhythmia risk between iPSC-CM treatment and control groups. In conclusion, this meta-analysis indicates iPSC-CM therapy's promise as a safe and beneficial intervention for enhancing heart function in IHD. However, due to observed heterogeneity, the efficacy of this treatment must be further explored through large randomized controlled trials based on rigorous research design.
en-copyright=
kn-copyright=

en-aut-name=VoQuan Duy
en-aut-sei=Vo
en-aut-mei=Quan Duy
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=SaitoYukihiro
en-aut-sei=Saito
en-aut-mei=Yukihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=NakamuraKazufumi
en-aut-sei=Nakamura
en-aut-mei=Kazufumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=IidaToshihiro
en-aut-sei=Iida
en-aut-mei=Toshihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=YuasaShinsuke
en-aut-sei=Yuasa
en-aut-mei=Shinsuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

affil-num=1
en-affil=Department of Cardiovascular Medicine, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Cardiovascular Medicine, Okayama University Hospital
kn-affil=

affil-num=3
en-affil=Department of Cardiovascular Medicine, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=4
en-affil=Department of Cardiovascular Medicine, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=5
en-affil=Department of Cardiovascular Medicine, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=induced pluripotent stem cell
kn-keyword=induced pluripotent stem cell
en-keyword=ischemic heart disease
kn-keyword=ischemic heart disease
en-keyword=outcomes
kn-keyword=outcomes
en-keyword=safety
kn-keyword=safety
en-keyword=meta-analysis
kn-keyword=meta-analysis
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=20231217
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Significant delayed conduction and characteristic ventricular tachycardias in patients with cardiac sarcoidosis and electrical storm
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Introduction: Electrical storm (ES) of ventricular tachyarrhythmias (VTAs) is an important cause of sudden death in patients with cardiac sarcoidosis (CS). VTAs in CS are associated with myocardial scarring and inflammation. However, little is known about the risk factors of ES in patients with CS and VTAs. The objective of this study is to clarify the characteristics and risk factors for the development of ES in patients with CS.<br>
Methods: The study population included consecutive 52 patients with CS and sustained VTA. Twenty-five out of 52 patients experienced ES. We evaluated clinical characteristics, imaging modalities, and electrocardiogram (ECG) parameters to determine the risk factors associated with ES.<br>
Results: Half of the patients experienced VTAs as the initial symptom of sarcoidosis, and eight patients had ES as the initial VTA episode. There were no differences in cardiac imaging abnormalities between patients with and without ES. Among ECG markers, significant QRS fragmentation (odds ratio [OR]: 7.9, p?=?.01) and epsilon waves (OR: 12.24, p?=?.02) were associated with ES. Among the ventricular tachycardia (VT) characteristics, multiple morphologies of monomorphic VTs (OR: 10.9, p?<?.01), short VT cycle lengths (OR: 12.5, p?<?.01), and polymorphic VT (OR: 13.5, p?<?.01) were associated with ES. Bidirectional VTs were detected in 10 patients with ES and one patient without ES. Immunosuppressive therapy relieved ES in some patients.<br>
Conclusions: ES was common in patients with CS and VTAs. Significant depolarization abnormalities that appeared as QRS fragmentation, epsilon waves, and specific VT characteristics were associated with ES.<br>
en-copyright=
kn-copyright=

en-aut-name=MoritaHiroshi
en-aut-sei=Morita
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NakagawaKoji
en-aut-sei=Nakagawa
en-aut-mei=Koji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=UeokaAkira
en-aut-sei=Ueoka
en-aut-mei=Akira
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MizunoTomofumi
en-aut-sei=Mizuno
en-aut-mei=Tomofumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=MasudaTakuro
en-aut-sei=Masuda
en-aut-mei=Takuro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=AsadaSaori
en-aut-sei=Asada
en-aut-mei=Saori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=MiyamotoMasakazu
en-aut-sei=Miyamoto
en-aut-mei=Masakazu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=KawadaSatoshi
en-aut-sei=Kawada
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=NishiiNobuhiro
en-aut-sei=Nishii
en-aut-mei=Nobuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=NakamuraKazufumi
en-aut-sei=Nakamura
en-aut-mei=Kazufumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

affil-num=1
en-affil=Department of Cardiovascular Therapeutics, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Cardiovascular Medicine, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine and Dentistry
kn-affil=

affil-num=3
en-affil=Department of Cardiovascular Medicine, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine and Dentistry
kn-affil=

affil-num=4
en-affil=Department of Cardiovascular Medicine, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine and Dentistry
kn-affil=

affil-num=5
en-affil=Department of Cardiovascular Medicine, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine and Dentistry
kn-affil=

affil-num=6
en-affil=Department of Cardiovascular Medicine, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine and Dentistry
kn-affil=

affil-num=7
en-affil=Department of Cardiovascular Medicine, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine and Dentistry
kn-affil=

affil-num=8
en-affil=Department of Cardiovascular Medicine, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine and Dentistry
kn-affil=

affil-num=9
en-affil=Department of Cardiovascular Therapeutics, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=10
en-affil=Department of Cardiovascular Medicine, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine and Dentistry
kn-affil=
en-keyword=cardiac sarcoidosis
kn-keyword=cardiac sarcoidosis
en-keyword=ventricular tachycardia
kn-keyword=ventricular tachycardia
en-keyword=electrical storm
kn-keyword=electrical storm
en-keyword=ventricular fibrillation
kn-keyword=ventricular fibrillation
en-keyword=sudden cardiac death
kn-keyword=sudden cardiac death
END

start-ver=1.4
cd-journal=joma
no-vol=135
cd-vols=
no-issue=3
article-no=
start-page=142
end-page=146
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=20231201
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Systemic amyloidosis : Diagnosis and treatment of transthyretin cardiac amyloidosis
kn-title=全身性アミロイドーシス― トランスサイレチン型心アミロイドーシスの診断と治療―
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=NakamuraKazufumi
en-aut-sei=Nakamura
en-aut-mei=Kazufumi
kn-aut-name=中村一文
kn-aut-sei=中村
kn-aut-mei=一文
aut-affil-num=1
ORCID=

affil-num=1
en-affil=Department of Cardiovascular Medicine, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=岡山大学学術研究院医歯薬学域　循環器内科学
en-keyword=トランスサイレチン
kn-keyword=トランスサイレチン
en-keyword=免疫グロブリン
kn-keyword=免疫グロブリン
en-keyword=ピロリン酸シンチグラフィー
kn-keyword=ピロリン酸シンチグラフィー
en-keyword=タファミジス
kn-keyword=タファミジス
en-keyword=核酸医薬
kn-keyword=核酸医薬
END

start-ver=1.4
cd-journal=joma
no-vol=13
cd-vols=
no-issue=3
article-no=
start-page=e12286
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=20230912
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Impact of malnutrition on prognosis in patients with pulmonary arterial hypertension
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Pulmonary arterial hypertension is a life-threatening disease that coexists with right heart failure. We evaluated the relationship between malnutrition and prognosis in patients with pulmonary arterial hypertension, as malnutrition is known as a prognosis determinant in chronic heart failure. We retrospectively reviewed data of patients with pulmonary arterial hypertension before treatment. The Geriatric Nutritional Risk Index, Prognostic Nutritional Index, and Controlling Nutritional Status scores on the day of diagnosis were calculated to assess the nutritional status. Clinical endpoints were defined as composite outcomes of all-cause death or lung transplantation. Eighty patients were enrolled (mean age, 50 years; 23 men). The mean pulmonary arterial pressure was 47?±?19?mmHg, Geriatric Nutritional Risk Index was 99.9?±?12.0, and Prognostic Nutritional Index was 46.3?±?10.0. The median Controlling Nutritional Status score was 2 (1?4). During the median 5.5-year follow-up period, 28 composite events occurred. Kaplan-Meier analysis demonstrated significant differences in the incidence of clinical endpoints between groups divided by each median Geriatric Nutritional Risk Index, Prognostic Nutritional Index, and Controlling Nutritional Status score (p?=?0.007, 0.039, and 0.010, respectively). In multivariate Cox regression analysis, clinical endpoints were significantly associated with Geriatric Nutritional Risk Index (hazard ratio: 0.953, 95% confidence interval: 0.918?0.990), Prognostic Nutritional Index (hazard ratio: 0.942, 95% confidence interval: 0.892?0.996), and Controlling Nutritional Status score (hazard ratio: 1.230, 95% confidence interval: 1.056?1.433) after adjustment for factors associated in univariate Cox regression analysis. Malnutrition at diagnosis is a useful prognostic predictor for patients with pulmonary arterial hypertension.
en-copyright=
kn-copyright=

en-aut-name=NakashimaMitsutaka
en-aut-sei=Nakashima
en-aut-mei=Mitsutaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=AkagiSatoshi
en-aut-sei=Akagi
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=EjiriKentaro
en-aut-sei=Ejiri
en-aut-mei=Kentaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=NakamuraKazufumi
en-aut-sei=Nakamura
en-aut-mei=Kazufumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=ItoHiroshi
en-aut-sei=Ito
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

affil-num=1
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=Controlling Nutritional Status score
kn-keyword=Controlling Nutritional Status score
en-keyword=Geriatric Nutritional Risk Index
kn-keyword=Geriatric Nutritional Risk Index
en-keyword=nutritional status
kn-keyword=nutritional status
en-keyword=Prognostic Nutritional Index
kn-keyword=Prognostic Nutritional Index
END

start-ver=1.4
cd-journal=joma
no-vol=10
cd-vols=
no-issue=
article-no=
start-page=1261330
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=20230907
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=In vivo tracking transplanted cardiomyocytes derived from human induced pluripotent stem cells using nuclear medicine imaging
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Introduction: Transplantation of human induced pluripotent stem cell-derived cardiomyocytes (iPSC-CMs) is a promising treatment for heart failure. Information on long-term cell engraftment after transplantation is clinically important. However, clinically applicable evaluation methods have not yet been established.<br>
Methods: In this study, to noninvasively assess transplanted cell engraftment, human SLC5A5, which encodes a sodium/iodide symporter (NIS) that transports radioactive tracers such as 125I, 18F-tetrafluoroborate (TFB), and 99mTc-pertechnetate (99mTcO4?), was transduced into human induced pluripotent stem cells (iPSCs), and nuclear medicine imaging was used to track engrafted human iPSC-CMs.<br>
Results: To evaluate the pluripotency of NIS-expressing human iPSCs, they were subcutaneously transplanted into immunodeficient rats. Teratomas were detected by 99mTcO4? single photon emission computed tomography (SPECT/CT) imaging. NIS expression and the uptake ability of 125I were maintained in purified human iPSC-CMs. NIS-expressing human iPSC-CMs transplanted into immunodeficient rats could be detected over time using 99mTcO4? SPECT/CT imaging. Unexpectedly, NIS expression affected cell proliferation of human iPSCs and iPSC-derived cells.<br>
Discussion: Such functionally designed iPSC-CMs have potential clinical applications as a noninvasive method of grafted cell evaluation, but further studies are needed to determine the effects of NIS transduction on cellular characteristics and functions.
en-copyright=
kn-copyright=

en-aut-name=SaitoYukihiro
en-aut-sei=Saito
en-aut-mei=Yukihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NoseNaoko
en-aut-sei=Nose
en-aut-mei=Naoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=IidaToshihiro
en-aut-sei=Iida
en-aut-mei=Toshihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=AkazawaKaoru
en-aut-sei=Akazawa
en-aut-mei=Kaoru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KannoTakayuki
en-aut-sei=Kanno
en-aut-mei=Takayuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=FujimotoYuki
en-aut-sei=Fujimoto
en-aut-mei=Yuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=SasakiTakanori
en-aut-sei=Sasaki
en-aut-mei=Takanori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=AkehiMasaru
en-aut-sei=Akehi
en-aut-mei=Masaru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=HiguchiTakahiro
en-aut-sei=Higuchi
en-aut-mei=Takahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=AkagiSatoshi
en-aut-sei=Akagi
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=YoshidaMasashi
en-aut-sei=Yoshida
en-aut-mei=Masashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=MiyoshiToru
en-aut-sei=Miyoshi
en-aut-mei=Toru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=ItoHiroshi
en-aut-sei=Ito
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=NakamuraKazufumi
en-aut-sei=Nakamura
en-aut-mei=Kazufumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

affil-num=1
en-affil=Department of Cardiovascular Medicine, Okayama University Hospital
kn-affil=

affil-num=2
en-affil=Molecular Imaging Project of RECTOR Program, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Cardiovascular Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=4
en-affil=Department of Cardiovascular Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=5
en-affil=Molecular Imaging Project of RECTOR Program, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=6
en-affil=Molecular Imaging Project of RECTOR Program, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=7
en-affil=Okayama Medical Innovation Center, Faculty of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=8
en-affil=Okayama Medical Innovation Center, Faculty of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=9
en-affil=Molecular Imaging Project of RECTOR Program, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=10
en-affil=Department of Cardiovascular Medicine, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=11
en-affil=Department of Chronic Kidney Disease and Cardiovascular Disease, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=12
en-affil=Department of Cardiovascular Medicine, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=13
en-affil=Department of General Internal Medicine 3, Kawasaki Medical School
kn-affil=

affil-num=14
en-affil=Department of Cardiovascular Medicine, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=sodium/iodide symporter
kn-keyword=sodium/iodide symporter
en-keyword=human induced pluripotent stem cell-derived cardiomyocytes
kn-keyword=human induced pluripotent stem cell-derived cardiomyocytes
en-keyword=single photon emission computed tomography
kn-keyword=single photon emission computed tomography
en-keyword=cell-based therapy
kn-keyword=cell-based therapy
en-keyword=in vivo imaging
kn-keyword=in vivo imaging
END

start-ver=1.4
cd-journal=joma
no-vol=28
cd-vols=
no-issue=18
article-no=
start-page=2059
end-page=2066
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2021
dt-pub=20210719
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Incremental prognostic value of non-alcoholic fatty liver disease over coronary computed tomography angiography findings in patients with suspected coronary artery disease
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Aims　This study aimed to investigate additional risk stratification benefits of hepatic steatosis (HS) concurrently assessed during coronary computed tomography angiography (CTA) in a large patient cohort with suspected stable coronary artery disease (CAD).<br>
Methods and results　In this prospective study, 1148 Japanese outpatients without a history of CAD who underwent coronary CTA for suspected stable CAD (mean age 64?±?14?years) were included. HS, defined on CT as a hepatic-to-spleen attenuation ratio of <1.0, was examined just before the evaluation of adverse CTA findings, defined as obstructive and/or high-risk plaque. The major adverse cardiac events (MACE) were the composite of cardiac death, acute coronary syndrome, and late revascularization. The incremental predictive value of HS was evaluated using the global χ2 test and C-statistic. HS was identified in 247 (22%) patients. During a median follow-up of 3.9?years, MACE was observed in 40 (3.5%) patients. HS was significantly associated with MACE in a model that included adverse CTA findings (hazard ratio 4.01, 95% confidence interval 2.12?7.59, P?<?0.001). By adding HS to the Framingham risk score and adverse CTA findings, the global χ2 score and C-statistic significantly increased from 29.0 to 49.5 (P?<?0.001) and 0.74 to 0.81 (P?=?0.026), respectively. In subgroup analyses in patients with diabetes mellitus and metabolic syndrome, HS had significant additive predictive value for MACE over the Framingham risk score and adverse CTA findings.<br>
Conclusion　In patients with suspected stable CAD, concurrent evaluation of HS during coronary CTA enables more accurate detection of patients at higher risk of MACE.
en-copyright=
kn-copyright=

en-aut-name=IchikawaKeishi
en-aut-sei=Ichikawa
en-aut-mei=Keishi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MiyoshiToru
en-aut-sei=Miyoshi
en-aut-mei=Toru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=OsawaKazuhiro
en-aut-sei=Osawa
en-aut-mei=Kazuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MikiTakashi
en-aut-sei=Miki
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=TodaHironobu
en-aut-sei=Toda
en-aut-mei=Hironobu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=EjiriKentaro
en-aut-sei=Ejiri
en-aut-mei=Kentaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=YoshidaMasashi
en-aut-sei=Yoshida
en-aut-mei=Masashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=NakamuraKazufumi
en-aut-sei=Nakamura
en-aut-mei=Kazufumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=MoritaHiroshi
en-aut-sei=Morita
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=ItoHiroshi
en-aut-sei=Ito
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

affil-num=1
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of General Internal Medicine 3, Kawasaki Medical School General Medical Center
kn-affil=

affil-num=4
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=6
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=7
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=8
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=9
en-affil=Department of Cardiovascular Therapeutics, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Science
kn-affil=

affil-num=10
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=Coronary artery disease
kn-keyword=Coronary artery disease
en-keyword=Computed tomography angiography
kn-keyword=Computed tomography angiography
en-keyword=Atherosclerotic plaque
kn-keyword=Atherosclerotic plaque
en-keyword=Risk assessment
kn-keyword=Risk assessment
en-keyword=Hepatic steatosis
kn-keyword=Hepatic steatosis
END

start-ver=1.4
cd-journal=joma
no-vol=29
cd-vols=
no-issue=3
article-no=
start-page=423
end-page=431
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2021
dt-pub=20211115
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=The number of circulating CD34-positive cells is an independent predictor of coronary artery calcification progression: Sub-analysis of a prospective multicenter study
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background: Decreases in circulating CD34-positive cells are associated with increases in cardiovascular events. We investigated the association between the number of CD34-positive cells and the progression of coronary artery calcification (CAC), a marker of atherosclerosis, in patients with hypercholesteremia under statin therapy in a sub-analysis of a multicenter study.<br>
Methods: In the principal study, patients with CAC scores of 1?999 were treated with pitavastatin. Measurement of CAC by non-enhanced computed tomography and a blood test were performed at baseline and at 1-year follow-up. Patients were divided into two groups: CAC progression (change in CAC score > 0) and non-progression. The number of circulating CD34-positive cells was counted using flow cytometry.<br>
Results: A total of 156 patients (mean age 67 years, 55% men) were included in this sub-analysis. CD34 positive cell numbers at baseline as a continuous variable was inversely correlated with annual change in the log-transformed CAC score (r = ?0.19, p = 0.02). When patients were divided into high and low CD34 groups based on the median value of 0.8 cells/μL, the adjusted change in CAC score in the low-CD34 group was significantly greater than that in the high-CD34 group (54.2% vs. 20.8%, respectively, p = 0.04). In multiple logistic analysis, a low CD34-positive cell number was an independent predictor of CAC progression, with an odds ratio of 2.88 (95% confidence interval 1.28?6.49, p = 0.01).<br>
Conclusions: Low numbers of CD34-positive cells are associated with CAC progression in patients with hypercholesterolemia under statin therapy. The number of CD34-positive cells may help to identify patients at increased cardiovascular risk.
en-copyright=
kn-copyright=

en-aut-name=IchikawaKeishi
en-aut-sei=Ichikawa
en-aut-mei=Keishi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MiyoshiToru
en-aut-sei=Miyoshi
en-aut-mei=Toru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=OsawaKazuhiro
en-aut-sei=Osawa
en-aut-mei=Kazuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MikiTakashi
en-aut-sei=Miki
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KohnoKunihisa
en-aut-sei=Kohno
en-aut-mei=Kunihisa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=NakamuraKazufumi
en-aut-sei=Nakamura
en-aut-mei=Kazufumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=KoyamaYasushi
en-aut-sei=Koyama
en-aut-mei=Yasushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=ItoHiroshi
en-aut-sei=Ito
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

affil-num=1
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Density and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Density and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Cardiovascular Medicine, Japanese Red Cross Okayama Hospital
kn-affil=

affil-num=4
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Density and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Density and Pharmaceutical Sciences
kn-affil=

affil-num=6
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Density and Pharmaceutical Sciences
kn-affil=

affil-num=7
en-affil=Department of Cardiology, Sakurabashi Watanabe Hospital
kn-affil=

affil-num=8
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Density and Pharmaceutical Sciences
kn-affil=
en-keyword=coronary artery calcification
kn-keyword=coronary artery calcification
en-keyword=computed tomography
kn-keyword=computed tomography
en-keyword=endothelial progenitor cells
kn-keyword=endothelial progenitor cells
en-keyword=hypercholesterolemia
kn-keyword=hypercholesterolemia
END

start-ver=1.4
cd-journal=joma
no-vol=135
cd-vols=
no-issue=2
article-no=
start-page=95
end-page=97
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=20230801
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Overview of the 44th Annual Meeting of the Cardiac Biopsy Conference: Myocardial biopsy for clarification and treatment
kn-title=第44回心筋生検研究会学術集会報告― 解明と治療を目指す心筋生検―
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=NakamuraKazufumi
en-aut-sei=Nakamura
en-aut-mei=Kazufumi
kn-aut-name=中村一文
kn-aut-sei=中村
kn-aut-mei=一文
aut-affil-num=1
ORCID=

en-aut-name=YoshidaMasashi
en-aut-sei=Yoshida
en-aut-mei=Masashi
kn-aut-name=吉田賢司
kn-aut-sei=吉田
kn-aut-mei=賢司
aut-affil-num=2
ORCID=

affil-num=1
en-affil=Department of Cardiovascular Medicine, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=岡山大学学術研究院医歯薬学域　循環器内科学

affil-num=2
en-affil=Department of Chronic Kidney Disease and Cardiovascular Disease, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=岡山大学学術研究院医歯薬学域　CKD・CVD地域連携包括医療学講座
END

start-ver=1.4
cd-journal=joma
no-vol=12
cd-vols=
no-issue=15
article-no=
start-page=5028
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=20230731
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Evidence for Hypoxia-Induced Shift in ATP Production from Glycolysis to Mitochondrial Respiration in Pulmonary Artery Smooth Muscle Cells in Pulmonary Arterial Hypertension
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background: The metabolic state of pulmonary artery smooth muscle cells (PASMCs) from patients with pulmonary arterial hypertension (PAH) is not well understood. In this study, we examined the balance between glycolysis and mitochondrial respiration in non-PAH-PASMCs and PAH-PASMCs under normoxia and hypoxia. Methods: We investigated the enzymes involved in glycolysis and mitochondrial respiration, and studied the two major energy-yielding pathways (glycolysis and mitochondrial respiration) by measuring extracellular acidification rate (ECAR) and cellular oxygen consumption rate (OCR) using the Seahorse extracellular flux technology. Results: Under both normoxia and hypoxia, the mRNA and protein levels of pyruvate dehydrogenase kinase 1 and pyruvate dehydrogenase were increased in PAH-PASMCs compared with non-PAH-PASMCs. The mRNA and protein levels of lactate dehydrogenase, as well as the intracellular lactate concentration, were also increased in PAH-PASMCs compared with non-PAH-PASMCs under normoxia. However, these were not significantly increased in PAH-PASMCs compared with non-PAH-PASMCs under hypoxia. Under normoxia, ATP production was significantly lower in PAH-PASMCs (59 ± 5 pmol/min) than in non-PAH-PASMCs (70 ± 10 pmol/min). On the other hand, ATP production was significantly higher in PAH-PASMCs (31 ± 5 pmol/min) than in non-PAH-PASMCs (14 ± 3 pmol/min) under hypoxia. Conclusions: There is an underlying change in the metabolic strategy to generate ATP production under the challenge of hypoxia.
en-copyright=
kn-copyright=

en-aut-name=AkagiSatoshi
en-aut-sei=Akagi
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NakamuraKazufumi
en-aut-sei=Nakamura
en-aut-mei=Kazufumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KondoMegumi
en-aut-sei=Kondo
en-aut-mei=Megumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=HirohataSatoshi
en-aut-sei=Hirohata
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=UdonoHeiichiro
en-aut-sei=Udono
en-aut-mei=Heiichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=NishidaMikako
en-aut-sei=Nishida
en-aut-mei=Mikako
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=SaitoYukihiro
en-aut-sei=Saito
en-aut-mei=Yukihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=YoshidaMasashi
en-aut-sei=Yoshida
en-aut-mei=Masashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=MiyoshiToru
en-aut-sei=Miyoshi
en-aut-mei=Toru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=ItoHiroshi
en-aut-sei=Ito
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

affil-num=1
en-affil=Department of Cardiovascular Medicine, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Cardiovascular Medicine, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Cardiovascular Medicine, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=4
en-affil=Department of Medical Technology, Graduate School of Health Sciences, Okayama University
kn-affil=

affil-num=5
en-affil=Department of Immunology, Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=6
en-affil=Department of Immunology, Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=7
en-affil=Department of Cardiovascular Medicine, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=8
en-affil=Department of Cardiovascular Medicine, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=9
en-affil=Department of Cardiovascular Medicine, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=10
en-affil=Department of Cardiovascular Medicine, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=glycolysis
kn-keyword=glycolysis
en-keyword=mitochondrial respiration
kn-keyword=mitochondrial respiration
en-keyword=pulmonary arterial hypertension
kn-keyword=pulmonary arterial hypertension
en-keyword=pulmonary artery smooth muscle cells
kn-keyword=pulmonary artery smooth muscle cells
en-keyword=Seahorse technology
kn-keyword=Seahorse technology
en-keyword=hypoxia
kn-keyword=hypoxia
en-keyword=ATP production
kn-keyword=ATP production
END

start-ver=1.4
cd-journal=joma
no-vol=12
cd-vols=
no-issue=10
article-no=
start-page=e028706
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=20230516
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Significant Delayed Activation on the Right Ventricular Outflow Tract Represents Complete Right Bundle-Branch Block Pattern in Brugada Syndrome
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background: The appearance of complete right bundle-branch block (CRBBB) in Brugada syndrome (BrS) is associated with an increased risk of ventricular fibrillation. The pathophysiological mechanism of CRBBB in patients with BrS has not been well established. We aimed to clarify the significance of a conduction delay zone associated with arrhythmias on CRBBB using body surface mapping in patients with BrS. <br>
Methods and Results: Body surface mapping was recorded in 11 patients with BrS and 8 control patients both with CRBBB. CRBBB in control patients was transiently exhibited by unintentional catheter manipulation (proximal RBBB). Ventricular activation time maps were constructed for both of the groups. We divided the anterior chest into 4 areas (inferolateral right ventricle [RV], RV outflow tract [RVOT], intraventricular septum, and left ventricle) and compared activation patterns between the 2 groups. Excitation propagated to the RV from the left ventricle through the intraventricular septum with activation delay in the entire RV in the control group (proximal RBBB pattern). In 7 patients with BrS, excitation propagated from the inferolateral RV to the RVOT with significant regional activation delay. The remaining 4 patients with BrS showed a proximal RBBB pattern with the RVOT activation delay. The ventricular activation time in the inferolateral RV was significantly shorter in patients with BrS without a proximal RBBB pattern than in control patients. <br>
Conclusions: The CRBBB morphology in patients with BrS consisted of 2 mechanisms: (1) significantly delayed conduction in the RVOT and (2) proximal RBBB with RVOT conduction delay. Significant RVOT conduction delay without proximal RBBB resulted in CRBBB morphology in patients with BrS.
en-copyright=
kn-copyright=

en-aut-name=MorimotoYoshimasa
en-aut-sei=Morimoto
en-aut-mei=Yoshimasa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MoritaHiroshi
en-aut-sei=Morita
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=EjiriKentaro
en-aut-sei=Ejiri
en-aut-mei=Kentaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MizunoTomofumi
en-aut-sei=Mizuno
en-aut-mei=Tomofumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=MasudaTakuro
en-aut-sei=Masuda
en-aut-mei=Takuro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=UeokaAkira
en-aut-sei=Ueoka
en-aut-mei=Akira
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=AsadaSaori
en-aut-sei=Asada
en-aut-mei=Saori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=MiyamotoMasakazu
en-aut-sei=Miyamoto
en-aut-mei=Masakazu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=KawadaSatoshi
en-aut-sei=Kawada
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=NakagawaKoji
en-aut-sei=Nakagawa
en-aut-mei=Koji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=NishiiNobuhiro
en-aut-sei=Nishii
en-aut-mei=Nobuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=NakamuraKazufumi
en-aut-sei=Nakamura
en-aut-mei=Kazufumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=ItoHiroshi
en-aut-sei=Ito
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

affil-num=1
en-affil=Department of Cardiovascular Medicine ,Okayama University Graduate School of Medicine, Dentistry, Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Cardiovascular Therapeutics , Okayama University Graduate School of Medicine, Dentistry, Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Cardiovascular Medicine ,Okayama University Graduate School of Medicine, Dentistry, Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of Cardiovascular Medicine ,Okayama University Graduate School of Medicine, Dentistry, Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of Cardiovascular Medicine ,Okayama University Graduate School of Medicine, Dentistry, Pharmaceutical Sciences
kn-affil=

affil-num=6
en-affil=Department of Cardiovascular Medicine ,Okayama University Graduate School of Medicine, Dentistry, Pharmaceutical Sciences
kn-affil=

affil-num=7
en-affil=Department of Cardiovascular Medicine ,Okayama University Graduate School of Medicine, Dentistry, Pharmaceutical Sciences
kn-affil=

affil-num=8
en-affil=Department of Cardiovascular Medicine ,Okayama University Graduate School of Medicine, Dentistry, Pharmaceutical Sciences
kn-affil=

affil-num=9
en-affil=Department of Cardiovascular Medicine ,Okayama University Graduate School of Medicine, Dentistry, Pharmaceutical Sciences
kn-affil=

affil-num=10
en-affil=Department of Cardiovascular Medicine ,Okayama University Graduate School of Medicine, Dentistry, Pharmaceutical Sciences
kn-affil=

affil-num=11
en-affil=Department of Cardiovascular Therapeutics , Okayama University Graduate School of Medicine, Dentistry, Pharmaceutical Sciences
kn-affil=

affil-num=12
en-affil=Department of Cardiovascular Medicine ,Okayama University Graduate School of Medicine, Dentistry, Pharmaceutical Sciences
kn-affil=

affil-num=13
en-affil=Department of Cardiovascular Medicine ,Okayama University Graduate School of Medicine, Dentistry, Pharmaceutical Sciences
kn-affil=
en-keyword=activation pattern
kn-keyword=activation pattern
en-keyword=body surface map
kn-keyword=body surface map
en-keyword=Brugada syndrome
kn-keyword=Brugada syndrome
en-keyword=complete right bundle-branch block
kn-keyword=complete right bundle-branch block
END

start-ver=1.4
cd-journal=joma
no-vol=12
cd-vols=
no-issue=6
article-no=
start-page=e027046
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=20230321
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Heat Exposure Following the Rainy Season Is Associated With an Increased Risk of Cardiovascular Emergency Among the Elderly in Japan
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background: Despite the impact of heat exposure caused by global warming, few studies have investigated the hourly effects of heat exposure and the risk of cardiovascular disease (CVD) in the elderly. We examined the associations between short-term heat exposure and the risk of CVD in the elderly in Japan and evaluated possible effect-measure modifications by rainy seasons that occur in East Asia. <br>
Methods and Results: We conducted a time-stratified case-crossover study. The study included 6527 residents in Okayama City, Japan, aged >= 65 years who were transported to emergency hospitals between 2012 and 2019 for the onset of CVD during and a few months after the rainy seasons. We examined the linear associations between temperature and CVD-related emergency calls for each year and for hourly preceding intervals before the emergency call during the most relevant months. Heat exposure during 1 month after the end of the rainy season was associated with CVD risk; the odds ratio (OR) for a 1 degrees C increase in temperature was 1.34 (95% CI, 1.29-1.40). When we further explored the nonlinear association by using the natural cubic spline model, we found a J-shaped relationship. Exposures 0 to 6 hours before the case event (preceding intervals 0-6 hours) were associated with CVD risk, particularly for the preceding interval 0 to 1 hour (OR, 1.33 [95% CI, 1.28-1.39]). For longer periods, the highest risk was at preceding intervals 0 to 23 hours (OR, 1.40 [95% CI, 1.34-1.46]).<br> 
Conclusions: Elderly individuals may be more susceptible to CVD after heat exposure during the month after the rainy season. As shown by finer temporal resolution analyses, short-term exposure to increasing temperature can trigger CVD onset.
en-copyright=
kn-copyright=

en-aut-name=FujimotoRyohei
en-aut-sei=Fujimoto
en-aut-mei=Ryohei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=SuzukiEtsuji
en-aut-sei=Suzuki
en-aut-mei=Etsuji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KashimaSaori
en-aut-sei=Kashima
en-aut-mei=Saori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=NakamuraKazufumi
en-aut-sei=Nakamura
en-aut-mei=Kazufumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=NaitoHiromichi
en-aut-sei=Naito
en-aut-mei=Hiromichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=NakaoAtsunori
en-aut-sei=Nakao
en-aut-mei=Atsunori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=ItoHiroshi
en-aut-sei=Ito
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=YorifujiTakashi
en-aut-sei=Yorifuji
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

affil-num=1
en-affil=Department of Epidemiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Epidemiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University 
kn-affil=

affil-num=3
en-affil=Environmental Health Sciences Laboratory, Graduate School of Advanced Science and Engineering, Hiroshima University
kn-affil=

affil-num=4
en-affil=Department of Cardiovascular Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=5
en-affil=Department of Emergency, Critical Care and Disaster Medicine, Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=6
en-affil=Department of Emergency, Critical Care and Disaster Medicine, Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=7
en-affil=Department of Cardiovascular Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=8
en-affil=Department of Epidemiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=cardiovascular disease
kn-keyword=cardiovascular disease
en-keyword=climate change
kn-keyword=climate change
en-keyword=end of the rainy season
kn-keyword=end of the rainy season
en-keyword=heat exposure
kn-keyword=heat exposure
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=20230327
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Prevalence of transthyretin amyloidosis among heart failure patients with preserved ejection fraction in Japan
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Aims Heart failure with preserved ejection fraction (HFpEF), which is caused by wide various conditions, has become a major public health problem. Transthyretin amyloid cardiomyopathy (ATTR-CM), which is thought to be an underdiagnosed disease, can cause HFpEF. Non-invasive diagnosis using 99mTechnetium (Tc)-pyrophosphate (PYP) scintigraphy enables accurate diagnosis of ATTR-CM. The aim of this study was to clarify the prevalence and characteristics of ATTR-CM among Japanese patients with HFpEF.<br>
Methods and results This study was a multicentre, prospective, observational study conducted in Japan. We enrolled 373 patients with HFpEF [left ventricular (LV) ejection fraction ?50%] aged ?65 years who were admitted to the department of cardiology from September 2018 to January 2022. A 99mTc-PYP scintigraphy scan was performed during admission in all eligible patients. Cardiac 99mTc-PYP retention was graded according to a previously reported visual scale ranging from 0 to 3 points. The scan was considered positive when it revealed moderate-to-severe 99mTc-PYP uptake (Grade 2?3) in both ventricles. Patients were divided into ATTR-CM and non-ATTR-CM patients according to positive (Grade 2?3) or negative (Grade 0?1) 99mTc-PYP scintigraphy, respectively. Medical history, blood tests, electrocardiogram, echocardiography, and magnetic resonance imaging in the two groups of patients were compared. Among the 373 patients with HFpEF, 53 patients (14.2%; 95% confidence interval: 10.7?17.7) showed positive uptake on 99mTc-PYP scintigraphy. An endomyocardial biopsy was performed in 32 patients and confirmed amyloidosis in all cases. There were no significant differences between the two groups in age, severity of heart failure as assessed by the New York Heart Association (NYHA) functional classification, renal function values, left ventricular ejection fraction, and tricuspid regurgitant pressure gradient (ATTR-CM, n = 53 vs. non-ATTR-CM, n = 320). Patients in the ATTR-CM group had a higher N-terminal pro-brain natriuretic peptide level [2314 (1081?3398) vs. 900 (415?1828), P < 0.001], higher sensitive troponin T level (0.074 ± 0.049 vs. 0.035 ± 0.038, P < 0.001), and higher mean LV maximal wall thickness [12.5 (11?14) vs. 10.5 (9.5?11.5), P < 0.001].<br>
Conclusions ATTR-CM is an underdiagnosed disease with a significant prevalence in Japanese patients with HFpEF. This study showed that results of examinations for ATTR-CM patients appear to be worse than those for non-ATTR-CM patients, but clinical severities of heart failure as assessed by the NYHA functional classification are similar in ATTR-CM and non-ATTR-CM patients, and the clinical overlap between ATTR-CM and non-ATTR-CM is high.
en-copyright=
kn-copyright=

en-aut-name=NaitoTakanori
en-aut-sei=Naito
en-aut-mei=Takanori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NakamuraKazufumi
en-aut-sei=Nakamura
en-aut-mei=Kazufumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=AbeYukio
en-aut-sei=Abe
en-aut-mei=Yukio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=WatanabeHiroyuki
en-aut-sei=Watanabe
en-aut-mei=Hiroyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=SakuragiSatoru
en-aut-sei=Sakuragi
en-aut-mei=Satoru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=KatayamaYusuke
en-aut-sei=Katayama
en-aut-mei=Yusuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=KiharaHajime
en-aut-sei=Kihara
en-aut-mei=Hajime
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=OkizakiAtsutaka
en-aut-sei=Okizaki
en-aut-mei=Atsutaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=KawaiYusuke
en-aut-sei=Kawai
en-aut-mei=Yusuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=YoshikawaMasaki
en-aut-sei=Yoshikawa
en-aut-mei=Masaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=TakaishiAtsushi
en-aut-sei=Takaishi
en-aut-mei=Atsushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=FujioHideki
en-aut-sei=Fujio
en-aut-mei=Hideki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=OtsukaHiroaki
en-aut-sei=Otsuka
en-aut-mei=Hiroaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=OguraSoichiro
en-aut-sei=Ogura
en-aut-mei=Soichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=ItoHiroshi
en-aut-sei=Ito
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

en-aut-name=ATTR HFpEF Registry Investigators
en-aut-sei=ATTR HFpEF Registry Investigators
en-aut-mei=
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=16
ORCID=

affil-num=1
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Cardiology, Osaka City General Hospital
kn-affil=

affil-num=4
en-affil=Department of Cardiovascular Medicine, Tokyo Bay Urayasu Ichikawa Medical Center
kn-affil=

affil-num=5
en-affil=Department of Cardiovascular Medicine, National Hospital Organization Iwakuni Clinical Center
kn-affil=

affil-num=6
en-affil=Department of Cardiovascular Medicine, National Hospital Organization Iwakuni Clinical Center
kn-affil=

affil-num=7
en-affil=Department of Internal Medicine, Kihara Cardiovascular Clinic
kn-affil=

affil-num=8
en-affil=Department of Radiology, Asahikawa Medical University
kn-affil=

affil-num=9
en-affil=Department of Cardiovascular Medicine, Okayama City Hospital
kn-affil=

affil-num=10
en-affil=Department of Cardiovascular Medicine, Fukuyama City Hospital
kn-affil=

affil-num=11
en-affil=Department of Cardiology, Mitoyo General Hospital
kn-affil=

affil-num=12
en-affil=Department of Cardiovascular Medicine, Japanese Red Cross Society Himeji Hospital
kn-affil=

affil-num=13
en-affil=Department of Cardiovascular Medicine, National Hospital Organization Iwakuni Clinical Center
kn-affil=

affil-num=14
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=15
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=16
en-affil=
kn-affil=
en-keyword=Transthyretin amyloidosis
kn-keyword=Transthyretin amyloidosis
en-keyword=Heart failure
kn-keyword=Heart failure
en-keyword=Scintigraphy
kn-keyword=Scintigraphy
en-keyword=Left ventricular hypertrophy
kn-keyword=Left ventricular hypertrophy
END

start-ver=1.4
cd-journal=joma
no-vol=15
cd-vols=
no-issue=3
article-no=
start-page=748
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=20230201
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Association between Cardiovascular Disease and Liver Disease, from a Clinically Pragmatic Perspective as a Cardiologist
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Cardiovascular diseases and liver diseases are closely related. Non-alcoholic fatty liver disease has the same risk factors as those for atherosclerotic cardiovascular disease and may also be a risk factor for atherosclerotic cardiovascular disease on its own. Heart failure causes liver fibrosis, and liver fibrosis results in worsened cardiac preload and congestion. Although some previous reports regard the association between cardiovascular diseases and liver disease, the management strategy for liver disease in patients with cardiovascular diseases is not still established. This review summarized the association between cardiovascular diseases and liver disease. In patients with non-alcoholic fatty liver disease, the degree of liver fibrosis progresses with worsening cardiovascular prognosis. In patients with heart failure, liver fibrosis could be a prognostic marker. Liver stiffness assessed with shear wave elastography, the fibrosis-4 index, and non-alcoholic fatty liver disease fibrosis score is associated with both liver fibrosis in patients with liver diseases and worse prognosis in patients with heart failure. With the current population ageing, the importance of management for cardiovascular diseases and liver disease has been increasing. However, whether management and interventions for liver disease improve the prognosis of cardiovascular diseases has not been fully understood. Future investigations are needed.
en-copyright=
kn-copyright=

en-aut-name=NakashimaMitsutaka
en-aut-sei=Nakashima
en-aut-mei=Mitsutaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NakamuraKazufumi
en-aut-sei=Nakamura
en-aut-mei=Kazufumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=NishiharaTakahiro
en-aut-sei=Nishihara
en-aut-mei=Takahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=IchikawaKeishi
en-aut-sei=Ichikawa
en-aut-mei=Keishi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=NakayamaRie
en-aut-sei=Nakayama
en-aut-mei=Rie
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=TakayaYoichi
en-aut-sei=Takaya
en-aut-mei=Yoichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=TohNorihisa
en-aut-sei=Toh
en-aut-mei=Norihisa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=AkagiSatoshi
en-aut-sei=Akagi
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=MiyoshiToru
en-aut-sei=Miyoshi
en-aut-mei=Toru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=AkagiTeiji
en-aut-sei=Akagi
en-aut-mei=Teiji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=ItoHiroshi
en-aut-sei=Ito
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

affil-num=1
en-affil=Department of Cardiovascular Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Cardiovascular Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Cardiovascular Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=4
en-affil=Department of Cardiovascular Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=5
en-affil=Department of Cardiovascular Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=6
en-affil=Department of Cardiovascular Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=7
en-affil=Department of Cardiovascular Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=8
en-affil=Department of Cardiovascular Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=9
en-affil=Department of Cardiovascular Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=10
en-affil=Department of Cardiovascular Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=11
en-affil=Department of Cardiovascular Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=liver disease
kn-keyword=liver disease
en-keyword=heart failure
kn-keyword=heart failure
en-keyword=atherosclerotic cardiovascular disease
kn-keyword=atherosclerotic cardiovascular disease
en-keyword=non-alcoholic fatty liver disease
kn-keyword=non-alcoholic fatty liver disease
END

start-ver=1.4
cd-journal=joma
no-vol=24
cd-vols=
no-issue=3
article-no=
start-page=1921
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=202302
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Microcalcification and Tc-99m-Pyrophosphate Uptake without Increased Bone Metabolism in Cardiac Tissue from Patients with Transthyretin Cardiac Amyloidosis
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Transthyretin cardiac amyloidosis (ATTR-CA) is characterized by high Tc-99m-labeled bone tracer uptake in the heart. However, the mechanism of bone tracer uptake into the heart remains controversial. Since bone tracer uptake into metastatic bone tumors is thought to be associated with increased bone metabolism, we examined Tc-99m-pyrophosphate (PYP) scintigraphy findings, endomyocardial biopsy (EMB) tissue findings, and the expression of bone metabolism-related genes in the EMB tissues in patients with ATTR-CA, amyloid light-chain cardiac amyloidosis (AL-CA), and noncardiac amyloidosis (non-CA) in this study. The uptake of Tc-99m-PYP in the heart was significantly higher in the ATTR-CA patients than in the AL-CA and non-CA patients. A higher percentage of ATTR-CA EMB tissue showed von Kossa-positive microparticles: ATTR-CA, 62%; AL-CA, 33%; and non-CA, 0%. Calcified microparticles were identified using transmission electron microscopy. However, none of the osteogenic marker genes, osteoclastic marker genes, or phosphate/pyrophosphate-related genes were upregulated in the EMB samples from ATTR-CA patients compared to those from AL-CA and non-CA patients. These results suggest that active calcification-promoting mechanisms are not involved in the microcalcification observed in the heart in ATTR-CA. The mechanisms explaining bone tracer uptake in the heart, which is stronger than that in the ribs, require further investigation.
en-copyright=
kn-copyright=

en-aut-name=MoriAtsushi
en-aut-sei=Mori
en-aut-mei=Atsushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=SaitoYukihiro
en-aut-sei=Saito
en-aut-mei=Yukihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=NakamuraKazufumi
en-aut-sei=Nakamura
en-aut-mei=Kazufumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=IidaToshihiro
en-aut-sei=Iida
en-aut-mei=Toshihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=AkagiSatoshi
en-aut-sei=Akagi
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=YoshidaMasashi
en-aut-sei=Yoshida
en-aut-mei=Masashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=TaniyamaMakiko
en-aut-sei=Taniyama
en-aut-mei=Makiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=MiyoshiToru
en-aut-sei=Miyoshi
en-aut-mei=Toru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=ItoHiroshi
en-aut-sei=Ito
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

affil-num=1
en-affil=Department of Cardiovascular Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Cardiovascular Medicine, Okayama University Hospital
kn-affil=

affil-num=3
en-affil=Department of Cardiovascular Medicine, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=4
en-affil=Department of Cardiovascular Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=5
en-affil=Department of Cardiovascular Medicine, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=6
en-affil=Department of Chronic Kidney Disease and Cardiovascular Disease, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=7
en-affil=Department of General Medicine, Tamano Division, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=8
en-affil=Department of Cardiovascular Medicine, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=9
en-affil=Department of Cardiovascular Medicine, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=ATTR
kn-keyword=ATTR
en-keyword=Tc-99m-labeled bone scintigraphy
kn-keyword=Tc-99m-labeled bone scintigraphy
en-keyword=calcified microparticle
kn-keyword=calcified microparticle
END

start-ver=1.4
cd-journal=joma
no-vol=10
cd-vols=
no-issue=11
article-no=
start-page=e06552
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2022
dt-pub=20221106
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=A hyperechoic mass in femoral vein
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Here, we present a case of fat embolism syndrome (FES) in which ultrasound sonography and computed tomography successfully visualized fat embolus in the femoral vein. A multimodality approach was particularly useful for early and specific diagnosis.
en-copyright=
kn-copyright=

en-aut-name=KakuNaoko
en-aut-sei=Kaku
en-aut-mei=Naoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=SugiyamaHiroki
en-aut-sei=Sugiyama
en-aut-mei=Hiroki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=NakamuraKazufumi
en-aut-sei=Nakamura
en-aut-mei=Kazufumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=FurutaniTomoki
en-aut-sei=Furutani
en-aut-mei=Tomoki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=HongoTakashi
en-aut-sei=Hongo
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=ItoHiroshi
en-aut-sei=Ito
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

affil-num=1
en-affil=Department of Internal Medicine, Okayama Saiseikai General Hospital
kn-affil=

affil-num=2
en-affil=Department of Internal Medicine, Okayama Saiseikai General Hospital
kn-affil=

affil-num=3
en-affil=Department of Cardiovascular Medicine, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=4
en-affil=Department of Orthopedic surgery, Okayama Saiseikai General Hospital
kn-affil=

affil-num=5
en-affil=Department of Emergency medicine, Okayama Saiseikai General Hospital
kn-affil=

affil-num=6
en-affil=Department of Cardiovascular Medicine, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=bone fractures
kn-keyword=bone fractures
en-keyword=fat embolism syndrome
kn-keyword=fat embolism syndrome
END

start-ver=1.4
cd-journal=joma
no-vol=9
cd-vols=
no-issue=11
article-no=
start-page=368
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2022
dt-pub=20221025
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Cardio-Ankle Vascular Index as an Arterial Stiffness Marker Improves the Prediction of Cardiovascular Events in Patients without Cardiovascular Diseases
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Several studies have reported that the cardio-ankle vascular index (CAVI), a non-invasive measurement of arterial stiffness, is associated with the incidence of cardiovascular events. We investigated whether adding CAVI to a risk score improves the prediction of cardiovascular events in the setting of primary prevention. This retrospective observational study included consecutive 554 outpatients with cardiovascular disease risk factors but without known cardiovascular disease (68 +/- 9 years, 64% men). The CAVI was measured using the VaSera vascular screening system. Major adverse cardiovascular events (MACE) included cardiovascular death, myocardial infarction, stroke, hospitalization for heart failure, and coronary revascularization. During a median follow-up of 4.3 years, cardiovascular events occurred in 65 patients (11.7%). Multivariate Cox analysis showed that abnormal CAVI (>9.0) was significantly associated with the incidence of MACE (hazard ratio 2.31, 95% confidence interval 1.27-4.18). The addition of CAVI to the Suita score, a conventional risk score for coronary heart disease in Japan, significantly improved the C statics from 0.642 to 0.713 (p = 0.04). In addition to a conventional risk score, CAVI improved the prediction of cardiovascular events in patients with cardiovascular disease risk factors but without known cardiovascular diseases.
en-copyright=
kn-copyright=

en-aut-name=OkamotoYuko
en-aut-sei=Okamoto
en-aut-mei=Yuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MiyoshiToru
en-aut-sei=Miyoshi
en-aut-mei=Toru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=IchikawaKeishi
en-aut-sei=Ichikawa
en-aut-mei=Keishi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TakayaYoichi
en-aut-sei=Takaya
en-aut-mei=Yoichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=NakamuraKazufumi
en-aut-sei=Nakamura
en-aut-mei=Kazufumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=ItoHiroshi
en-aut-sei=Ito
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

affil-num=1
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=6
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=arterial stiffness
kn-keyword=arterial stiffness
en-keyword=cardio-ankle vascular index
kn-keyword=cardio-ankle vascular index
en-keyword=cardiovascular events
kn-keyword=cardiovascular events
en-keyword=risk factors
kn-keyword=risk factors
END

start-ver=1.4
cd-journal=joma
no-vol=12
cd-vols=
no-issue=1
article-no=
start-page=15449
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2022
dt-pub=20220914
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Effects of luseogliflozin and voglibose on high-risk lipid profiles and inflammatory markers in diabetes patients with heart failure
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Sodium-glucose cotransporter 2 inhibitors could reduce cardiovascular events in patients with heart failure irrespective of diabetes status. In this prespecified sub-analysis of randomised-controlled trial, we investigated the efficacy of luseogliflozin (2.5 mg daily), a sodium-glucose cotransporter 2 inhibitor, with that of voglibose (0.6 mg daily), an alpha-glucosidase inhibitor, on high-risk lipid profile and inflammatory markers in patients with type-2 diabetes and heart failure. Among the 157 patients studied, there were no significant differences in the mean malondialdehyde LDL or small-dense LDL cholesterol levels between the luseogliflozin and voglibose groups (percent change: 0.2% vs. - 0.6%, p = 0.93; - 1.7% vs. - 8.6%, p= 0.21) after 12 weeks in comparison to levels at the baseline. No significant difference was observed between the two groups in the adiponectin and high-sensitivity C-reactive protein levels after 12 weeks compared to the baseline levels (percent change, - 1.6% vs. - 4.0% and 22.5% vs. 10.0%; p = 0.52 and p = 0.55, respectively). In conclusion, in patients with type-2 diabetes and heart failure, compared to voglibose, luseogliflozin did not significantly improve the high-risk lipoprotein profile including malondialdehyde LDL and small-dense LDL cholesterol or the levels of inflammatory markers, including adiponectin and high-sensitivity C-reactive protein.
en-copyright=
kn-copyright=

en-aut-name=EjiriKentaro
en-aut-sei=Ejiri
en-aut-mei=Kentaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MiyoshiToru
en-aut-sei=Miyoshi
en-aut-mei=Toru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KiharaHajime
en-aut-sei=Kihara
en-aut-mei=Hajime
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=HataYoshiki
en-aut-sei=Hata
en-aut-mei=Yoshiki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=NaganoToshihiko
en-aut-sei=Nagano
en-aut-mei=Toshihiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=TakaishiAtsushi
en-aut-sei=Takaishi
en-aut-mei=Atsushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=TodaHironobu
en-aut-sei=Toda
en-aut-mei=Hironobu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=NambaSeiji
en-aut-sei=Namba
en-aut-mei=Seiji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=NakamuraYoichi
en-aut-sei=Nakamura
en-aut-mei=Yoichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=AkagiSatoshi
en-aut-sei=Akagi
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=SakuragiSatoru
en-aut-sei=Sakuragi
en-aut-mei=Satoru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=MinagawaTaro
en-aut-sei=Minagawa
en-aut-mei=Taro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=KawaiYusuke
en-aut-sei=Kawai
en-aut-mei=Yusuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=NishiiNobuhiro
en-aut-sei=Nishii
en-aut-mei=Nobuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=FukeSoichiro
en-aut-sei=Fuke
en-aut-mei=Soichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

en-aut-name=YoshikawaMasaki
en-aut-sei=Yoshikawa
en-aut-mei=Masaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=16
ORCID=

en-aut-name=NakamuraKazufumi
en-aut-sei=Nakamura
en-aut-mei=Kazufumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=17
ORCID=

en-aut-name=ItoHiroshi
en-aut-sei=Ito
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=18
ORCID=

en-aut-name=The MUSCAT-HF Study  Investigators
en-aut-sei=The MUSCAT-HF Study  Investigators
en-aut-mei=
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=19
ORCID=

affil-num=1
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and  Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and  Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Internal Medicine, Kihara Cardiovascular Clinic
kn-affil=

affil-num=4
en-affil=Department of Cardiology, Minamino Cardiovascular Hospital
kn-affil=

affil-num=5
en-affil=Department  of Internal Medicine, Iwasa Hospital
kn-affil=

affil-num=6
en-affil=Department of Cardiology, Mitoyo General Hospital
kn-affil=

affil-num=7
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and  Pharmaceutical Sciences
kn-affil=

affil-num=8
en-affil=Department  of Cardiology, Okayama Rosai Hospital
kn-affil=

affil-num=9
en-affil=Department of Cardiovascular Medicine, Specifed  Clinic of Soyokaze Cardiovascular Medicine and Diabetes Care
kn-affil=

affil-num=10
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and  Pharmaceutical Sciences
kn-affil=

affil-num=11
en-affil=Department of Cardiovascular Medicine,  Iwakuni Clinical Center
kn-affil=

affil-num=12
en-affil=Department of Internal Medicine, Minagawa Cardiovascular Clinic
kn-affil=

affil-num=13
en-affil=Department of Cardiovascular Medicine, Okayama City Hospital
kn-affil=

affil-num=14
en-affil=Department  of Internal Medicine, Yoshinaga Hospital
kn-affil=

affil-num=15
en-affil=Department of Cardiovascular Medicine, Japanese Red  Cross Okayama Hospital
kn-affil=

affil-num=16
en-affil=Department of Cardiology, Fukuyama City Hospital
kn-affil=

affil-num=17
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and  Pharmaceutical Sciences
kn-affil=

affil-num=18
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and  Pharmaceutical Sciences
kn-affil=

affil-num=19
en-affil=
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=86
cd-vols=
no-issue=8
article-no=
start-page=1312
end-page=1318
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2022
dt-pub=2022725
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Overview of the 86th Annual Scientific Meeting of the Japanese Circulation Society　― Cardiology Spreading Its Wings ―
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The 86th Annual Scientific Meeting of the Japanese Circulation Society was held in a web-based format on March 11-13, 2022. In accordance with the internationalization policy of the JCS, the meeting was held with the Asian Pacific Society of Cardiology Congress 2022. The main theme was "Cardiology Spreading its Wings". The number of patients with heart failure and other cardiovascular diseases is increasing dramatically, and the fields dealt with by cardiovascular medicine are also greatly expanding. This conference was both intellectually satisfying and exciting for all participants, who numbered over 14,900. The meeting was completed with great success, and the enormous amount of cooperation and support from all involved was greatly appreciated.
en-copyright=
kn-copyright=

en-aut-name=NakamuraKazufumi
en-aut-sei=Nakamura
en-aut-mei=Kazufumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MiyoshiToru
en-aut-sei=Miyoshi
en-aut-mei=Toru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=AkagiSatoshi
en-aut-sei=Akagi
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TohNorihisa
en-aut-sei=Toh
en-aut-mei=Norihisa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=SaitoYukihiro
en-aut-sei=Saito
en-aut-mei=Yukihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=TakayaYoichi
en-aut-sei=Takaya
en-aut-mei=Yoichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=YoshidaMasatoki
en-aut-sei=Yoshida
en-aut-mei=Masatoki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=NakagawaKoji
en-aut-sei=Nakagawa
en-aut-mei=Koji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=KawadaSatoshi
en-aut-sei=Kawada
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=TodaHironobu
en-aut-sei=Toda
en-aut-mei=Hironobu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=MikiTakashi
en-aut-sei=Miki
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=NakayamaRie
en-aut-sei=Nakayama
en-aut-mei=Rie
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=YokohamaFumi
en-aut-sei=Yokohama
en-aut-mei=Fumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=IchikawaKeishi
en-aut-sei=Ichikawa
en-aut-mei=Keishi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=YoshidaMasashi
en-aut-sei=Yoshida
en-aut-mei=Masashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

en-aut-name=TaniyamaMakiko
en-aut-sei=Taniyama
en-aut-mei=Makiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=16
ORCID=

en-aut-name=NishiiNobuhiro
en-aut-sei=Nishii
en-aut-mei=Nobuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=17
ORCID=

en-aut-name=AkagiTeiji
en-aut-sei=Akagi
en-aut-mei=Teiji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=18
ORCID=

en-aut-name=MoritaHiroshi
en-aut-sei=Morita
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=19
ORCID=

en-aut-name=ItoHiroshi
en-aut-sei=Ito
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=20
ORCID=

affil-num=1
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=6
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=7
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=8
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=9
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=10
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=11
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=12
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=13
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=14
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=15
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=16
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=17
en-affil=Department of Cardiovascular Therapeutics, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=18
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=19
en-affil=Department of Cardiovascular Therapeutics, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=20
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=Cardiology
kn-keyword=Cardiology
en-keyword=Heart failure
kn-keyword=Heart failure
en-keyword=Internationalization
kn-keyword=Internationalization
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2022
dt-pub=20220731
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=High platelet reactivity is a predictor of left ventricular remodelling in patients with acute myocardial infarction
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Aims Acute myocardial infarction (AMI) is associated with left ventricular remodelling (LVR), which leads to progressive heart failure. Platelets play a pivotal role in promoting systemic and cardiac inflammatory responses during the complex process of myocardial wound healing or repair following AMI. This study aimed to investigate the impact of platelet reactivity immediately after primary percutaneous coronary intervention (PCI) on LVR in AMI patients with ST-segment (STEMI) and nonST-segment elevation (NSTEMI). <br>
Methods and results This prospective, single-centre, observational study included 182 patients with AMI who underwent primary PCI (107 patient with STEMI and 75 patients with NSTEMI). Patients were administered a loading dose of aspirin plus prasugrel before the procedure, and platelet reactivity was assessed using the VerifyNow P2Y12 assay immediately after PCI. Echocardiography was performed before discharge and during the chronic phase (8 +/- 3 months after discharge). LVR was defined as a relative >= 20% increase in left ventricular end-diastolic volume index (LVEDVI). LVR in chronic phase was found in 34 patients (18.7%) whose platelet reactivity was significantly higher than those without LVR (259.6 +/- 61.5 and 213.1 +/- 74.8 P2Y12 reaction units [PRU]; P = 0.001). The occurrence of LVR did not differ between patients with STEMI and patients with NSTEMI (21.5% and 14.7%; P = 0.33). The optimal cut-off value of platelet reactivity for discriminating LVR was >= 245 PRU. LVEDVI significantly decreased at chronic phase in patients without high platelet reactivity (<245 PRU) (from 49.2 +/- 13.5 to 45.4 +/- 15.8 ml/m(2); P = 0.02), but not in patients with high platelet reactivity (>= d245 PRU) (P = 0.06). Multivariate logistic analysis showed that high platelet reactivity was an independent predictor of LVR after adjusting for LVEDVI before discharge (odds ratio, 4.13; 95% confidence interval, 1.85-9.79). <br>
Conclusions High platelet reactivity measured immediately after PCI was a predictor of LVR in patients with AMI during the chronic phase. The role of antiplatelet therapy on inflammation in the myocardium is a promising area for further research.
en-copyright=
kn-copyright=

en-aut-name=TsujiMasahiro
en-aut-sei=Tsuji
en-aut-mei=Masahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KawaiYusuke
en-aut-sei=Kawai
en-aut-mei=Yusuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=MiyoshiToru
en-aut-sei=Miyoshi
en-aut-mei=Toru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=SaitoEisuke
en-aut-sei=Saito
en-aut-mei=Eisuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KawamuraKohei
en-aut-sei=Kawamura
en-aut-mei=Kohei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=OnoTamaki
en-aut-sei=Ono
en-aut-mei=Tamaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=TokiokaKoji
en-aut-sei=Tokioka
en-aut-mei=Koji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=OheTohru
en-aut-sei=Ohe
en-aut-mei=Tohru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=NakamuraKazufumi
en-aut-sei=Nakamura
en-aut-mei=Kazufumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=ItoHiroshi
en-aut-sei=Ito
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

affil-num=1
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Cardiovascular Medicine, Okayama City Hospital
kn-affil=

affil-num=3
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of Cardiovascular Medicine, Okayama City Hospital
kn-affil=

affil-num=5
en-affil=Department of Cardiovascular Medicine, Okayama City Hospital
kn-affil=

affil-num=6
en-affil=Department of Cardiovascular Medicine, Okayama City Hospital
kn-affil=

affil-num=7
en-affil=Department of Cardiovascular Medicine, Okayama City Hospital
kn-affil=

affil-num=8
en-affil=Department of Cardiovascular Medicine, Okayama City Hospital
kn-affil=

affil-num=9
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences 
kn-affil=

affil-num=10
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences 
kn-affil=
en-keyword=Myocardial infarction
kn-keyword=Myocardial infarction
en-keyword=Left ventricular remodelling
kn-keyword=Left ventricular remodelling
en-keyword=Platelet reactivity
kn-keyword=Platelet reactivity
en-keyword=Inflammation
kn-keyword=Inflammation
en-keyword=Reverse remodelling
kn-keyword=Reverse remodelling
en-keyword=Prasugrel
kn-keyword=Prasugrel
END

start-ver=1.4
cd-journal=joma
no-vol=9
cd-vols=
no-issue=
article-no=
start-page=904215
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2022
dt-pub=20220630
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Pemafibrate Prevents Rupture of Angiotensin II-Induced Abdominal Aortic Aneurysms
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background: Abdominal aortic aneurysm (AAA) is a life-threatening disease that lacks effective preventive therapies. This study aimed to evaluate the effect of pemafibrate, a selective peroxisome proliferator-activated receptor alpha (PPAR alpha) agonist, on AAA formation and rupture. <br>
Methods: Experimental AAA was induced by subcutaneous angiotensin II (AngII) infusion in ApoE(-)(/)(-) mice for 4 weeks. Pemafibrate (0.1 mg/kg/day) was administered orally. Dihydroethidium staining was used to evaluate the reactive oxygen species (ROS). <br>
Results: The size of the AngII-induced AAA did not differ between pemafibrate- and vehicle-treated groups. However, a decreased mortality rate due to AAA rupture was observed in pemafibrate-treated mice. Pemafibrate ameliorated AngII-induced ROS and reduced the mRNA expression of interleukin-6 and tumor necrosis factor-alpha in the aortic wall. Gelatin zymography analysis demonstrated significant inhibition of matrix metalloproteinase-2 activity by pemafibrate. AngII-induced ROS production in human vascular smooth muscle cells was inhibited by pre-treatment with pemafibrate and was accompanied by an increase in catalase activity. Small interfering RNA-mediated knockdown of catalase or PPAR alpha significantly attenuated the anti-oxidative effect of pemafibrate. <br>
Conclusion: Pemafibrate prevented AAA rupture in a murine model, concomitant with reduced ROS, inflammation, and extracellular matrix degradation in the aortic wall. The protective effect against AAA rupture was partly mediated by the anti-oxidative effect of catalase induced by pemafibrate in the smooth muscle cells.
en-copyright=
kn-copyright=

en-aut-name=AmiokaNaofumi
en-aut-sei=Amioka
en-aut-mei=Naofumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MiyoshiToru
en-aut-sei=Miyoshi
en-aut-mei=Toru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=YonezawaTomoko
en-aut-sei=Yonezawa
en-aut-mei=Tomoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KondoMegumi
en-aut-sei=Kondo
en-aut-mei=Megumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=AkagiSatoshi
en-aut-sei=Akagi
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=YoshidaMasashi
en-aut-sei=Yoshida
en-aut-mei=Masashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=SaitoYukihiro
en-aut-sei=Saito
en-aut-mei=Yukihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=NakamuraKazufumi
en-aut-sei=Nakamura
en-aut-mei=Kazufumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=ItoHiroshi
en-aut-sei=Ito
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

affil-num=1
en-affil=Department of Cardiovascular Medicine, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Cardiovascular Medicine, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Molecular Biology and Biochemistry, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=4
en-affil=Department of Cardiovascular Medicine, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=5
en-affil=Department of Cardiovascular Medicine, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=6
en-affil=Department of Cardiovascular Medicine, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=7
en-affil=Department of Cardiovascular Medicine, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=8
en-affil=Department of Cardiovascular Medicine, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=9
en-affil=Department of Cardiovascular Medicine, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=pemafibrate
kn-keyword=pemafibrate
en-keyword=angiotensin II
kn-keyword=angiotensin II
en-keyword=abdominal aortic aneurysm
kn-keyword=abdominal aortic aneurysm
en-keyword=oxidative stress
kn-keyword=oxidative stress
en-keyword=catalase
kn-keyword=catalase
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2022
dt-pub=20220713
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Differences in extracellular fluid volume between acute heart failure patients with and without high systolic blood pressure
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Aims Some reports have suggested that hypertensive acute heart failure (AHF) is caused by intravascular congestion, not interstitial congestion. We evaluated the differences in extracellular fluid volume assessed by bioelectrical impedance analysis (BIA) between AHF patients with and without high systolic blood pressure (sBP). <br>
Methods This prospective single-centre study (UMIN000030266) included 178 patients hospitalized due to AHF between September 2017 and August 2018. We calculated extracellular water (ECW), intracellular water (ICW), total body water (TBW), and ECW-to-TBW ratio (oedema index: EI) by BIA and evaluated conventional parameters as follows: weight, N-terminal pro brain natriuretic peptide values, and echocardiography parameters on admission and before discharge. One-year outcomes included all-cause death and re-admission due to heart failure. We compared patients with sBP > 140 mmHg on admission [clinical scenario 1 (CS1) group] and with sBP of <= 140 mmHg on admission (non-CS1 group). <br>
Results The mean age of the patients was 79.5 +/- 11.1 years, and 48.9% of the patients were female. EI on admission of 83 patients in the CS1 group was lower than that of 95 patients in the non-CS1 group. The change in EI from admission to before discharge was no significant in the CS1 group but was significant in the non-CS1 group. Comparing the changes from admission to before discharge between the CS1 and the non-CS1 group, delta ECW, delta ICW, delta TBW, and delta EI of the CS1 group were significantly smaller than those of the non-CS1 group. During the 1-year follow-up period after discharge of the 178 patients, the numbers of deaths and re-admissions due to acute HF were 26 (15%) and 49 (28%), respectively. Patients with high EI before discharge [> 0.408 (median)] had significantly more cardiac events than patients with low EI [hazard ratio (HR): 2.15, 95% confidence interval (CI): 1.30-3.55]. Cox regression analysis revealed that higher EI as a continuous variable was significantly associated with worse outcome in non-CS1 group (HR: 1.46, 95% CI: 1.13-1.87), but not significantly associated with worse outcome in CS1 group (HR: 1.29, 95% CI: 0.98-1.69). <br>
Conclusions EI on admission in patients with high sBP was not elevated, and changes in ECW, ICW, TBW, and EI in patients with high sBP were smaller than those in patients without high sBP. EI measured by BIA could distinguish AHF with interstitial or intravascular congestion.
en-copyright=
kn-copyright=

en-aut-name=NambaYusuke
en-aut-sei=Namba
en-aut-mei=Yusuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=YunokiKei
en-aut-sei=Yunoki
en-aut-mei=Kei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=NakamuraKazufumi
en-aut-sei=Nakamura
en-aut-mei=Kazufumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=EjiriKentaro
en-aut-sei=Ejiri
en-aut-mei=Kentaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=OkaTakefumi
en-aut-sei=Oka
en-aut-mei=Takefumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=ItoHiroshi
en-aut-sei=Ito
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

affil-num=1
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Cardiovascular Medicine, Tsuyama Chuo Hospital
kn-affil=

affil-num=3
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of Cardiovascular Medicine, Tsuyama Chuo Hospital
kn-affil=

affil-num=6
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=Acute heart failure
kn-keyword=Acute heart failure
en-keyword=High systolic blood pressure
kn-keyword=High systolic blood pressure
en-keyword=Fluid volume
kn-keyword=Fluid volume
en-keyword=Oedema index
kn-keyword=Oedema index
END

start-ver=1.4
cd-journal=joma
no-vol=12
cd-vols=
no-issue=5
article-no=
start-page=684
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2022
dt-pub=20220505
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Quantification of Lung Perfusion Blood Volume in Dual-Energy Computed Tomography in Patients with Pulmonary Hypertension
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Dual-energy computed tomography (DECT) is a promising technique for the assessment of the lung perfused blood volume (LPBV) in the lung parenchyma. This study was performed to compare the LPBV by DECT of patients with pulmonary hypertension (PH) and controls and to evaluate the association between the LPBV and the perfusion ratio derived by lung perfusion scintigraphy. This study involved 45 patients who underwent DECT (25 patients with PH and 20 controls). We measured the total LPBV and distribution of the LPBV in each lung. The total LPBV was significantly lower in the PH group than the control group (38 +/- 9 vs. 45 +/- 8 HU, p = 0.024). Significant differences were observed between the LPBV of the upper lung of the PH and control groups (34 +/- 10 vs. 47 +/- 10, p = 0.021 and 37 +/- 10 vs. 47 +/- 8, p < 0.001). A significant correlation was observed between the LPBV and the lung perfusion scintigraphy. A lower total LPBV and lower LPBV of the upper lung as detected by DECT might be specific findings of PH.
en-copyright=
kn-copyright=

en-aut-name=UgawaSatoko
en-aut-sei=Ugawa
en-aut-mei=Satoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=AkagiSatoshi
en-aut-sei=Akagi
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=EjiriKentaro
en-aut-sei=Ejiri
en-aut-mei=Kentaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=NakamuraKazufumi
en-aut-sei=Nakamura
en-aut-mei=Kazufumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=ItoHiroshi
en-aut-sei=Ito
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

affil-num=1
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=
en-keyword=pulmonary vascular bed
kn-keyword=pulmonary vascular bed
en-keyword=pulmonary arterial hypertension
kn-keyword=pulmonary arterial hypertension
en-keyword=lung perfusion scintigraphy
kn-keyword=lung perfusion scintigraphy
END

start-ver=1.4
cd-journal=joma
no-vol=12
cd-vols=
no-issue=1
article-no=
start-page=8776
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2022
dt-pub=20220524
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Impact of shear wave dispersion slope analysis for assessing the severity of myocarditis
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=This study aimed to elucidate the utility of a novel ultrasound-based technique, shear wave dispersion slope (SWDS) analysis, which estimates tissue viscosity, for evaluating the severity of myocardial inflammation. Experimental autoimmune myocarditis (EAM) at different disease phases [3-week (acute phase): n = 10, 5-week (subacute phase): n = 9, and 7-week (late phase): n = 11] were developed in male Lewis rats. SWDS was measured in the right and the left ventricular free walls (RVFW and LVFW) under a retrograde perfusion condition. Histological myocardial inflammation was evaluated by CD68 staining. The accumulation of CD68-positive cells was severe in the myocardium of the EAM 3-week group. The median (interquartile range) SWDS of RVFW was significantly higher in the EAM 3-week group [9.9 (6.5-11.0) m/s/kHz] than in the control group [5.4 (4.5-6.8) m/s/kHz] (P = 0.034). The median SWDS of LVFW was also significantly higher in the EAM 3-week group [8.1 (6.4-11.0) m/s/kHz] than in the control group [4.4 (4.2-4.8) m/s/kHz] (P = 0.003). SWDS and the percentage of CD68-positive area showed a significant correlation in RVFW (R-2 = 0.64, P < 0.001) and LVFW (R-2 = 0.73, P < 0.001). This study showed that SWDS was elevated in ventricular walls with acute inflammation and also significantly correlated with the degree of myocardial inflammation. These results suggest the potential of SWDS in estimating the histological severity of acute myocarditis.
en-copyright=
kn-copyright=

en-aut-name=AmiokaNaofumi
en-aut-sei=Amioka
en-aut-mei=Naofumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TakayaYoichi
en-aut-sei=Takaya
en-aut-mei=Yoichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=NakamuraKazufumi
en-aut-sei=Nakamura
en-aut-mei=Kazufumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KondoMegumi
en-aut-sei=Kondo
en-aut-mei=Megumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=AkazawaKaoru
en-aut-sei=Akazawa
en-aut-mei=Kaoru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=OhnoYuko
en-aut-sei=Ohno
en-aut-mei=Yuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=IchikawaKeishi
en-aut-sei=Ichikawa
en-aut-mei=Keishi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=NakayamaRie
en-aut-sei=Nakayama
en-aut-mei=Rie
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=SaitoYukihiro
en-aut-sei=Saito
en-aut-mei=Yukihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=AkagiSatoshi
en-aut-sei=Akagi
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=MiyoshiToru
en-aut-sei=Miyoshi
en-aut-mei=Toru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=YoshidaMasashi
en-aut-sei=Yoshida
en-aut-mei=Masashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=MoritaHiroshi
en-aut-sei=Morita
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=ItoHiroshi
en-aut-sei=Ito
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

affil-num=1
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and  Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and  Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and  Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and  Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and  Pharmaceutical Sciences
kn-affil=

affil-num=6
en-affil=Kawasaki University of Medical  Welfare
kn-affil=

affil-num=7
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and  Pharmaceutical Sciences
kn-affil=

affil-num=8
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and  Pharmaceutical Sciences
kn-affil=

affil-num=9
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and  Pharmaceutical Sciences
kn-affil=

affil-num=10
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and  Pharmaceutical Sciences
kn-affil=

affil-num=11
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and  Pharmaceutical Sciences
kn-affil=

affil-num=12
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and  Pharmaceutical Sciences
kn-affil=

affil-num=13
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and  Pharmaceutical Sciences
kn-affil=

affil-num=14
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and  Pharmaceutical Sciences
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=12
cd-vols=
no-issue=1
article-no=
start-page=4930
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2022
dt-pub=20220323
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=LCZ696 ameliorates doxorubicin-induced cardiomyocyte toxicity in rats
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Doxorubicin (DOX)-based chemotherapy induces cardiotoxicity, which is considered the main bottleneck for its clinical application. In this study, we investigated the potential benefit of LCZ696, an angiotensin receptor-neprilysin inhibitor against DOX-induced cardiotoxicity in rats and H9c2 cells and determined whether the mechanism underlying any such effects involves its antioxidant activity. Male Sprague-Dawley rats were randomly separated into four groups, each consisting of 15 rats (DOX (1.5 mg/kg/day intraperitoneally for 10 days followed by non-treatment for 8 days); DOX + valsartan (31 mg/kg/day by gavage from day 1 to day 18); DOX + LCZ696 (68 mg/kg/day by gavage from day 1 to day 18); and control (saline intraperitoneally for 10 days). DOX-induced elevation of cardiac troponin T levels on day 18 was significantly reduced by LCZ696, but not valsartan. The DOX-induced increase in myocardial reactive oxygen species (ROS) levels determined using dihydroethidium was significantly ameliorated by LCZ696, but not valsartan, and was accompanied by the suppression of DOX-induced increase in p47phox. LCZ696 recovered the DOX-induced decrease in phosphorylation of adenosine monophosphate-activated protein kinase and increased the ratio of Bax and Bcl-2. In H9c2 cardiomyocytes, LCZ696 reduced DOX-induced mitochondrial ROS generation and improved cell viability more than valsartan. Our findings indicated that LCZ696 ameliorated DOX-induced cardiotoxicity in rat hearts in vivo and in vitro, possibly by mediating a decrease in oxidative stress.
en-copyright=
kn-copyright=

en-aut-name=MiyoshiToru
en-aut-sei=Miyoshi
en-aut-mei=Toru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NakamuraKazufumi
en-aut-sei=Nakamura
en-aut-mei=Kazufumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=AmiokaNaofumi
en-aut-sei=Amioka
en-aut-mei=Naofumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=HatipogluOmer F.
en-aut-sei=Hatipoglu
en-aut-mei=Omer F.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=YonezawaTomoko
en-aut-sei=Yonezawa
en-aut-mei=Tomoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=SaitoYukihiro
en-aut-sei=Saito
en-aut-mei=Yukihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=YoshidaMasashi
en-aut-sei=Yoshida
en-aut-mei=Masashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=AkagiSatoshi
en-aut-sei=Akagi
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=ItoHiroshi
en-aut-sei=Ito
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

affil-num=1
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry  and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry  and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry  and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=4
en-affil=Department of Pharmacology, Kindai University
kn-affil=

affil-num=5
en-affil=Department of Molecular Biology and  Biochemistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Science
kn-affil=

affil-num=6
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry  and Pharmaceutical Sciences
kn-affil=

affil-num=7
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry  and Pharmaceutical Sciences
kn-affil=

affil-num=8
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry  and Pharmaceutical Sciences
kn-affil=

affil-num=9
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry  and Pharmaceutical Sciences
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=13
cd-vols=
no-issue=1
article-no=
start-page=141
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2022
dt-pub=20220401
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Enhancement of pacing function by HCN4 overexpression in human pluripotent stem cell-derived cardiomyocytes
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background The number of patients with bradyarrhythmia and the number of patients with cardiac pacemakers are increasing with the aging population and the increase in the number of patients with heart diseases. Some patients in whom a cardiac pacemaker has been implanted experience problems such as pacemaker infection and inconvenience due to electromagnetic interference. We have reported that overexpression of HCN channels producing a pacemaker current in mouse embryonic stem cell-derived cardiomyocytes showed enhanced pacing function in vitro and in vivo. The aim of this study was to determine whether HCN4 overexpression in human induced pluripotent stem cell-derived cardiomyocytes (iPSC-CMs) can strengthen the pacing function of the cells. Methods Human HCN4 was transduced in the AAVS1 locus of human induced pluripotent stem cells by nucleofection and HCN4-overexpressing iPSC-CMs were generated. Gene expression profiles, frequencies of spontaneous contraction and pacing abilities of HCN4-overexpressing and non-overexpressing iPSC-CMs in vitro were compared. Results HCN4-overexpressing iPSC-CMs showed higher spontaneous contraction rates than those of non-overexpressing iPSC-CMs. They responded to an HCN channel blocker and beta adrenergic stimulation. The pacing rates against parent iPSC line-derived cardiomyocytes were also higher in HCN4-overexpressing iPSC-CMs than in non-overexpressing iPSC-CMs. Conclusions Overexpression of HCN4 showed enhancement of I-f current, spontaneous firing and pacing function in iPSC-CMs. These data suggest this transgenic cell line may be useful as a cardiac pacemaker.
en-copyright=
kn-copyright=

en-aut-name=SaitoYukihiro
en-aut-sei=Saito
en-aut-mei=Yukihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NakamuraKazufumi
en-aut-sei=Nakamura
en-aut-mei=Kazufumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=YoshidaMasashi
en-aut-sei=Yoshida
en-aut-mei=Masashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=SugiyamaHiroki
en-aut-sei=Sugiyama
en-aut-mei=Hiroki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=AkagiSatoshi
en-aut-sei=Akagi
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=MiyoshiToru
en-aut-sei=Miyoshi
en-aut-mei=Toru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=MoritaHiroshi
en-aut-sei=Morita
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=ItoHiroshi
en-aut-sei=Ito
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

affil-num=1
en-affil=Department of Cardiovascular Medicine, Okayama University Hospital
kn-affil=

affil-num=2
en-affil=Department of Cardiovascular Medicine, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine
kn-affil=

affil-num=3
en-affil=Department of Chronic Kidney Disease and Cardiovascular Disease, Dentistry, and Pharmaceutical Science, Okayama University Graduate School of Medicine
kn-affil=

affil-num=4
en-affil=Department of Internal Medicine, Okayama Saiseikai General Hospital
kn-affil=

affil-num=5
en-affil=Department of Cardiovascular Medicine, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine
kn-affil=

affil-num=6
en-affil=Department of Cardiovascular Medicine, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine
kn-affil=

affil-num=7
en-affil=Department of Cardiovascular Therapeutics, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine
kn-affil=

affil-num=8
en-affil=Department of Cardiovascular Medicine, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine
kn-affil=
en-keyword=Hyperpolarization-activated cyclic nucleotide-gated potassium channel 4
kn-keyword=Hyperpolarization-activated cyclic nucleotide-gated potassium channel 4
en-keyword=Human induced pluripotent stem cell-derived cardiomyocytes
kn-keyword=Human induced pluripotent stem cell-derived cardiomyocytes
en-keyword=Pacing
kn-keyword=Pacing
END

start-ver=1.4
cd-journal=joma
no-vol=23
cd-vols=
no-issue=7
article-no=
start-page=3587
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2022
dt-pub=20220325
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Pathophysiology and Treatment of Diabetic Cardiomyopathy and Heart Failure in Patients with Diabetes Mellitus
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=There is a close relationship between diabetes mellitus and heart failure, and diabetes is an independent risk factor for heart failure. Diabetes and heart failure are linked by not only the complication of ischemic heart disease, but also by metabolic disorders such as glucose toxicity and lipotoxicity based on insulin resistance. Cardiac dysfunction in the absence of coronary artery disease, hypertension, and valvular disease is called diabetic cardiomyopathy. Diabetes-induced hyperglycemia and hyperinsulinemia lead to capillary damage, myocardial fibrosis, and myocardial hypertrophy with mitochondrial dysfunction. Lipotoxicity with extensive fat deposits or lipid droplets is observed on cardiomyocytes. Furthermore, increased oxidative stress and inflammation cause cardiac fibrosis and hypertrophy. Treatment with a sodium glucose cotransporter 2 (SGLT2) inhibitor is currently one of the most effective treatments for heart failure associated with diabetes. However, an effective treatment for lipotoxicity of the myocardium has not yet been established, and the establishment of an effective treatment is needed in the future. This review provides an overview of heart failure in diabetic patients for the clinical practice of clinicians.
en-copyright=
kn-copyright=

en-aut-name=NakamuraKazufumi
en-aut-sei=Nakamura
en-aut-mei=Kazufumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MiyoshiToru
en-aut-sei=Miyoshi
en-aut-mei=Toru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=YoshidaMasashi
en-aut-sei=Yoshida
en-aut-mei=Masashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=AkagiSatoshi
en-aut-sei=Akagi
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=SaitoYukihiro
en-aut-sei=Saito
en-aut-mei=Yukihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=EjiriKentaro
en-aut-sei=Ejiri
en-aut-mei=Kentaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=MatsuoNaoaki
en-aut-sei=Matsuo
en-aut-mei=Naoaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=IchikawaKeishi
en-aut-sei=Ichikawa
en-aut-mei=Keishi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=IwasakiKeiichiro
en-aut-sei=Iwasaki
en-aut-mei=Keiichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=NaitoTakanori
en-aut-sei=Naito
en-aut-mei=Takanori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=NambaYusuke
en-aut-sei=Namba
en-aut-mei=Yusuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=YoshidaMasatoki
en-aut-sei=Yoshida
en-aut-mei=Masatoki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=SugiyamaHiroki
en-aut-sei=Sugiyama
en-aut-mei=Hiroki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=ItoHiroshi
en-aut-sei=Ito
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

affil-num=1
en-affil=Department of Cardiovascular Medicine, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Cardiovascular Medicine, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Cardiovascular Medicine, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=4
en-affil=Department of Cardiovascular Medicine, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=5
en-affil=Department of Cardiovascular Medicine, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=6
en-affil=Department of Cardiovascular Medicine, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=7
en-affil=Department of Cardiovascular Medicine, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=8
en-affil=Department of Cardiovascular Medicine, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=9
en-affil=Department of Cardiovascular Medicine, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=10
en-affil=Department of Cardiovascular Medicine, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=11
en-affil=Department of Cardiovascular Medicine, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=12
en-affil=Department of Cardiovascular Medicine, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=13
en-affil=Department of Internal Medicine, Okayama Saiseikai General Hospital
kn-affil=

affil-num=14
en-affil=Department of Cardiovascular Medicine, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=heart failure
kn-keyword=heart failure
en-keyword=lipotoxicity
kn-keyword=lipotoxicity
en-keyword=SGLT2 inhibitor
kn-keyword=SGLT2 inhibitor
END

start-ver=1.4
cd-journal=joma
no-vol=79
cd-vols=
no-issue=3
article-no=
start-page=446
end-page=452
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2022
dt-pub=20223
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Fragmented QRS as a predictor of cardiac events in patients with cardiac sarcoidosis
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background: Multiple spikes within the QRS complex, known as fragmented QRS (fQRS),
are associated with the occurrences of ventricular arrhythmic events (VAEs) in patients with
Brugada syndrome and hypertrophic cardiomyopathy. However, the association between
fQRS and occurrence of VAEs in patients with cardiac sarcoidosis (CS) has not been
elucidated.<br>
Methods: We evaluated the associations between fQRS and cardiac events including VAEs
(non-sustained ventricular tachycardia [NSVT], sustained ventricular tachycardia [VT], and
ventricular fibrillation [VF]), hospitalization for heart failure, and all cause death in 68
patients with CS (30 patients with fQRS vs. 38 patients without fQRS) over a 5-year period.<br>
Results: Cardiac events occurred in 22 patients with fQRS and 18 patients without fQRS
(73% vs. 47%, P=0.009). Of the cardiac events that occurred in CS patients, VAEs occurred
more frequently in patients with fQRS than in patients without fQRS (VAEs: 70% vs. 45%,
P=0.017; NSVT: 70% vs. 45%, P=0.010; VT: 43% vs. 18%, P=0.011, and VF: 6.7% vs.
2.6%, P=0.34), whereas there was no significant difference in hospitalization for heart failure
or all-cause death between patients with and those without fQRS (hospitalization for heart
failure: 6.7% vs. 5.3%, P=0.75; all-cause death: 6.7% vs. 5.3%, P=0.64). Multivariate analysis
showed that fQRS in the baseline ECG was independently associated with VAEs (hazard ratio
[HR]: 2.21, 95% confidence interval [CI]: 1.15?4.25, P=0.017).<br>
Conclusion: fQRS is a predictor of VAEs in patients with CS.<br>
en-copyright=
kn-copyright=

en-aut-name=OguraSoichiro
en-aut-sei=Ogura
en-aut-mei=Soichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NakamuraKazufumi
en-aut-sei=Nakamura
en-aut-mei=Kazufumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=MoritaHiroshi
en-aut-sei=Morita
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=NakagawaKoji
en-aut-sei=Nakagawa
en-aut-mei=Koji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=NishiiNobuhiro
en-aut-sei=Nishii
en-aut-mei=Nobuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=AkagiSatoshi
en-aut-sei=Akagi
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=TohNorihisa
en-aut-sei=Toh
en-aut-mei=Norihisa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=TakayaYoichi
en-aut-sei=Takaya
en-aut-mei=Yoichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=YoshidaMasashi
en-aut-sei=Yoshida
en-aut-mei=Masashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=MiyoshiToru
en-aut-sei=Miyoshi
en-aut-mei=Toru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=WatanabeAtsuyuki
en-aut-sei=Watanabe
en-aut-mei=Atsuyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=ItoHiroshi
en-aut-sei=Ito
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

affil-num=1
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=6
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=7
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=8
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=9
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=10
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=11
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=12
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=2022
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2022
dt-pub=20220117
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Assessment of congestion and clinical outcomes in patients with chronic heart failure using shear wave elasticity
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Aims The relief of congestion is essential for the prevention of worsening heart failure (HF) resulting in hospitalizations. Assessment of the degree of organ congestion in the chronic phase of HF is important for determining therapeutic strategies. The aim of this study was to evaluate the efficacy of shear wave (SW) elasticity for assessing congestion and clinical outcomes in patients with chronic HF. Methods and results We prospectively enrolled 345 consecutive patients with chronic HF who underwent SW elastography at outpatient clinic. Patients were divided into two groups according to the median value of SW elasticity: low group (SW elasticity <6.4 kPa, n = 176) and high group (SW elasticity >= 6.4 kPa, n = 169). The endpoint was cardiovascular death or hospitalization for HF. During the median follow-up period of 19 months (range: 7-36 months), cardiovascular death or hospitalization for HF occurred in 4 patients of low group and 27 patients of high group. In high group, 8 patients died, and 19 patients were hospitalized for HF. In low group, 3 patients died, and 1 patient was hospitalized. Kaplan-Meier analysis showed that the event-free survival rate was worse in high group than in low group (log-rank test, P = 0.004). After adjusting for variables, high SW elasticity was independently related to cardiac events. In multivariate regression analysis, SW elasticity was correlated with left atrial volume index, early diastolic mitral inflow velocity to mitral annular velocity ratio, and inferior vena cava diameter. Conclusions The SW elasticity reflected haemodynamic congestion in patients with chronic HF, which was related to cardiac events.
en-copyright=
kn-copyright=

en-aut-name=NakayamaRie
en-aut-sei=Nakayama
en-aut-mei=Rie
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TakayaYoichi
en-aut-sei=Takaya
en-aut-mei=Yoichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=NakamuraKazufumi
en-aut-sei=Nakamura
en-aut-mei=Kazufumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TakemotoRika
en-aut-sei=Takemoto
en-aut-mei=Rika
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=TohNorihisa
en-aut-sei=Toh
en-aut-mei=Norihisa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=ItoHiroshi
en-aut-sei=Ito
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

affil-num=1
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Division of Medical Support, Okayama University Hospital
kn-affil=

affil-num=5
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=6
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=Congestion
kn-keyword=Congestion
en-keyword=Heart failure
kn-keyword=Heart failure
en-keyword=Prognosis
kn-keyword=Prognosis
en-keyword=Shear wave elasticity
kn-keyword=Shear wave elasticity
END

start-ver=1.4
cd-journal=joma
no-vol=23
cd-vols=
no-issue=1
article-no=
start-page=25
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2021
dt-pub=20211221
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Molecular Mechanisms of Cardiac Amyloidosis
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Cardiac involvement has a profound effect on the prognosis of patients with systemic amyloidosis. Therapeutic methods for suppressing the production of causative proteins have been developed for ATTR amyloidosis and AL amyloidosis, which show cardiac involvement, and the prognosis has been improved. However, a method for removing deposited amyloid has not been established. Methods for reducing cytotoxicity caused by amyloid deposition and amyloid precursor protein to protect cardiovascular cells are also needed. In this review, we outline the molecular mechanisms and treatments of cardiac amyloidosis.
en-copyright=
kn-copyright=

en-aut-name=SaitoYukihiro
en-aut-sei=Saito
en-aut-mei=Yukihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NakamuraKazufumi
en-aut-sei=Nakamura
en-aut-mei=Kazufumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=ItoHiroshi
en-aut-sei=Ito
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

affil-num=1
en-affil=Department of Cardiovascular Medicine, Okayama University Hospital
kn-affil=

affil-num=2
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=amyloid
kn-keyword=amyloid
en-keyword=cytotoxicity
kn-keyword=cytotoxicity
en-keyword=transthyretin
kn-keyword=transthyretin
en-keyword=immunoglobulin light chain
kn-keyword=immunoglobulin light chain
END

start-ver=1.4
cd-journal=joma
no-vol=11
cd-vols=
no-issue=1
article-no=
start-page=22812
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2021
dt-pub=20211124
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Efficacy of shear wave elasticity for evaluating myocardial hypertrophy in hypertensive rats
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Shear wave (SW) imaging is a novel ultrasound-based technique for assessing tissue characteristics. SW elasticity may be useful to assess the severity of hypertensive left ventricular (LV) hypertrophy. This study aimed to evaluate the efficacy of SW elasticity for assessing the degree of myocardial hypertrophy using hypertensive rats. Rats were divided into hypertension group and control group. SW elasticity was measured on the excised heart. Myocardial hypertrophy was assessed histologically. LV weight was greater in hypertension group. An increase in interventricular septum and LV free wall thicknesses was observed in hypertension group. SW elasticity was significantly higher in hypertension group than in control group (14.6 +/- 4.3 kPa vs. 6.5 +/- 1.1 kPa, P < 0.01). The cross-sectional area of cardiomyocytes was larger in hypertension group than in control group (397 +/- 50 mu m(2) vs. 243 +/- 14 mu m(2), P < 0.01), and SW elasticity was positively correlated with the cross-sectional area of cardiomyocytes (R = 0.96, P < 0.01). This study showed that SW elasticity was higher in hypertensive rats and was closely correlated with the degree of myocardial hypertrophy, suggesting the efficacy of SW elasticity for estimating the severity of hypertensive LV hypertrophy.
en-copyright=
kn-copyright=

en-aut-name=TakayaYoichi
en-aut-sei=Takaya
en-aut-mei=Yoichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NakamuraKazufumi
en-aut-sei=Nakamura
en-aut-mei=Kazufumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=NakayamaRie
en-aut-sei=Nakayama
en-aut-mei=Rie
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=OhtsukaHiroaki
en-aut-sei=Ohtsuka
en-aut-mei=Hiroaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=AmiokaNaofumi
en-aut-sei=Amioka
en-aut-mei=Naofumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=KondoMegumi
en-aut-sei=Kondo
en-aut-mei=Megumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=AkazawaKaoru
en-aut-sei=Akazawa
en-aut-mei=Kaoru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=OhnoYuko
en-aut-sei=Ohno
en-aut-mei=Yuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=IchikawaKeishi
en-aut-sei=Ichikawa
en-aut-mei=Keishi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=SaitoYukihiro
en-aut-sei=Saito
en-aut-mei=Yukihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=AkagiSatoshi
en-aut-sei=Akagi
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=YoshidaMasashi
en-aut-sei=Yoshida
en-aut-mei=Masashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=MiyoshiToru
en-aut-sei=Miyoshi
en-aut-mei=Toru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=ItoHiroshi
en-aut-sei=Ito
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

affil-num=1
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=6
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=7
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=8
en-affil=Kawasaki University of Medical Welfare
kn-affil=

affil-num=9
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=10
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=11
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=12
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=13
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=14
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2021
dt-pub=20211103
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Effects of luseogliflozin on estimated plasma volume in patients with heart failure with preserved ejection fraction
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Aims<br>
Sodium glucose co-transporter 2 inhibitors have diuretic effects in both patients with glycosuria and with natriuresis. We sought to assess the effect of luseogliflozin on estimated plasma volume (ePV) in patients with type 2 diabetes and heart failure with preserved ejection fraction (HFpEF). <br>
Methods and results<br>
This study was a post-hoc analysis of the MUSCAT-HF trial (UMIN000018395), a multicentre, prospective, open-label, randomized controlled trial that assessed the effect of 12 weeks of luseogliflozin (2.5 mg, once daily, n = 83) as compared with voglibose (0.2 mg, three times daily, n = 82) on the reduction in brain natriuretic peptide (BNP) in patients with type 2 diabetes and HFpEF. The analysis compared the change in ePV calculated by the Straus formula from baseline to Weeks 4, 12, and 24, using a mixed-effects model for repeated measures. We also estimated the association between changes in ePV and changes in other clinical parameters, including BNP levels. Luseogliflozin significantly reduced ePV as compared to voglibose at Week 4 {adjusted mean group-difference -6.43% [95% confidence interval (CI): -9.11 to -3.74]}, at Week 12 [-8.73% (95%CI: -11.40 to -6.05)], and at Week 24 [-11.02% (95%CI: -13.71 to -8.33)]. The effect of luseogliflozin on these parameters was mostly consistent across various patient clinical characteristics. The change in ePV at Week 12 was significantly associated with log-transformed BNP (r = 0.197, P = 0.015) and left atrial volume index (r = 0.283, P = 0.019). <br>
Conclusions<br>
Luseogliflozin significantly reduced ePV in patients with type 2 diabetes and HFpEF, as compared with voglibose. The reduction of intravascular volume by luseogliflozin may provide clinical benefits to patients with type 2 diabetes and HFpEF.
en-copyright=
kn-copyright=

en-aut-name=NakashimaMitsutaka
en-aut-sei=Nakashima
en-aut-mei=Mitsutaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MiyoshiToru
en-aut-sei=Miyoshi
en-aut-mei=Toru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=EjiriKentaro
en-aut-sei=Ejiri
en-aut-mei=Kentaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KiharaHajime
en-aut-sei=Kihara
en-aut-mei=Hajime
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=HataYoshiki
en-aut-sei=Hata
en-aut-mei=Yoshiki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=NaganoToshihiko
en-aut-sei=Nagano
en-aut-mei=Toshihiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=TakaishiAtsushi
en-aut-sei=Takaishi
en-aut-mei=Atsushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=TodaHironobu
en-aut-sei=Toda
en-aut-mei=Hironobu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=NanbaSeiji
en-aut-sei=Nanba
en-aut-mei=Seiji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=NakamuraYoichi
en-aut-sei=Nakamura
en-aut-mei=Yoichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=AkagiSatoshi
en-aut-sei=Akagi
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=SakuragiSatoru
en-aut-sei=Sakuragi
en-aut-mei=Satoru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=MinagawaTaro
en-aut-sei=Minagawa
en-aut-mei=Taro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=KawaiYusuke
en-aut-sei=Kawai
en-aut-mei=Yusuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=NishiiNobuhiro
en-aut-sei=Nishii
en-aut-mei=Nobuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

en-aut-name=FukeSoichiro
en-aut-sei=Fuke
en-aut-mei=Soichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=16
ORCID=

en-aut-name=YoshikawaMasaki
en-aut-sei=Yoshikawa
en-aut-mei=Masaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=17
ORCID=

en-aut-name=NakamuraKazufumi
en-aut-sei=Nakamura
en-aut-mei=Kazufumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=18
ORCID=

en-aut-name=ItoHiroshi
en-aut-sei=Ito
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=19
ORCID=

en-aut-name=MUSCAT-HF Study Investigators
en-aut-sei=MUSCAT-HF Study Investigators
en-aut-mei=
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=20
ORCID=

affil-num=1
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of Internal Medicine, Kihara Cardiovascular Clinic
kn-affil=

affil-num=5
en-affil=Department of Cardiology, Minamino Cardiovascular Hospital
kn-affil=

affil-num=6
en-affil=Department of Internal Medicine, Iwasa Hospital,
kn-affil=

affil-num=7
en-affil=Department of Cardiology, Mitoyo General Hospital
kn-affil=

affil-num=8
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=9
en-affil=Department of Cardiology, Okayama Rosai Hospital
kn-affil=

affil-num=10
en-affil=Department of Cardiovascular Medicine, Specified Clinic of Soyokaze CardioVascular Medicine and Diabetes Care, Matsuyama
kn-affil=

affil-num=11
en-affil=Department of Internal Medicine, Akaiwa Medical Association Hospital
kn-affil=

affil-num=12
en-affil=Department of Cardiovascular Medicine, Iwakuni Clinical Center
kn-affil=

affil-num=13
en-affil=Department of Internal Medicine, Minagawa Cardiovascular Clinic
kn-affil=

affil-num=14
en-affil=Department of Cardiovascular Medicine, Okayama City Hospital
kn-affil=

affil-num=15
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=16
en-affil=Department of Cardiovascular Medicine, Japanese Red Cross Okayama Hospital
kn-affil=

affil-num=17
en-affil=Department of Cardiology, Fukuyama City Hospital
kn-affil=

affil-num=18
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=19
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=20
en-affil=
kn-affil=
en-keyword=Estimated plasma volume
kn-keyword=Estimated plasma volume
en-keyword=Heart failure with preserved ejection fraction
kn-keyword=Heart failure with preserved ejection fraction
en-keyword=Luseogliflozin
kn-keyword=Luseogliflozin
en-keyword=Sodium glucose co-transporter 2 inhibitors
kn-keyword=Sodium glucose co-transporter 2 inhibitors
en-keyword=Voglibose
kn-keyword=Voglibose
END

start-ver=1.4
cd-journal=joma
no-vol=16
cd-vols=
no-issue=3
article-no=
start-page=e0245502
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2021
dt-pub=20210304
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Usefulness of right ventriculography compared with computed tomography for ruling out the possibility of lead perforation before lead extraction
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Purpose High-risk patients can be identified by preprocedural computed tomography (CT) before lead extraction. However, CT evaluation may be difficult especially for lead tip identification due to artifacts in the leads. Selective right ventriculography (RVG) may enable preprocedural evaluation of lead perforation. We investigated the efficacy of RVG for identifying right ventricular (RV) lead perforation compared with CT in patients who underwent lead extraction. Methods Ninety-five consecutive patients who were examined by thin-section non-ECG-gated multi-detector CT and RVG before lead extraction were investigated retrospectively. Newly recognized pericardial effusion after lead extraction was used as a reference standard for lead perforation. We analyzed the prevalence of RV lead perforation diagnosed by each method. The difference in the detection rates of lead perforation by RVG and CT was evaluated. Results Of the 115 RV leads in the 95 patients, lead perforation was diagnosed for 35 leads using CT, but the leads for 29 (83%) of those 35 leads diagnosed as lead perforation by CT were shown to be within the right ventricle by RVG. Three patients with 5 leads could not be evaluated by CT due to motion artifacts. The diagnostic accuracies of RVG and CT were significantly different (p < 0.001). There was no complication of pericardial effusion caused by RV lead extraction. Conclusion RVG for identification of RV lead perforation leads to fewer false-positives compared to non-ECG-gated CT. However, even in cases in which lead perforation is diagnosed, most leads may be safely extracted by transvenous lead extraction.
en-copyright=
kn-copyright=

en-aut-name=AsadaSaori
en-aut-sei=Asada
en-aut-mei=Saori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NishiiNobuhiro
en-aut-sei=Nishii
en-aut-mei=Nobuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=ShinyaTakayoshi
en-aut-sei=Shinya
en-aut-mei=Takayoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MiyoshiAkihito
en-aut-sei=Miyoshi
en-aut-mei=Akihito
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=MorimotoYoshimasa
en-aut-sei=Morimoto
en-aut-mei=Yoshimasa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=MiyamotoMasakazu
en-aut-sei=Miyamoto
en-aut-mei=Masakazu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=NakagawaKoji
en-aut-sei=Nakagawa
en-aut-mei=Koji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=NakamuraKazufumi
en-aut-sei=Nakamura
en-aut-mei=Kazufumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=MoritaHiroshi
en-aut-sei=Morita
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=ItoHiroshi
en-aut-sei=Ito
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

affil-num=1
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Cardiovascular Therapeutics, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Pediatric Radiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=6
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=7
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=8
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=9
en-affil=Department of Cardiovascular Therapeutics, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=10
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=78
cd-vols=
no-issue=1
article-no=
start-page=17
end-page=23
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2021
dt-pub=20210207
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Efficacy of shear wave elastography for evaluating right ventricular myocardial fibrosis in monocrotaline-induced pulmonary hypertension rats
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background: Right ventricular (RV) function is important for outcomes in pulmonary hypertension. Evaluation of RV myocardial characteristics is useful to assess the disease severity. Shear wave elastography (SWE) provides information of shear wave (SW) elasticity, which is related to tissue hardness, and SW dispersion slope, which reflects tissue viscosity. This study aimed to test the hypothesis that SW elasticity is increased and SW dispersion slope is decreased in the right ventricle of monocrotaline (MCT)-induced pulmonary hypertension rats. <br>
<br>
Methods: Rats were divided into MCT-induced pulmonary hypertension group (n = 10) and control group (n = 10). SW elasticity and SW dispersion slope were measured on excised hearts. Myocardial fibrosis was evaluated histologically. <br>
<br>
Results: RV hypertrophy was observed in the MCT group. SW elasticity of right ventricle was higher in the MCT group than in the control group (3.5 ± 0.9 kPa vs. 2.5 ± 0.4 kPa, p < 0.01). SW dispersion slope of right ventricle was lower in the MCT group than in the control group (5.3 ± 1.7 m/s/kHz vs. 7.7 ± 1.5 m/s/kHz, p < 0.01). The fibrosis area of right ventricle was increased in MCT group compared with control group (18 ± 5% vs. 8 ± 3%, p < 0.01), and was positively related to SW elasticity and negatively related to SW dispersion slope. <br>
<br>
Conclusions: Higher SW elasticity and lower SW dispersion slope were observed in the fibrotic myocardium of right ventricle in MCT-induced pulmonary hypertension rats. SWE may have the potential to evaluate RV function by assessing myocardial characteristics. 
en-copyright=
kn-copyright=

en-aut-name=NakayamaRie
en-aut-sei=Nakayama
en-aut-mei=Rie
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TakayaYoichi
en-aut-sei=Takaya
en-aut-mei=Yoichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=NakamuraKazufumi
en-aut-sei=Nakamura
en-aut-mei=Kazufumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KondoMegumi
en-aut-sei=Kondo
en-aut-mei=Megumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KobayashiKaoru
en-aut-sei=Kobayashi
en-aut-mei=Kaoru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=OhnoYuko
en-aut-sei=Ohno
en-aut-mei=Yuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=AmiokaNaofumi
en-aut-sei=Amioka
en-aut-mei=Naofumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=AkagiSatoshi
en-aut-sei=Akagi
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=YoshidaMasashi
en-aut-sei=Yoshida
en-aut-mei=Masashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=MiyoshiToru
en-aut-sei=Miyoshi
en-aut-mei=Toru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=ItoHiroshi
en-aut-sei=Ito
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

affil-num=1
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=6
en-affil=Kawasaki University of Medical Welfare
kn-affil=

affil-num=7
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=8
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=9
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=10
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=11
en-affil= Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=Dispersion
kn-keyword=Dispersion
en-keyword=Elasticity
kn-keyword=Elasticity
en-keyword=Myocardium
kn-keyword=Myocardium
en-keyword=Right ventricular function
kn-keyword=Right ventricular function
en-keyword=Shear wave elastography
kn-keyword=Shear wave elastography
END

start-ver=1.4
cd-journal=joma
no-vol=78
cd-vols=
no-issue=1
article-no=
start-page=12
end-page=16
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2020
dt-pub=20201230
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Inhibitory effects of RAGE-aptamer on development of monocrotaline-induced pulmonary arterial hypertension in rats
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background: The receptor for advanced glycation end products (RAGE), a transmembrane receptor belonging to the immunoglobulin superfamily, is overexpressed in pulmonary artery smooth muscle cells (PASMCs) in patients with pulmonary arterial hypertension (PAH) and is implicated in the etiology of PAH. Recently, we reported that RAGE-aptamer, a short and single-stranded DNA directed against RAGE, inhibited an inappropriate increase in cultured PASMCs in PAH. The aim of this study was to determine the efficacy of RAGEaptamer in monocrotaline-induced PAH in rats.<br><br>
Methods and Results: Rats were assigned to either an untreated control group, a group that received continuous subcutaneous administration of RAGE-aptamer immediately after monocrotaline injection, or a group that received control-aptamer immediately after monocrotaline injection. All rats survived 21 days after injection of monocrotaline and control-aptamer or RAGE-aptamer. Injection of monocrotaline with continuous subcutaneous delivery of control-aptamer resulted in higher right ventricular systolic pressure compared with controls. This increase was attenuated by continuous subcutaneous delivery of RAGE-aptamer. The proportion of small pulmonary arteries with full muscularization was greater in the monocrotaline and control-aptamer group than in the control group. Continuous subcutaneous delivery of RAGE-aptamer significantly reduced the percentage of small pulmonary arteries with full muscularization Conclusions: Continuous subcutaneous delivery of RAGE-aptamer suppresses development of monocrotaline-induced PAH in rats. Inhibition of RAGE ameliorates muscularization of 3 small pulmonary arteries. Treatment with RAGE-aptamer might be a new therapeutic option for PAH.
en-copyright=
kn-copyright=

en-aut-name=NakamuraKazufumi
en-aut-sei=Nakamura
en-aut-mei=Kazufumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=AkagiSatoshi
en-aut-sei=Akagi
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=EjiriKentaro
en-aut-sei=Ejiri
en-aut-mei=Kentaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=YoshidaMasashi
en-aut-sei=Yoshida
en-aut-mei=Masashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=MiyoshiToru
en-aut-sei=Miyoshi
en-aut-mei=Toru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=SakaguchiMasakiyo
en-aut-sei=Sakaguchi
en-aut-mei=Masakiyo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=AmiokaNaofumi
en-aut-sei=Amioka
en-aut-mei=Naofumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=SuastikaLuh Oliva Saraswati
en-aut-sei=Suastika
en-aut-mei=Luh Oliva Saraswati
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=KondoMegumi
en-aut-sei=Kondo
en-aut-mei=Megumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=NakayamaRie
en-aut-sei=Nakayama
en-aut-mei=Rie
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=TakayaYoichi
en-aut-sei=Takaya
en-aut-mei=Yoichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=HigashimotoYuichiro
en-aut-sei=Higashimoto
en-aut-mei=Yuichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=FukamiKei
en-aut-sei=Fukami
en-aut-mei=Kei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=MatsubaraHiromi
en-aut-sei=Matsubara
en-aut-mei=Hiromi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=ItoHiroshi
en-aut-sei=Ito
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

affil-num=1
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=6
en-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=7
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=8
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=9
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=10
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=11
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=12
en-affil=Department of Chemistry, Kurume University School of Medicine
kn-affil=

affil-num=13
en-affil=Division of Nephrology, Department of Medicine, Kurume University School of Medicine
kn-affil=

affil-num=14
en-affil=Department of Cardiology, National Hospital Organization Okayama Medical Center
kn-affil=

affil-num=15
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=pulmonary artery smooth muscle cells
kn-keyword=pulmonary artery smooth muscle cells
en-keyword=RAGE
kn-keyword=RAGE
en-keyword=aptamer
kn-keyword=aptamer
END

start-ver=1.4
cd-journal=joma
no-vol=8
cd-vols=
no-issue=3
article-no=
start-page=1751
end-page=1758
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2021
dt-pub=20210324
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Efficacy of shear wave elastography for assessment of liver function in patients with heart failure
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Aims</br>
Liver dysfunction is important for prognosis in heart failure (HF). Shear wave elastography (SWE), which is a novel ultrasound technique for charactering tissues, has been used in liver diseases. However, clinical implication of SWE, including dispersion slope, remains unknown in heart diseases. This study aimed to evaluate the efficacy of SWE assessing liver function in the severity of HF.</br>
Methods and results</br>
We enrolled 316 consecutive patients with or suspected heart diseases, who were classified according to the American College of Cardiology Foundation/American Heart Association stage of HF, including 37 with Stage A, 139 with Stage B, 114 with Stage C, and 26 with Stage D, and 45 normal subjects. Elasticity and dispersion slope of shear wave were assessed according to the HF stage. Elasticity and dispersion slope were not elevated in normal subjects and patients with Stage A. Elasticity was slightly increased from Stage A to Stage C and was remarkably elevated in Stage D (normal: 5.2 ± 1.1 kPa, Stage A: 5.4 ± 1.2 kPa, Stage B: 6.4 ± 1.8 kPa, Stage C: 7.8 ± 3.5 kPa, and Stage D: 17.7 ± 12.7 kPa), whereas dispersion slope was gradually increased from Stage A to Stage D (normal: 9.7 ± 1.7m/s/kHz, Stage A: 10.4 ± 1.6m/s/kHz, Stage B: 11.7 ± 2.4m/s/kHz, Stage C: 13.2 ± 3.4m/s/kHz, and Stage D: 17.6 ± 5.6 m/s/kHz). In the early HF stage, dispersion slope was elevated. In the advanced HF stage, both elasticity and dispersion slope were elevated. Liver function test abnormalities were observed only from Stage C or Stage D.</br>
Conclusions</br>
Dispersion slope could detect early liver damage, and the combination of elasticity and dispersion slope could clarify the progression of liver dysfunction in HF. SWE may be valuable to manage therapeutic strategies in patients with HF.
en-copyright=
kn-copyright=

en-aut-name=NakayamaRie
en-aut-sei=Nakayama
en-aut-mei=Rie
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TakayaYoichi
en-aut-sei=Takaya
en-aut-mei=Yoichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=NakamuraKazufumi
en-aut-sei=Nakamura
en-aut-mei=Kazufumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TohNorihisa
en-aut-sei=Toh
en-aut-mei=Norihisa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=ItoHiroshi
en-aut-sei=Ito
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

affil-num=1
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Science
kn-affil=

affil-num=2
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Science
kn-affil=

affil-num=3
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Science
kn-affil=

affil-num=4
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Science
kn-affil=

affil-num=5
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Science
kn-affil=
en-keyword=Shear wave elastography
kn-keyword=Shear wave elastography
en-keyword=Elasticity
kn-keyword=Elasticity
en-keyword=Dispersion slope
kn-keyword=Dispersion slope
en-keyword=Liver dysfunction
kn-keyword=Liver dysfunction
en-keyword=Heart failure
kn-keyword=Heart failure
END

start-ver=1.4
cd-journal=joma
no-vol=9
cd-vols=
no-issue=1
article-no=
start-page=2045894019831217
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2019
dt-pub=20190215
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Improvement of lung function and pulmonary hypertension after pulmonary aneurysm repair: case series 
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Pulmonary artery aneurysms (PAA) can be complicated with pulmonary arterial hypertension (PAH), causing sudden death due to PA rupture and dissection. Because treatment with PAH-targeted drugs does not always prevent PAA progression, prophylactic surgical repair of the PAA seems a promising alternative. However, although it avoids rupture and dissection of the PAs, additional benefits have not been forthcoming. We therefore present two patients with co-existing PAH and a PAA who underwent surgical repair of the aneurysm. Following the surgery, their lung function and pulmonary hypertension improved. Optimal treatment of PAA remains uncertain, however, with no clear guidelines regarding the best therapeutic approach. This case series provides physicians with reasons to repair PAA surgically in patients with PAH.
en-copyright=
kn-copyright=

en-aut-name=AkagiSatoshi
en-aut-sei=Akagi
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=EjiriKentaro
en-aut-sei=Ejiri
en-aut-mei=Kentaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KasaharaShingo
en-aut-sei=Kasahara
en-aut-mei=Shingo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=NakamuraKazufumi
en-aut-sei=Nakamura
en-aut-mei=Kazufumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=ItoHiroshi
en-aut-sei=Ito
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

affil-num=1
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Science
kn-affil=

affil-num=2
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Science
kn-affil=

affil-num=3
en-affil=Department of Cardiovascular Surgery, Okayama University Hospital
kn-affil=

affil-num=4
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Science
kn-affil=

affil-num=5
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Science
kn-affil=
en-keyword=vital capacity
kn-keyword=vital capacity
en-keyword=pulmonary artery pressure
kn-keyword=pulmonary artery pressure
en-keyword=lung perfusion and oxygenation
kn-keyword=lung perfusion and oxygenation
END

start-ver=1.4
cd-journal=joma
no-vol=75
cd-vols=
no-issue=1
article-no=
start-page=45
end-page=53
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2021
dt-pub=202102
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Possible Protective Effect of Remote Ischemic Preconditioning on Acute Kidney Injury Following Elective Percutaneous Coronary Intervention: Secondary Analysis of a Multicenter, Randomized Study
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Remote ischemic preconditioning (RIPC) is a promising strategy for protecting against ischemic reperfusion injury. This study is a secondary analysis of a randomized study that aimed to evaluate the effect of RIPC on the early increase in serum creatinine (SCr) following percutaneous coronary intervention (PCI), which is associ-ated with contrast-induced acute kidney injury. Patients with stable angina undergoing elective PCI were assigned to control, RIPC, and continuous infusion of nicorandil (nicorandil) groups. The endpoint of this study was the incidence of the early increase in SCr, a predictor of contrast-induced acute kidney injury, which was defined as either a > 20% or absolute increase by 0.3 mg/dl of SCr levels after 24 h of PCI. This study included 220 patients for whom a dataset of SCr values was available. The incidence of the early increase in SCr was significantly lower in the RIPC than in the control (1.3% vs 10.8%, p = 0.03) group, but was not significantly different between the nicorandil and control groups. In multivariate analysis, RIPC remained a significant fac-tor associated with a reduction in the incidence of early increase in SCr. RIPC reduces the incidence of early increase in SCr in patients with stable angina following elective PCI.
en-copyright=
kn-copyright=

en-aut-name=OtsukaHiroaki
en-aut-sei=Otsuka
en-aut-mei=Hiroaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MiyoshiToru
en-aut-sei=Miyoshi
en-aut-mei=Toru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=EjiriKentaro
en-aut-sei=Ejiri
en-aut-mei=Kentaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KohnoKunihisa
en-aut-sei=Kohno
en-aut-mei=Kunihisa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=NakahamaMakoto
en-aut-sei=Nakahama
en-aut-mei=Makoto
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=DoiMasayuki
en-aut-sei=Doi
en-aut-mei=Masayuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=MunemasaMitsuru
en-aut-sei=Munemasa
en-aut-mei=Mitsuru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=MurakamiMasaaki
en-aut-sei=Murakami
en-aut-mei=Masaaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=NakamuraKazufumi
en-aut-sei=Nakamura
en-aut-mei=Kazufumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=ItoHiroshi
en-aut-sei=Ito
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

affil-num=1
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Density and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Density and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Density and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Density and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of Cardiology, Fukuyama City Hospital
kn-affil=

affil-num=6
en-affil=Department of Cardiology, Kagawa Prefectural Central Hospital
kn-affil=

affil-num=7
en-affil=Department of Cardiology, Okayama Medical Center
kn-affil=

affil-num=8
en-affil=Department of Cardiology, Okayama Heart Clinic
kn-affil=

affil-num=9
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Density and Pharmaceutical Sciences
kn-affil=

affil-num=10
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Density and Pharmaceutical Sciences
kn-affil=
en-keyword=remote ischemic preconditioning
kn-keyword=remote ischemic preconditioning
en-keyword=stable angina
kn-keyword=stable angina
en-keyword=serum creatinine
kn-keyword=serum creatinine
en-keyword=acute kidney injury
kn-keyword=acute kidney injury
END

start-ver=1.4
cd-journal=joma
no-vol=20
cd-vols=
no-issue=1
article-no=
start-page=2021
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2021
dt-pub=20210107
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Prognostic value of non-alcoholic fatty liver disease for predicting cardiovascular events in patients with diabetes mellitus with suspected coronary artery disease: a prospective cohort study
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background</br>
Risk stratification of cardiovascular events in patients with type 2 diabetes mellitus (T2DM) has not been established. Coronary artery calcium score (CACS) and non-alcoholic fatty liver disease (NAFLD) are independently associated with cardiovascular events in T2DM patients. This study examined the incremental prognostic value of NAFLD assessed by non-enhanced computed tomography (CT) in addition to CACS and Framingham risk score (FRS) for cardiovascular events in T2DM patients.</br>
Methods</br>
This prospective pilot study included 529 T2DM outpatients with no history of cardiovascular disease who underwent CACS measurement because of suspected coronary artery disease. NAFLD was defined on CT images as a liver:spleen attenuation ratio?<?1.0. Cardiovascular events were defined as cardiovascular death, nonfatal myocardial infarction, late coronary revascularization, nonfatal stroke, or hospitalization for heart failure.</br>
Results</br>
Among 529 patients (61% men, mean age 65 years), NAFLD was identified in 143 (27%). Forty-four cardiovascular events were documented during a median follow-up of 4.4 years. In multivariate Cox regression analysis, NAFLD, CACS, and FRS were associated with cardiovascular events (hazard ratios and 95% confidence intervals 5.43, 2.82?10.44, p?<?0.001; 1.56, 1.32?1.86, p?<?0.001; 1.23, 1.08?1.39, p?=?0.001, respectively). The global χ2 score for predicting cardiovascular events increased significantly from 27.0 to 49.7 by adding NAFLD to CACS and FRS (p?<?0.001). The addition of NAFLD to a model including CACS and FRS significantly increased the C-statistic from 0.71 to 0.80 (p?=?0.005). The net reclassification achieved by adding CACS and FRS was 0.551 (p?<?0.001).</br>
Conclusions</br>
NAFLD assessed by CT, in addition to CACS and FRS, could be useful for identifying T2DM patients at higher risk of cardiovascular events.
en-copyright=
kn-copyright=

en-aut-name=IchikawaKeishi
en-aut-sei=Ichikawa
en-aut-mei=Keishi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MiyoshiToru
en-aut-sei=Miyoshi
en-aut-mei=Toru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=OsawaKazuhiro
en-aut-sei=Osawa
en-aut-mei=Kazuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MikiTakashi
en-aut-sei=Miki
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=TodaHironobu
en-aut-sei=Toda
en-aut-mei=Hironobu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=EjiriKentaro
en-aut-sei=Ejiri
en-aut-mei=Kentaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=YoshidaMasatoki
en-aut-sei=Yoshida
en-aut-mei=Masatoki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=NanbaYusuke
en-aut-sei=Nanba
en-aut-mei=Yusuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=YoshidaMasashi
en-aut-sei=Yoshida
en-aut-mei=Masashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=NakamuraKazufumi
en-aut-sei=Nakamura
en-aut-mei=Kazufumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=MoritaHiroshi
en-aut-sei=Morita
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=ItoHiroshi
en-aut-sei=Ito
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

affil-num=1
en-affil=Department of Cardiovascular Medicine, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine
kn-affil=

affil-num=2
en-affil=Department of Cardiovascular Medicine, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine
kn-affil=

affil-num=3
en-affil=Department of Cardiovascular Medicine, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine
kn-affil=

affil-num=4
en-affil=Department of Cardiovascular Medicine, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine
kn-affil=

affil-num=5
en-affil=Department of Cardiovascular Medicine, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine
kn-affil=

affil-num=6
en-affil=Department of Cardiovascular Medicine, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine
kn-affil=

affil-num=7
en-affil=Department of Cardiovascular Medicine, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine
kn-affil=

affil-num=8
en-affil=Department of Cardiovascular Medicine, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine
kn-affil=

affil-num=9
en-affil=Department of Cardiovascular Medicine, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine
kn-affil=

affil-num=10
en-affil=Department of Cardiovascular Medicine, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine
kn-affil=

affil-num=11
en-affil=Department of Cardiovascular Therapeutics, Dentistry, and Pharmaceutical Sciences, Okayama University Graduate School of Medicine
kn-affil=

affil-num=12
en-affil=Department of Cardiovascular Medicine, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine
kn-affil=
en-keyword=Cardiovascular disease
kn-keyword=Cardiovascular disease
en-keyword=Computed tomography
kn-keyword=Computed tomography
en-keyword=Coronary artery calcium
kn-keyword=Coronary artery calcium
en-keyword=Non-alcoholic fatty liver disease
kn-keyword=Non-alcoholic fatty liver disease
en-keyword=Risk stratification
kn-keyword=Risk stratification
END

start-ver=1.4
cd-journal=joma
no-vol=84
cd-vols=
no-issue=2
article-no=
start-page=245
end-page=251
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2020
dt-pub=20200124
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Marked Reduction of Pulmonary Artery Pressure After Registration for Lung Transplantation Is Associated With Long-Term Survival in Patients With Pulmonary Arterial Hypertension　― Cohort Study ―
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background:The waiting period for lung transplantation (LT) is approximately 3 years in Japan. The prognosis of patients with pulmonary arterial hypertension (PAH) awaiting LT is poor without LT. Patients at the present center often survive in the long term after registration for LT. The aim of this study was to elucidate why some patients survive in the long term by investigating changes in pulmonary artery pressure (PAP) after registration, and medication used.</br>
Methods?and?Results:This study involved 57 patients with PAH who were enrolled in a registry for LT at Okayama University Hospital. We divided patients into 3 groups according to outcome: LT (n=27); death without LT (n=21); and survival without LT (n=9). The median interval from PAH diagnosis to epoprostenol treatment was shorter in the survival group (58 days) than in the LT group (378 days) and death group (545 days). Eight patients in the survival group, 13 in the LT group, and 13 in the death group underwent right heart catheterization after registration. Percent change in mean PAP after registration was significantly greater in the survival group (?32%) than in the LT group (?13%) and death group (1%; P<0.01).</br>
Conclusions:Even after LT registration, patients who received epoprostenol infusion soon after diagnosis of PAH often had marked reduction in PAP and long-term survival without LT.
en-copyright=
kn-copyright=

en-aut-name=AkagiSatoshi
en-aut-sei=Akagi
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MatsubaraHiromi
en-aut-sei=Matsubara
en-aut-mei=Hiromi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=NakamuraKazufumi
en-aut-sei=Nakamura
en-aut-mei=Kazufumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=OtoTakahiro
en-aut-sei=Oto
en-aut-mei=Takahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=EjiriKentaro
en-aut-sei=Ejiri
en-aut-mei=Kentaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=ItoHiroshi
en-aut-sei=Ito
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

affil-num=1
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Science
kn-affil=

affil-num=2
en-affil=Division of Cardiology, Okayama Medical Center
kn-affil=

affil-num=3
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Science
kn-affil=

affil-num=4
en-affil=Department of Organ Transplant Center, Okayama University Hospital
kn-affil=

affil-num=5
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Science
kn-affil=

affil-num=6
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Science
kn-affil=
en-keyword=Lung transplantation
kn-keyword=Lung transplantation
en-keyword=Pulmonary artery hypertension
kn-keyword=Pulmonary artery hypertension
en-keyword=Pulmonary artery pressure
kn-keyword=Pulmonary artery pressure
en-keyword=Survival
kn-keyword=Survival
END

start-ver=1.4
cd-journal=joma
no-vol=19
cd-vols=
no-issue=1
article-no=
start-page=213
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2020
dt-pub=20201214
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Correction to: Combination therapy with pemafibrate (K-877) and pitavastatin improves vascular endothelial dysfunction in dahl/salt-sensitive rats fed a high-salt and high-fat diet
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=YoshidaMasatoki
en-aut-sei=Yoshida
en-aut-mei=Masatoki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NakamuraKazufumi
en-aut-sei=Nakamura
en-aut-mei=Kazufumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=MiyoshiToru
en-aut-sei=Miyoshi
en-aut-mei=Toru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=YoshidaMasashi
en-aut-sei=Yoshida
en-aut-mei=Masashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KondoMegumi
en-aut-sei=Kondo
en-aut-mei=Megumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=AkazawaKaoru
en-aut-sei=Akazawa
en-aut-mei=Kaoru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=KimuraTomonari
en-aut-sei=Kimura
en-aut-mei=Tomonari
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=OhtsukaHiroaki
en-aut-sei=Ohtsuka
en-aut-mei=Hiroaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=OhnoYuko
en-aut-sei=Ohno
en-aut-mei=Yuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=MiuraDaiji
en-aut-sei=Miura
en-aut-mei=Daiji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=ItoHiroshi
en-aut-sei=Ito
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

affil-num=1
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=6
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=7
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=8
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=9
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=10
en-affil=Department of Basic and Clinical Medicine, Nagano College of Nursing
kn-affil=

affil-num=11
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=9
cd-vols=
no-issue=16
article-no=
start-page=e015103
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2020
dt-pub=20200818
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Effect of Luseogliflozin on Heart Failure With Preserved Ejection Fraction in Patients With Diabetes Mellitus
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background</br>
Effects of sodium‐glucose cotransporter 2 inhibitors on reducing hospitalization for heart failure have been reported in randomized controlled trials, but their effects on patients with heart failure with preserved ejection fraction (HFpEF) are unknown. This study aimed to evaluate the drug efficacy of luseogliflozin, a sodium‐glucose cotransporter 2 inhibitor, in patients with type 2 diabetes mellitus and HFpEF.</br>
Methods and Results</br>
We performed a multicenter, open‐label, randomized, controlled trial for comparing luseogliflozin 2.5 mg once daily with voglibose 0.2 mg 3 times daily in patients with type 2 diabetes mellitus suffering from HFpEF (left ventricular ejection fraction >45% and BNP [B‐type natriuretic peptide] concentrations ?35 pg/mL) in a 1:1 randomization fashion. The primary outcome was the difference from baseline in BNP levels after 12 weeks of treatment between the 2 drugs. A total of 173 patients with diabetes mellitus and HFpEF were included. Of these, 83 patients were assigned to receive luseogliflozin and 82 to receive voglibose. There was no significant difference in the reduction in BNP concentrations after 12 weeks from baseline between the 2 groups. The ratio of the mean BNP value at week 12 to the baseline value was 0.79 in the luseogliflozin group and 0.87 in the voglibose group (percent change, ?9.0% versus ?1.9%; ratio of change with luseogliflozin versus voglibose, 0.93; 95% CI, 0.78?1.10; P=0.26).</br>
Conclusion</br>
In patients with type 2 diabetes mellitus and HFpEF, there is no significant difference in the degree of reduction in BNP concentrations after 12 weeks between luseogliflozin and voglibose.
en-copyright=
kn-copyright=

en-aut-name=EjiriKentaro
en-aut-sei=Ejiri
en-aut-mei=Kentaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MiyoshiToru
en-aut-sei=Miyoshi
en-aut-mei=Toru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KiharaHajime
en-aut-sei=Kihara
en-aut-mei=Hajime
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=HataYoshiki
en-aut-sei=Hata
en-aut-mei=Yoshiki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=NaganoToshihiko
en-aut-sei=Nagano
en-aut-mei=Toshihiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=TakaishiAtsushi
en-aut-sei=Takaishi
en-aut-mei=Atsushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=TodaHironobu
en-aut-sei=Toda
en-aut-mei=Hironobu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=NanbaSeiji
en-aut-sei=Nanba
en-aut-mei=Seiji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=NakamuraYoichi
en-aut-sei=Nakamura
en-aut-mei=Yoichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=AkagiSatoshi
en-aut-sei=Akagi
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=SakuragiSatoru
en-aut-sei=Sakuragi
en-aut-mei=Satoru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=MinagawaTaro
en-aut-sei=Minagawa
en-aut-mei=Taro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=KawaiYusuke
en-aut-sei=Kawai
en-aut-mei=Yusuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=NishiiNobuhiro
en-aut-sei=Nishii
en-aut-mei=Nobuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=FukeSoichiro
en-aut-sei=Fuke
en-aut-mei=Soichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

en-aut-name=YoshikawaMasaki
en-aut-sei=Yoshikawa
en-aut-mei=Masaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=16
ORCID=

en-aut-name=NakamuraKazufumi
en-aut-sei=Nakamura
en-aut-mei=Kazufumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=17
ORCID=

en-aut-name=ItoHiroshi
en-aut-sei=Ito
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=18
ORCID=

affil-num=1
en-affil=Okayama University Graduate School of Medicine, Density and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Okayama University Graduate School of Medicine, Density and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Internal Medicine, Kihara Cardiovascular Clinic
kn-affil=

affil-num=4
en-affil=Department of Cardiology, Minamino Cardiovascular Hospital
kn-affil=

affil-num=5
en-affil=Department of Internal Medicine, Iwasa Hospital
kn-affil=

affil-num=6
en-affil=Department of Cardiology, Mitoyo General Hospital
kn-affil=

affil-num=7
en-affil=Okayama University Graduate School of Medicine, Density and Pharmaceutical Sciences
kn-affil=

affil-num=8
en-affil=Department of Cardiology, Okayama Rosai Hospital
kn-affil=

affil-num=9
en-affil=Department of Cardiovascular Medicine, Specified Clinic of Soyokaze Cardiovascular Medicine and Diabetes Care
kn-affil=

affil-num=10
en-affil=Okayama University Graduate School of Medicine, Density and Pharmaceutical Sciences
kn-affil=

affil-num=11
en-affil=Department of Cardiovascular Medicine, Iwakuni Clinical Center
kn-affil=

affil-num=12
en-affil=Department of Internal Medicine, Minagawa Cardiovascular Clinic
kn-affil=

affil-num=13
en-affil=Department of Cardiovascular Medicine, Okayama City Hospital
kn-affil=

affil-num=14
en-affil=Okayama University Graduate School of Medicine, Density and Pharmaceutical Sciences
kn-affil=

affil-num=15
en-affil=Department of Cardiovascular Medicine, Japanese Red Cross Okayama Hospital
kn-affil=

affil-num=16
en-affil=Department of Cardiology, Fukuyama City Hospital
kn-affil=

affil-num=17
en-affil=Okayama University Graduate School of Medicine, Density and Pharmaceutical Sciences
kn-affil=

affil-num=18
en-affil=Okayama University Graduate School of Medicine, Density and Pharmaceutical Sciences
kn-affil=
en-keyword=B-type natriuretic peptide
kn-keyword=B-type natriuretic peptide
en-keyword=diabetes mellitus
kn-keyword=diabetes mellitus
en-keyword=heart failure
kn-keyword=heart failure
en-keyword=sodium-glucose cotransporter 2 inhibitor
kn-keyword=sodium-glucose cotransporter 2 inhibitor
END

start-ver=1.4
cd-journal=joma
no-vol=19
cd-vols=
no-issue=1
article-no=
start-page=149
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2020
dt-pub=20200926
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Combination therapy with pemafibrate (K-877) and pitavastatin improves vascular endothelial dysfunction in dahl/salt-sensitive rats fed a high-salt and high-fat diet
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background Statins suppress the progression of atherosclerosis by reducing low-density lipoprotein (LDL) cholesterol levels. Pemafibrate (K-877), a novel selective peroxisome proliferator-activated receptor alpha modulator, is expected to reduce residual risk factors including high triglycerides (TGs) and low high-density lipoprotein (HDL) cholesterol during statin treatment. However, it is not known if statin therapy with add-on pemafibrate improves the progression of atherosclerosis. The aim of this study was to assess the effect of combination therapy with pitavastatin and pemafibrate on lipid profiles and endothelial dysfunction in hypertension and insulin resistance model rats. Methods Seven-week-old male Dahl salt-sensitive (DS) rats were divided into the following five treatment groups (normal diet (ND) plus vehicle, high-salt and high-fat diet (HD) plus vehicle, HD plus pitavastatin (0.3 mg/kg/day), HD plus pemafibrate (K-877) (0.5 mg/kg/day), and HD plus combination of pitavastatin and pemafibrate) and treated for 12 weeks. At 19 weeks, endothelium-dependent relaxation of the thoracic aorta in response to acetylcholine was evaluated. Results After feeding for 12 weeks, systolic blood pressure and plasma levels of total cholesterol were significantly higher in the HD-vehicle group compared with the ND-vehicle group. Combination therapy with pitavastatin and pemafibrate significantly reduced systolic blood pressure, TG levels, including total, chylomicron (CM), very LDL (VLDL), HDL-TG, and cholesterol levels, including total, CM, VLDL, and LDL-cholesterol, compared with vehicle treatment. Acetylcholine caused concentration-dependent relaxation of thoracic aorta rings that were pre-contracted with phenylephrine in all rats. Relaxation rates in the HD-vehicle group were significantly lower compared with the ND-vehicle group. Relaxation rates in the HD-combination of pitavastatin and pemafibrate group significantly increased compared with the HD-vehicle group, although neither medication alone ameliorated relaxation rates significantly. Western blotting experiments showed increased phosphorylated endothelial nitric oxide synthase protein expression in aortas from rats in the HD-pemafibrate group and the HD-combination group compared with the HD-vehicle group. However, the expression levels did not respond significantly to pitavastatin alone. Conclusions Combination therapy with pitavastatin and pemafibrate improved lipid profiles and endothelial dysfunction in hypertension and insulin resistance model rats. Pemafibrate as an add-on strategy to statins may be useful for preventing atherosclerosis progression.
en-copyright=
kn-copyright=

en-aut-name=YoshidaMasatoki
en-aut-sei=Yoshida
en-aut-mei=Masatoki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NakamuraKazufumi
en-aut-sei=Nakamura
en-aut-mei=Kazufumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=MiyoshiToru
en-aut-sei=Miyoshi
en-aut-mei=Toru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=YoshidaMasashi
en-aut-sei=Yoshida
en-aut-mei=Masashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KondoMegumi
en-aut-sei=Kondo
en-aut-mei=Megumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=AkazawaKaoru
en-aut-sei=Akazawa
en-aut-mei=Kaoru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=KimuraTomonari
en-aut-sei=Kimura
en-aut-mei=Tomonari
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=OhtsukaHiroaki
en-aut-sei=Ohtsuka
en-aut-mei=Hiroaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=OhnoYuko
en-aut-sei=Ohno
en-aut-mei=Yuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=MiuraDaiji
en-aut-sei=Miura
en-aut-mei=Daiji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=ItoHiroshi
en-aut-sei=Ito
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

affil-num=1
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=6
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=7
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=8
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=9
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=10
en-affil=Department of Basic and Clinical Medicine, Nagano College of Nursing
kn-affil=

affil-num=11
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=Pemafibrate
kn-keyword=Pemafibrate
en-keyword=Statin
kn-keyword=Statin
en-keyword=Endothelial function
kn-keyword=Endothelial function
END

start-ver=1.4
cd-journal=joma
no-vol=10
cd-vols=
no-issue=1
article-no=
start-page=6869
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2020
dt-pub=20200422
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Deficiency of CD44 prevents thoracic aortic dissection in a murine model
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Thoracic aortic dissection (TAD) is a life-threatening vascular disease. We showed that CD44, a widely distributed cell surface adhesion molecule, has an important role in inflammation. In this study, we examined the role of CD44 in the development of TAD. TAD was induced by the continuous infusion of beta-aminopropionitrile (BAPN), a lysyl oxidase inhibitor, and angiotensin II (AngII) for 7 days in wild type (WT) mice and CD44 deficient (CD44(-/-)) mice. The incidence of TAD in CD44(-/-) mice was significantly reduced compared with WT mice (44% and 6%, p<0.01). Next, to evaluate the initial changes, aortic tissues at 24hours after BAPN/AngII infusion were examined. Neutrophil accumulation into thoracic aortic adventitia in CD44(-/-) mice was significantly decreased compared with that in WT mice (5.7 +/- 0.3% and 1.6 +/- 0.4%, p<0.01). In addition, BAPN/AngII induced interleukin-6, interleukin-1 beta, matrix metalloproteinase-2 and matrix metalloproteinase-9 in WT mice, all of which were significantly reduced in CD44(-/-) mice (all p<0.01). In vitro transmigration of neutrophils from CD44(-/-) mice through an endothelial monolayer was significantly decreased by 18% compared with WT mice (p<0.01). Our findings indicate that CD44 has a critical role in TAD development in association with neutrophil infiltration into adventitia.
en-copyright=
kn-copyright=

en-aut-name=HatipogluOmer F.
en-aut-sei=Hatipoglu
en-aut-mei=Omer F.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MiyoshiToru
en-aut-sei=Miyoshi
en-aut-mei=Toru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=YonezawaTomoko
en-aut-sei=Yonezawa
en-aut-mei=Tomoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KondoMegumi
en-aut-sei=Kondo
en-aut-mei=Megumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=AmiokaNaofumi
en-aut-sei=Amioka
en-aut-mei=Naofumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=YoshidaMasashi
en-aut-sei=Yoshida
en-aut-mei=Masashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=AkagiSatoshi
en-aut-sei=Akagi
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=NakamuraKazufumi
en-aut-sei=Nakamura
en-aut-mei=Kazufumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=HirohataSatoshi
en-aut-sei=Hirohata
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=ItoHiroshi
en-aut-sei=Ito
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

affil-num=1
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Science
kn-affil=

affil-num=2
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Science
kn-affil=

affil-num=3
en-affil=Department of Molecular Biology and Biochemistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Science
kn-affil=

affil-num=4
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Science
kn-affil=

affil-num=5
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Science
kn-affil=

affil-num=6
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Science
kn-affil=

affil-num=7
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Science
kn-affil=

affil-num=8
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Science
kn-affil=

affil-num=9
en-affil=Department of Medical Technology, Graduate School of Health Sciences, Okayama University
kn-affil=

affil-num=10
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Science
kn-affil=
en-keyword=Aneurysm
kn-keyword=Aneurysm
en-keyword=Aortic diseases
kn-keyword=Aortic diseases
END

start-ver=1.4
cd-journal=joma
no-vol=21
cd-vols=
no-issue=15
article-no=
start-page=5455
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2020
dt-pub=20200730
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Effects of Eicosapentaenoic Acid on Arterial Calcification
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Arterial calcification is a hallmark of advanced atherosclerosis and predicts cardiovascular events. However, there is no clinically accepted therapy that prevents progression of arterial calcification. HMG-CoA reductase inhibitors, statins, lower low-density lipoprotein-cholesterol and reduce cardiovascular events, but coronary artery calcification is actually promoted by statins. The addition of eicosapentaenoic acid (EPA) to statins further reduced cardiovascular events in clinical trials, JELIS and REDUCE-IT. Additionally, we found that EPA significantly suppressed arterial calcification in vitro and in vivo via suppression of inflammatory responses, oxidative stress and Wnt signaling. However, so far there is a lack of evidence showing the effect of EPA on arterial calcification in a clinical situation. We reviewed the molecular mechanisms of the inhibitory effect of EPA on arterial calcification and the results of some clinical trials.
en-copyright=
kn-copyright=

en-aut-name=SaitoYukihiro
en-aut-sei=Saito
en-aut-mei=Yukihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NakamuraKazufumi
en-aut-sei=Nakamura
en-aut-mei=Kazufumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=ItoHiroshi
en-aut-sei=Ito
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

affil-num=1
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=eicosapentaenoic acid
kn-keyword=eicosapentaenoic acid
en-keyword=atherosclerosis
kn-keyword=atherosclerosis
en-keyword=Klotho
kn-keyword=Klotho
END

start-ver=1.4
cd-journal=joma
no-vol=84
cd-vols=
no-issue=3
article-no=
start-page=487
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2020
dt-pub=20200225
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=New Appearance of Fragmented QRS as a Predictor of Ventricular Arrhythmic Events in Patients With Hypertrophic Cardiomyopathy
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background: Multiple spikes in the QRS complex (fragmented QRS [fQRS]) on 12-lead electrocardiography have been associated with ventricular arrhythmic events (VAEs) in patients with hypertrophic cardiomyopathy (HCM). The aim of this study was to assess the association between new appearances of fQRS and cardiac events in patients with HCM.Methods and Results:The association between baseline fQRS and cardiac events, namely VAEs, heart failure-related hospitalization, and all-cause death, was evaluated retrospectively in 146 HCM patients (46 patients with fQRS, 100 without fQRS). The median follow-up was 5.3 years. Cardiac events occurred in 29 patients with baseline fQRS and 32 patients without baseline fQRS (63% vs. 32%; P<0.001). VAEs occurred in a significantly larger percentage of patients with than without baseline fQRS (54% vs. 23%, respectively; P<0.001). Of the 100 patients without baseline fQRS, 33 had a new appearance of fQRS during the 4.6-year follow-up, whereas 67 did not. VAEs occurred more frequently in the 33 patients with the appearance of fQRS than in those without (42% vs. 13%, respectively; P=0.001). Multivariable analysis showed that the new appearance of fQRS documented before VAEs was associated with VAEs (hazard ratio 4.29, 95% confidence interval 1.81-10.2; P=0.001).<br/>
Conclusions: The new appearance of fQRS was associated with an increased risk of VAEs in HCM patients.
en-copyright=
kn-copyright=

en-aut-name=OguraSoichiro
en-aut-sei=Ogura
en-aut-mei=Soichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NakamuraKazufumi
en-aut-sei=Nakamura
en-aut-mei=Kazufumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=MoritaHiroshi
en-aut-sei=Morita
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TohNorihisa
en-aut-sei=Toh
en-aut-mei=Norihisa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=NakagawaKoji
en-aut-sei=Nakagawa
en-aut-mei=Koji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=YoshidaMasashi
en-aut-sei=Yoshida
en-aut-mei=Masashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=WatanabeAtsuyuki
en-aut-sei=Watanabe
en-aut-mei=Atsuyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=NishiiNobuhiro
en-aut-sei=Nishii
en-aut-mei=Nobuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=MiyoshiToru
en-aut-sei=Miyoshi
en-aut-mei=Toru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=ItoHiroshi
en-aut-sei=Ito
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

affil-num=1
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=6
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=7
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=8
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=9
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=10
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=Electrocardiography
kn-keyword=Electrocardiography
en-keyword=Fragmented QRS
kn-keyword=Fragmented QRS
en-keyword=Hospitalization
kn-keyword=Hospitalization
en-keyword=Hypertrophic cardiomyopathy
kn-keyword=Hypertrophic cardiomyopathy
en-keyword=Ventricular arrhythmia.
kn-keyword=Ventricular arrhythmia.
END

start-ver=1.4
cd-journal=joma
no-vol=20
cd-vols=
no-issue=23
article-no=
start-page=5885
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2019
dt-pub=20191123
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Current Treatment Strategies and Nanoparticle-Mediated Drug Delivery Systems for Pulmonary Arterial Hypertension
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=There are three critical pathways for the pathogenesis and progression of pulmonary arterial hypertension (PAH): the prostacyclin (prostaglandin I-2) (PGI(2)), nitric oxide (NO), and endothelin pathways. The current approved drugs targeting these three pathways, including prostacyclin (PGI(2)), phosphodiesterase type-5 (PDE5) inhibitors, and endothelin receptor antagonists (ERAs), have been shown to be effective, however, PAH remains a severe clinical condition and the long-term survival of patients with PAH is still suboptimal. The full therapeutic abilities of available drugs are reduced by medication, patient non-compliance, and side effects. Nanoparticles are expected to address these problems by providing a novel drug delivery approach for the treatment of PAH. Drug-loaded nanoparticles for local delivery can optimize the efficacy and minimize the adverse effects of drugs. Prostacyclin (PGI(2)) analogue, PDE5 inhibitors, ERA, pitavastatin, imatinib, rapamycin, fasudil, and oligonucleotides-loaded nanoparticles have been reported to be effective in animal PAH models and in vitro studies. However, the efficacy and safety of nanoparticle mediated-drug delivery systems for PAH treatment in humans are unknown and further clinical studies are required to clarify these points.
en-copyright=
kn-copyright=

en-aut-name=NakamuraKazufumi
en-aut-sei=Nakamura
en-aut-mei=Kazufumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=AkagiSatoshi
en-aut-sei=Akagi
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=EjiriKentaro
en-aut-sei=Ejiri
en-aut-mei=Kentaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=YoshidaMasashi
en-aut-sei=Yoshida
en-aut-mei=Masashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=MiyoshiToru
en-aut-sei=Miyoshi
en-aut-mei=Toru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=TohNorihisa
en-aut-sei=Toh
en-aut-mei=Norihisa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=NakagawaKoji
en-aut-sei=Nakagawa
en-aut-mei=Koji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=TakayaYoichi
en-aut-sei=Takaya
en-aut-mei=Yoichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=MatsubaraHiromi
en-aut-sei=Matsubara
en-aut-mei=Hiromi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=ItoHiroshi
en-aut-sei=Ito
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

affil-num=1
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil= Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil= Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil= Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil= Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=6
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=7
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=8
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=9
en-affil=Division of Cardiology, National Hospital Organization Okayama Medical Center
kn-affil=

affil-num=10
en-affil= Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=pulmonary arterial hypertension
kn-keyword=pulmonary arterial hypertension
en-keyword=prostaglandin I-2
kn-keyword=prostaglandin I-2
en-keyword=nitric oxide
kn-keyword=nitric oxide
en-keyword=endothelin
kn-keyword=endothelin
END

start-ver=1.4
cd-journal=joma
no-vol=9
cd-vols=
no-issue=4
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2019
dt-pub=20191218
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Liver transplantation in a patient with hereditary haemorrhagic telangiectasia and pulmonary hypertension
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract= Hereditary haemorrhagic telangiectasia or Rendu-Osler-Weber syndrome is a systemic vascular disease with autosomal dominant inheritance, mucocutaneous telangiectasia, and repeated nasal bleeding due to vascular abnormalities. Hereditary haemorrhagic telangiectasia may occasionally lead to complications, including arteriovenous malformations and pulmonary hypertension. We present a case of a 52-year-old female patient with hereditary haemorrhagic telangiectasia who was referred to our hospital for treatment of pulmonary hypertension. She had been diagnosed with hereditary haemorrhagic telangiectasia during adolescence and was being followed up. Six months prior to presentation, she had undergone coil embolization for pulmonary haemorrhage due to pulmonary arteriovenous malformations. She was in World Health Organization functional class IV, with a mean of pulmonary arterial pressure of 38 mmHg, a pulmonary capillary wedge pressure of 10 mmHg, and a right atrial pressure of 22 mmHg. A contrast-enhanced computed tomography angiography showed large arteriovenous malformations in the liver. Right heart catheterization revealed an increase in oxygen saturation in the inferior vena cava between the supra- and infra-hepatic veins, low pulmonary vascular resistance, and high right atrial pressure. Hence, she was diagnosed with hereditary haemorrhagic telangiectasia with pulmonary hypertension due to major arteriovenous shunt resulting from arteriovenous malformations in the liver. Therefore, we considered liver transplantation as an essential treatment option. She underwent cadaveric liver transplantation after a year resulting in dramatic haemodynamic improvement to World Health Organization functional class I. Liver transplantation is a promising treatment in patients with hereditary haemorrhagic telangiectasia and pulmonary hypertension resulting from arteriovenous shunt caused by arteriovenous malformations in the liver.
en-copyright=
kn-copyright=

en-aut-name=
en-aut-sei=
en-aut-mei=
kn-aut-name=EjiriKentaro
kn-aut-sei=Ejiri
kn-aut-mei=Kentaro
aut-affil-num=1
ORCID=

en-aut-name=AkagiSatoshi
en-aut-sei=Akagi
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=NakamuraKazufumi
en-aut-sei=Nakamura
en-aut-mei=Kazufumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=AmiokaNaofumi
en-aut-sei=Amioka
en-aut-mei=Naofumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=IchikawaKeishi
en-aut-sei=Ichikawa
en-aut-mei=Keishi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=YagiTakahito
en-aut-sei=Yagi
en-aut-mei=Takahito
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=ItoHiroshi
en-aut-sei=Ito
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

affil-num=1
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=6
en-affil=Department of Hepato-Biliary-Pancreatic Surgery, Okayama University Hospital
kn-affil=

affil-num=7
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=Rendu-Osler-Weber syndrome
kn-keyword=Rendu-Osler-Weber syndrome
en-keyword=arteriovenous malformation
kn-keyword=arteriovenous malformation
en-keyword=pulmonary haemorrhage
kn-keyword=pulmonary haemorrhage
END

start-ver=1.4
cd-journal=joma
no-vol=42
cd-vols=
no-issue=425
article-no=
start-page=752
end-page=753
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2019
dt-pub=20190214
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=The optimal amount of salt intake.
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=NakamuraKazufumi
en-aut-sei=Nakamura
en-aut-mei=Kazufumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MiyoshiToru
en-aut-sei=Miyoshi
en-aut-mei=Toru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

affil-num=1
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama
kn-affil=

affil-num=2
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=70
cd-vols=
no-issue=5
article-no=
start-page=397
end-page=400
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2016
dt-pub=201610
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Feasibility of Repairing Defects Followed by Treatment with Pulmonary Hypertension-specific Drugs (Repair and Treat) in Patients with Pulmonary Hypertension Associated with Atrial Septal Defect: Study Protocol for Interventional Trial
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=A treatment strategy for patients with pulmonary hypertension (PH) and atrial septal defect (ASD) remains unclear. This study was designed to evaluate the effects of initial repair of ASD followed by treatment with PH-specific drugs in patients with PH and ASD. Eligible patients receive transcatheter ASD closure followed by treatment with bosentan and sildenafil. Right heart catheterization is performed at baseline and at 12, 24 and 48 weeks. The primary endpoint is change in pulmonary artery pressure and pulmonary vascular resistance from baseline to follow-up. This study should provide valuable information to establish a therapeutic strategy for PH and ASD.
en-copyright=
kn-copyright=

en-aut-name=AkagiSatoshi
en-aut-sei=Akagi
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NakamuraKazufumi
en-aut-sei=Nakamura
en-aut-mei=Kazufumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=AkagiTeiji
en-aut-sei=Akagi
en-aut-mei=Teiji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=NakagawaKoji
en-aut-sei=Nakagawa
en-aut-mei=Koji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=TakayaYoichi
en-aut-sei=Takaya
en-aut-mei=Yoichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=SarashinaToshihiro
en-aut-sei=Sarashina
en-aut-mei=Toshihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=EjiriKentaro
en-aut-sei=Ejiri
en-aut-mei=Kentaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=ItoHiroshi
en-aut-sei=Ito
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

affil-num=1
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Science
kn-affil=

affil-num=2
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Science
kn-affil=

affil-num=3
en-affil=Cardiac Intensive Care Unit, Okayama University Hospital
kn-affil=

affil-num=4
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Science
kn-affil=

affil-num=5
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Science
kn-affil=

affil-num=6
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Science
kn-affil=

affil-num=7
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Science
kn-affil=

affil-num=8
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Science
kn-affil=
en-keyword=pulmonary hypertension
kn-keyword=pulmonary hypertension
en-keyword=atrial septal defect
kn-keyword=atrial septal defect
en-keyword=repair and treat
kn-keyword=repair and treat
en-keyword=transcatheter closure
kn-keyword=transcatheter closure
END

start-ver=1.4
cd-journal=joma
no-vol=69
cd-vols=
no-issue=3
article-no=
start-page=129
end-page=136
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2015
dt-pub=201506
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Epoprostenol Therapy for Pulmonary Arterial Hypertension
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Pulmonary arterial hypertension (PAH) is characterized by elevation of pulmonary artery pressure caused by pulmonary vasoconstriction and vascular remodeling, which leads to right heart failure and death. Epoprostenol (prostaglandin I2) has a potent short-acting vasodilator property, and intravenous continuous epoprostenol is therefore used for treatment of PAH. Here we review evidence for the usefulness of intravenous continuous epoprostenol therapy in patients with PAH. Epoprostenol therapy is effective in idiopathic PAH patients and in patients with PAH associated with connective tissue disease, portal hypertension or congenital heart diseases, but it is not effective in patients with pulmonary veno-occlusive disease or pulmonary capillary hemangiomatosis. High-dose epoprostenol therapy markedly improved hemodynamics in some patients with PAH, possibly due to reverse remodeling of pulmonary arteries. This therapy has several side effects and complications such as headache, hypotension and catheter-related infections. Intravenous continuous epoprostenol is an effective treatment, but there are still some problems to be resolved.
en-copyright=
kn-copyright=

en-aut-name=AkagiSatoshi
en-aut-sei=Akagi
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NakamuraKazufumi
en-aut-sei=Nakamura
en-aut-mei=Kazufumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=MatsubaraHiromi
en-aut-sei=Matsubara
en-aut-mei=Hiromi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=OgawaAiko
en-aut-sei=Ogawa
en-aut-mei=Aiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=SarashinaToshihiro
en-aut-sei=Sarashina
en-aut-mei=Toshihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=EjiriKentaro
en-aut-sei=Ejiri
en-aut-mei=Kentaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=ItoHiroshi
en-aut-sei=Ito
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

affil-num=1
en-affil=
kn-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine

affil-num=2
en-affil=
kn-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine

affil-num=3
en-affil=
kn-affil=Department of Clinical Science, National Hospital Organization Okayama Medical Center

affil-num=4
en-affil=
kn-affil=Department of Clinical Science, National Hospital Organization Okayama Medical Center

affil-num=5
en-affil=
kn-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine

affil-num=6
en-affil=
kn-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine

affil-num=7
en-affil=
kn-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine
en-keyword=pulmonary arterial hypertension
kn-keyword=pulmonary arterial hypertension
en-keyword=epoprostenol
kn-keyword=epoprostenol
en-keyword=high-dose
kn-keyword=high-dose
en-keyword=complications
kn-keyword=complications
en-keyword=side effects
kn-keyword=side effects
END

start-ver=1.4
cd-journal=joma
no-vol=63
cd-vols=
no-issue=20
article-no=
start-page=2131
end-page=2138
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2014
dt-pub=20140527
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Electrocardiographic Parameters and Fatal Arrhythmic Events in Patients With Brugada Syndrome
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Objectives This study aimed to determine the usefulness of the combination of several electrocardiographic markers on risk assessment of ventricular fibrillation (VF) in patients with Brugada syndrome (BrS). 

Background Detection of high-/low-risk BrS patients using a noninvasive method is an important issue in the clinical setting. Several electrocardiographic markers related to depolarization and repolarization abnormalities have been reported, but the relationship and usefulness of these parameters in VF events are unclear. 

Methods Baseline characteristics of 246 consecutive patients (236 men; mean age, 47.6 +/- 13.6 years) with a Brugada-type electrocardiogram, including 13 patients with a history of VF and 40 patients with a history of syncope episodes, were retrospectively analyzed. During the mean follow-up period of 45.1 months, VF in 23 patients and sudden cardiac death (SCD) in 1 patient were observed. Clinical/ genetic and electrocardiographic parameters were compared with VF/SCD events. 

Results On univariate analysis, a history of VF and syncope episodes, paroxysmal atrial fibrillation, spontaneous type 1 pattern in the precordial leads, and electrocardiographic markers of depolarization abnormalities (QRS duration >= 120 ms, and fragmented QRS [f-QRS]) and those of repolarization abnormalities (inferolateral early repolarization [ER] pattern and QT prolongation) were associated with later cardiac events. On multivariable analysis, a history of VF and syncope episodes, inferolateral ER pattern, and f-QRS were independent predictors of documented VF and SCD (odds ratios: 19.61, 28.57, 2.87, and 5.21, respectively; p < 0.05). Kaplan-Meier curves showed that the presence/ absence of inferolateral ER and f-QRS predicted a worse/better prognosis (log-rank test, p < 0.01). 

Conclusions The combination of depolarization and repolarization abnormalities in BrS is associated with later VF events. The combination of these abnormalities is useful for detecting high-and low-risk BrS patients.
en-copyright=
kn-copyright=

en-aut-name=TokiokaKoji
en-aut-sei=Tokioka
en-aut-mei=Koji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KusanoKengo F.
en-aut-sei=Kusano
en-aut-mei=Kengo F.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=MoritaHiroshi
en-aut-sei=Morita
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MiuraDaiji
en-aut-sei=Miura
en-aut-mei=Daiji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=NishiiNobuhiro
en-aut-sei=Nishii
en-aut-mei=Nobuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=NagaseSatoshi
en-aut-sei=Nagase
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=NakamuraKazufumi
en-aut-sei=Nakamura
en-aut-mei=Kazufumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=KohnoKunihisa
en-aut-sei=Kohno
en-aut-mei=Kunihisa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=ItoHiroshi
en-aut-sei=Ito
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=OheTohru
en-aut-sei=Ohe
en-aut-mei=Tohru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

affil-num=1
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Cardiovasc Med

affil-num=2
en-affil=
kn-affil=Natl Cerebral & Cardiovasc Ctr, Dept Cardiovasc Med

affil-num=3
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Cardiovasc Med

affil-num=4
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Cardiovasc Med

affil-num=5
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Cardiovasc Med

affil-num=6
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Cardiovasc Med

affil-num=7
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Cardiovasc Med

affil-num=8
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Cardiovasc Med

affil-num=9
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Cardiovasc Med

affil-num=10
en-affil=
kn-affil=Sakakibara Heart Inst Okayama
en-keyword=Brugada syndrome
kn-keyword=Brugada syndrome
en-keyword=early repolarization
kn-keyword=early repolarization
en-keyword=fragmented QRS
kn-keyword=fragmented QRS
en-keyword=noninvasive risk assessment
kn-keyword=noninvasive risk assessment
en-keyword=ventricular fibrillation
kn-keyword=ventricular fibrillation
END

start-ver=1.4
cd-journal=joma
no-vol=76
cd-vols=
no-issue=9
article-no=
start-page=2266
end-page=2272
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2012
dt-pub=201209
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Impact of Chronic Kidney Disease on Left Main Coronary Artery Disease and Prognosis in Japanese Patients
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background: Renal insufficiency plays a critical role in the pathogenesis of ischemic heart disease. The aim of the present study was to investigate the prevalence of renal dysfunction and its impact on prognosis in patients with left main coronary artery disease (LMCAD) and stable angina pectoris. 

Methods and Results: A total of 626 consecutive patients with significant coronary artery stenosis were enrolled. Renal insufficiency was graded using estimated glomerular filtration rate (eGFR) before coronary angiography. Chronic kidney disease (CKD) was defined as eGFR <60 ml.min(-1) 1.73 m(-2) and/or proteinuria. Patients with LMCAD (n=95) had a significantly higher prevalence of CKD than those without LMCAD (P=0.02). Multiple logistic regression analysis showed that CKD was independently associated with LMCAD (adjusted odds ratio, 1.74; 95% confidence interval [CI]: 1.09-2.76, P=0.01). A 1-year follow-up of patients with LMCAD showed that the cumulative incidence of major adverse cardiovascular events among patients with eGFR <30 ml.min(-1).1.73 m(-2) was higher than that among patients with eGFR >= 60 ml.min(-1).1.73 m(-2) (P=0.03). The hazard ratio for a cardiovascular event was 9.54 (95% CI: 3.15-28.89, P<0.01) when comparing patients with LMCAD and eGFR <30 ml.min(-1).1.73 m(-2) vs. patients without LMCAD and eGFR >= 60 ml.min(-1).1.73 m(-2). 

Conclusions: Renal insufficiency is a risk factor for LMCAD and predicts poor prognosis in Japanese patients.
en-copyright=
kn-copyright=

en-aut-name=DanKazuhiro
en-aut-sei=Dan
en-aut-mei=Kazuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MiyoshiToru
en-aut-sei=Miyoshi
en-aut-mei=Toru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=UeedaMasayuki
en-aut-sei=Ueeda
en-aut-mei=Masayuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=OhtsukaHiroaki
en-aut-sei=Ohtsuka
en-aut-mei=Hiroaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=UgawaSatoko
en-aut-sei=Ugawa
en-aut-mei=Satoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=OhnishiNobuhiko
en-aut-sei=Ohnishi
en-aut-mei=Nobuhiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=TakaishiAtsushi
en-aut-sei=Takaishi
en-aut-mei=Atsushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=NakamuraKazufumi
en-aut-sei=Nakamura
en-aut-mei=Kazufumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=KusanoKengo
en-aut-sei=Kusano
en-aut-mei=Kengo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=ItoHiroshi
en-aut-sei=Ito
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

affil-num=1
en-affil=
kn-affil=Okayama Univ, Dept Cardiovasc Med, Grad Sch Med Dent & Pharmaceut Sci

affil-num=2
en-affil=
kn-affil=Okayama Univ, Dept Cardiovasc Med, Grad Sch Med Dent & Pharmaceut Sci

affil-num=3
en-affil=
kn-affil=Mitoyo Gen Hosp, Dept Cardiovasc Med

affil-num=4
en-affil=
kn-affil=Mitoyo Gen Hosp, Dept Cardiovasc Med

affil-num=5
en-affil=
kn-affil=Mitoyo Gen Hosp, Dept Cardiovasc Med

affil-num=6
en-affil=
kn-affil=Mitoyo Gen Hosp, Dept Cardiovasc Med

affil-num=7
en-affil=
kn-affil=Mitoyo Gen Hosp, Dept Cardiovasc Med

affil-num=8
en-affil=
kn-affil=Okayama Univ, Dept Cardiovasc Med, Grad Sch Med Dent & Pharmaceut Sci

affil-num=9
en-affil=
kn-affil=Okayama Univ, Dept Cardiovasc Med, Grad Sch Med Dent & Pharmaceut Sci

affil-num=10
en-affil=
kn-affil=Okayama Univ, Dept Cardiovasc Med, Grad Sch Med Dent & Pharmaceut Sci
en-keyword=Chronic kidney disease
kn-keyword=Chronic kidney disease
en-keyword=Coronary artery disease
kn-keyword=Coronary artery disease
en-keyword=Left main coronary artery
kn-keyword=Left main coronary artery
en-keyword=Risk factor
kn-keyword=Risk factor
END

start-ver=1.4
cd-journal=joma
no-vol=8
cd-vols=
no-issue=2
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2013
dt-pub=20130219
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=A Decreased Level of Serum Soluble Klotho Is an Independent Biomarker Associated with Arterial Stiffness in Patients with Chronic Kidney Disease
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background: Klotho was originally identified in a mutant mouse strain unable to express the gene that consequently showed shortened life spans. In humans, low serum Klotho levels are related to the prevalence of cardiovascular diseases in community-dwelling adults. However, it is unclear whether the serum Klotho levels are associated with signs of vascular dysfunction such as arterial stiffness, a major determinant of prognosis, in human subjects with chronic kidney disease (CKD). 

Methods: We determined the levels of serum soluble Klotho in 114 patients with CKD using ELISA and investigated the relationship between the level of Klotho and markers of CKD-mineral and bone disorder (CKD-MBD) and various types of vascular dysfunction, including flow-mediated dilatation, a marker of endothelial dysfunction, ankle-brachial pulse wave velocity (baPWV), a marker of arterial stiffness, intima-media thickness (IMT), a marker of atherosclerosis, and the aortic calcification index (ACI), a marker of vascular calcification. 

Results: The serum Klotho level significantly correlated with the 1,25-dihydroxyvitamin D level and inversely correlated with the parathyroid hormone level and the fractional excretion of phosphate. There were significant decreases in serum Klotho in patients with arterial stiffness defined as baPWV >= 1400 cm/sec, atherosclerosis defined as maximum IMT >= 1.1 mm and vascular calcification scores of ACI>0%. The serum Klotho level was a significant determinant of arterial stiffness, but not endothelial dysfunction, atherosclerosis or vascular calcification, in the multivariate analysis in either metabolic model, the CKD model or the CKD-MBD model. The adjusted odds ratio of serum Klotho for the baPWV was 0.60 (p = 0.0075). 

Conclusions: Decreases in the serum soluble Klotho levels are independently associated with signs of vascular dysfunction such as arterial stiffness in patients with CKD. Further research exploring whether therapeutic approaches to maintain or elevate the Klotho level could improve arterial stiffness in CKD patients is warranted.
en-copyright=
kn-copyright=

en-aut-name=KitagawaMasashi
en-aut-sei=Kitagawa
en-aut-mei=Masashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=SugiyamaHitoshi
en-aut-sei=Sugiyama
en-aut-mei=Hitoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=MorinagaHiroshi
en-aut-sei=Morinaga
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=InoueTatsuyuki
en-aut-sei=Inoue
en-aut-mei=Tatsuyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=TakiueKeiichi
en-aut-sei=Takiue
en-aut-mei=Keiichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=OgawaAyu
en-aut-sei=Ogawa
en-aut-mei=Ayu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=YamanariToshio
en-aut-sei=Yamanari
en-aut-mei=Toshio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=KikumotoYoko
en-aut-sei=Kikumoto
en-aut-mei=Yoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=UchidaHaruhito Adam
en-aut-sei=Uchida
en-aut-mei=Haruhito Adam
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=KitamuraShinji
en-aut-sei=Kitamura
en-aut-mei=Shinji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=MaeshimaYohei
en-aut-sei=Maeshima
en-aut-mei=Yohei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=NakamuraKazufumi
en-aut-sei=Nakamura
en-aut-mei=Kazufumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=ItoHiroshi
en-aut-sei=Ito
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=MakinoHirofumi
en-aut-sei=Makino
en-aut-mei=Hirofumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

affil-num=1
en-affil=
kn-affil=Okayama Univ, Dept Med & Clin Sci, Grad Sch Med Dent & Pharmaceut Sci

affil-num=2
en-affil=
kn-affil=Okayama Univ, Dept Med & Clin Sci, Grad Sch Med Dent & Pharmaceut Sci

affil-num=3
en-affil=
kn-affil=Okayama Univ, Dept Med & Clin Sci, Grad Sch Med Dent & Pharmaceut Sci

affil-num=4
en-affil=
kn-affil=Okayama Univ, Dept Med & Clin Sci, Grad Sch Med Dent & Pharmaceut Sci

affil-num=5
en-affil=
kn-affil=Okayama Univ, Dept Med & Clin Sci, Grad Sch Med Dent & Pharmaceut Sci

affil-num=6
en-affil=
kn-affil=Okayama Univ, Dept Med & Clin Sci, Grad Sch Med Dent & Pharmaceut Sci

affil-num=7
en-affil=
kn-affil=Okayama Univ, Dept Med & Clin Sci, Grad Sch Med Dent & Pharmaceut Sci

affil-num=8
en-affil=
kn-affil=Okayama Univ, Dept Med & Clin Sci, Grad Sch Med Dent & Pharmaceut Sci

affil-num=9
en-affil=
kn-affil=Okayama Univ, Dept Med & Clin Sci, Grad Sch Med Dent & Pharmaceut Sci

affil-num=10
en-affil=
kn-affil=Okayama Univ, Dept Med & Clin Sci, Grad Sch Med Dent & Pharmaceut Sci

affil-num=11
en-affil=
kn-affil=Okayama Univ, Dept Med & Clin Sci, Grad Sch Med Dent & Pharmaceut Sci

affil-num=12
en-affil=
kn-affil=Okayama Univ, Dept Cardiovasc Med, Grad Sch Med Dent & Pharmaceut Sci

affil-num=13
en-affil=
kn-affil=Okayama Univ, Dept Cardiovasc Med, Grad Sch Med Dent & Pharmaceut Sci

affil-num=14
en-affil=
kn-affil=Okayama Univ, Dept Med & Clin Sci, Grad Sch Med Dent & Pharmaceut Sci
END

start-ver=1.4
cd-journal=joma
no-vol=2013
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2013
dt-pub=2013
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Dual Antiplatelet Therapy Can Be Discontinued at Three Months after Implantation of Zotarolimus-Eluting Stent in Patients with Coronary Artery Disease
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Dual antiplatelet therapy (DAPT) after percutaneous coronary intervention increases the risk of bleeding. We studied the safety and clinical outcomes of switching from DAPT to aspirin monotherapy at 3 months after ZES implantation. We retrospectively evaluated 168 consecutive patients with coronary artery disease who had been implanted with a ZES from June 2009 through March 2010. After excluding 40 patients according to exclusion criteria such as myocardial infarction, 128 patients were divided into a 3-month DAPT group (67 patients, 88 lesions) and a 12-month conventional DAPT group (61 patients, 81 lesions). Coronary angiographic followup and clinical followup were conducted at more than 8 months and at 12 months after ZES implantation, respectively. Minor and major bleeding events, stent thrombosis (ST), and major adverse cardiac events (MACE) (death, myocardial infarction, cerebrovascular accident, target lesion revascularization, and target vessel revascularization) were evaluated. There were no statistically significant differences in the incidences of ST and MACE between the two groups. The incidence of bleeding events was significantly lower in the 3-month group than in the 12-month group (1.5% versus 11.5%, ). DAPT can be safely discontinued at 3 months after ZES implantation, which reduces bleeding risk.
en-copyright=
kn-copyright=

en-aut-name=WadaTadashi
en-aut-sei=Wada
en-aut-mei=Tadashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NakahamaMakoto
en-aut-sei=Nakahama
en-aut-mei=Makoto
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=TodaHironobu
en-aut-sei=Toda
en-aut-mei=Hironobu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=WatanabeAtsuyuki
en-aut-sei=Watanabe
en-aut-mei=Atsuyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=HashimotoKatsushi
en-aut-sei=Hashimoto
en-aut-mei=Katsushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=TerasakaRitsuko
en-aut-sei=Terasaka
en-aut-mei=Ritsuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=NakamuraKazufumi
en-aut-sei=Nakamura
en-aut-mei=Kazufumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=YamadaNobuyuki
en-aut-sei=Yamada
en-aut-mei=Nobuyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=ItoHiroshi
en-aut-sei=Ito
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

affil-num=1
en-affil=
kn-affil=Department of Cardiology, Fukuyama City Hospital

affil-num=2
en-affil=
kn-affil=Department of Cardiology, Fukuyama City Hospital

affil-num=3
en-affil=
kn-affil=Department of Cardiology, Fukuyama City Hospital

affil-num=4
en-affil=
kn-affil=Department of Cardiology, Fukuyama City Hospital

affil-num=5
en-affil=
kn-affil=Department of Cardiology, Fukuyama City Hospital

affil-num=6
en-affil=
kn-affil=Department of Cardiology, Fukuyama City Hospital

affil-num=7
en-affil=
kn-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=8
en-affil=
kn-affil=Department of Cardiology, Fukuyama City Hospital

affil-num=9
en-affil=
kn-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
END

start-ver=1.4
cd-journal=joma
no-vol=19
cd-vols=
no-issue=4
article-no=
start-page=E35
end-page=E39
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2013
dt-pub=201308
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Serum cystatin C as a biomarker of cardiac diastolic dysfunction in patients with cardiac disease and preserved ejection fraction
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Diastolic dysfunction of the heart is correlated with cardiac mortality. Serum cystatin C (CysC) is an endogenous marker of kidney function. It is not clear whether serum CysC is associated with diastolic dysfunction in patients with varying cardiac conditions with concomitant diastolic abnormalities and preserved ejection fraction (EF). The authors measured serum CysC levels in patients with cardiac diseases and examined the relationships between serum CysC levels and diastolic function. Serum CysC was measured and echocardiography was performed in 124 consecutive patients with cardiac diseases. Transmitral flow (TMF) patterns surrogating diastolic function were categorized into two groups: a normal group and an abnormal group. Serum CysC and BNP showed a significant positive correlation. There were no significant differences in serum CysC among those cardiac diseases. Seventy-eight patients with cardiac disease and preserved EF (left ventricular EF ?50%) and without renal dysfunction (estimated glomerular filtration rate ?60 mL/minute/1.73 m(2) ) were examined. Multivariate linear regression analysis demonstrated that left atrium diameter and abnormal TMF patterns were independent determinants of serum CysC. Furthermore, patients with elevated serum CysC levels had poor prognosis. Serum CysC is associated with diastolic dysfunction in patients with various cardiac diseases and preserved EF. Serum CysC might be a biomarker of cardiac diastolic dysfunction in patients with preserved EF.
en-copyright=
kn-copyright=

en-aut-name=NosakaKazumasa
en-aut-sei=Nosaka
en-aut-mei=Kazumasa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NakamuraKazufumi
en-aut-sei=Nakamura
en-aut-mei=Kazufumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KusanoKengo
en-aut-sei=Kusano
en-aut-mei=Kengo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TohNorihisa
en-aut-sei=Toh
en-aut-mei=Norihisa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=TadaTakeshi
en-aut-sei=Tada
en-aut-mei=Takeshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=MiyoshiToru
en-aut-sei=Miyoshi
en-aut-mei=Toru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=DoiMasayuki
en-aut-sei=Doi
en-aut-mei=Masayuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=KohnoKunihisa
en-aut-sei=Kohno
en-aut-mei=Kunihisa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=MoritaHiroshi
en-aut-sei=Morita
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=ItoHiroshi
en-aut-sei=Ito
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

affil-num=1
en-affil=
kn-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=2
en-affil=
kn-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=3
en-affil=
kn-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=4
en-affil=
kn-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=5
en-affil=
kn-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=6
en-affil=
kn-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=7
en-affil=
kn-affil=Department of Cardiology, Kagawa Prefectural Central Hospital

affil-num=8
en-affil=
kn-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=9
en-affil=
kn-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=10
en-affil=
kn-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
END

start-ver=1.4
cd-journal=joma
no-vol=124
cd-vols=
no-issue=1
article-no=
start-page=71
end-page=73
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2012
dt-pub=20120401
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Guidelines for treatment of chronic heart failure
kn-title=慢性心不全治療ガイドライン
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=NakamuraKazufumi
en-aut-sei=Nakamura
en-aut-mei=Kazufumi
kn-aut-name=中村一文
kn-aut-sei=中村
kn-aut-mei=一文
aut-affil-num=1
ORCID=

en-aut-name=ItoHiroshi
en-aut-sei=Ito
en-aut-mei=Hiroshi
kn-aut-name=伊藤浩
kn-aut-sei=伊藤
kn-aut-mei=浩
aut-affil-num=2
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学病院　循環器内科

affil-num=2
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　循環器内科学
END

start-ver=1.4
cd-journal=joma
no-vol=118
cd-vols=
no-issue=3
article-no=
start-page=187
end-page=192
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2007
dt-pub=20070104
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=原発性肺高血圧症の進行メカニズムの解明と治療薬の開発
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=
en-aut-sei=
en-aut-mei=
kn-aut-name=小川愛子
kn-aut-sei=小川
kn-aut-mei=愛子
aut-affil-num=1
ORCID=

en-aut-name=
en-aut-sei=
en-aut-mei=
kn-aut-name=中村一文
kn-aut-sei=中村
kn-aut-mei=一文
aut-affil-num=2
ORCID=

en-aut-name=
en-aut-sei=
en-aut-mei=
kn-aut-name=松原広己
kn-aut-sei=松原
kn-aut-mei=広己
aut-affil-num=3
ORCID=

en-aut-name=
en-aut-sei=
en-aut-mei=
kn-aut-name=藤尾栄起
kn-aut-sei=藤尾
kn-aut-mei=栄起
aut-affil-num=4
ORCID=

en-aut-name=
en-aut-sei=
en-aut-mei=
kn-aut-name=池田哲也
kn-aut-sei=池田
kn-aut-mei=哲也
aut-affil-num=5
ORCID=

en-aut-name=
en-aut-sei=
en-aut-mei=
kn-aut-name=宮地克維
kn-aut-sei=宮地
kn-aut-mei=克維
aut-affil-num=6
ORCID=

en-aut-name=
en-aut-sei=
en-aut-mei=
kn-aut-name=三浦大志
kn-aut-sei=三浦
kn-aut-mei=大志
aut-affil-num=7
ORCID=

en-aut-name=
en-aut-sei=
en-aut-mei=
kn-aut-name=三浦綾
kn-aut-sei=三浦
kn-aut-mei=綾
aut-affil-num=8
ORCID=

en-aut-name=
en-aut-sei=
en-aut-mei=
kn-aut-name=永瀬聡
kn-aut-sei=永瀬
kn-aut-mei=聡
aut-affil-num=9
ORCID=

en-aut-name=
en-aut-sei=
en-aut-mei=
kn-aut-name=草野研吾
kn-aut-sei=草野
kn-aut-mei=研吾
aut-affil-num=10
ORCID=

en-aut-name=
en-aut-sei=
en-aut-mei=
kn-aut-name=伊達洋至
kn-aut-sei=伊達
kn-aut-mei=洋至
aut-affil-num=11
ORCID=

en-aut-name=
en-aut-sei=
en-aut-mei=
kn-aut-name=大江透
kn-aut-sei=大江
kn-aut-mei=透
aut-affil-num=12
ORCID=

affil-num=1
en-affil=
kn-affil=University of California, San Diego, Division of Pulmonary and Critical Care Medicine

affil-num=2
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科循環器内科

affil-num=3
en-affil=
kn-affil=国立病院機構岡山医療センター循環器科

affil-num=4
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科循環器内科

affil-num=5
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科循環器内科

affil-num=6
en-affil=
kn-affil=国立病院機構岡山医療センター循環器科

affil-num=7
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科循環器内科

affil-num=8
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科循環器内科

affil-num=9
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科循環器内科

affil-num=10
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科循環器内科

affil-num=11
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科腫瘍・胸部外科

affil-num=12
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科循環器内科
en-keyword=原発性肺高血圧症
kn-keyword=原発性肺高血圧症
en-keyword=平滑筋細胞
kn-keyword=平滑筋細胞
en-keyword=prednisolone
kn-keyword=prednisolone
en-keyword=細胞周期
kn-keyword=細胞周期
END

start-ver=1.4
cd-journal=joma
no-vol=126
cd-vols=
no-issue=3
article-no=
start-page=427
end-page=429
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2008
dt-pub=20080622
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Expression of monocyte chemoattractant protein-1 in idiopathic dilated cardiomyopathy
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=<p>Immunological factors have been involved in the pathogenesis of dilated cardiomyopathy (DCM). The cytotoxic action of macrophages is one of the main factors causing cardiac myocyte damage. Monocyte chemoattractant protein-1 (MCP-1) is a major signal for the accumulation of monocytes/macrophages. We examined whether MCP-1 was expressed in the myocardium of DCM patients and whether the expression level was correlated with the degree of impairment of cardiac function. The expression of MCP-1 in the myocardium was determined by immunohistochemistry in endomyocardial biopsy samples from 13 patients. The expression of MCP-1 was found in all myocardial samples from DCM patients but not in those from control subjects. Positive staining for MCP-1 was distinct in cardiac myocytes, interstitium and infiltrating cells. Semi-quantitative analysis revealed that the expression of MCP-1 was inversely correlated with left ventricular ejection fraction. In conclusion, the expression level of MCP-1 in the myocardium was correlated with the degree of impairment of cardiac function in patients with DCM.</p>

en-copyright=
kn-copyright=

en-aut-name=KobayashiMakoto
en-aut-sei=Kobayashi
en-aut-mei=Makoto
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NakamuraKazufumi
en-aut-sei=Nakamura
en-aut-mei=Kazufumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KusanoKengo Fukushima
en-aut-sei=Kusano
en-aut-mei=Kengo Fukushima
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=NakamuraYoichi
en-aut-sei=Nakamura
en-aut-mei=Yoichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=Ohta-OgoKeiko
en-aut-sei=Ohta-Ogo
en-aut-mei=Keiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=NagaseSatoshi
en-aut-sei=Nagase
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=SakuragiSatoru
en-aut-sei=Sakuragi
en-aut-mei=Satoru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=OheTohru
en-aut-sei=Ohe
en-aut-mei=Tohru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

affil-num=1
en-affil=
kn-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=2
en-affil=
kn-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=3
en-affil=
kn-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=4
en-affil=
kn-affil=aDepartment of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=5
en-affil=
kn-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=6
en-affil=
kn-affil=aDepartment of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=7
en-affil=
kn-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=8
en-affil=
kn-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
en-keyword=cardiomyopathy
kn-keyword=cardiomyopathy
en-keyword=immunohistochemistry
kn-keyword=immunohistochemistry
en-keyword=monocyte
kn-keyword=monocyte
END

start-ver=1.4
cd-journal=joma
no-vol=58
cd-vols=
no-issue=1
article-no=
start-page=29
end-page=35
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2004
dt-pub=200402
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Usefulness of body surface mapping to differentiate patients with Brugada syndrome from patients with asymptomatic Brugada syndrome.
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=<p>We attempted to determine the usefulness of body surface mapping (BSM) for differentiating patients with Brugada syndrome (BS) from patients with asymptomatic Brugada syndrome (ABS). Electrocardiograms (ECG) and BSM were recorded in 7 patients with BS and 35 patients with ABS. Following the administration of Ic antiarrhythmic drugs, BSM was recorded in 5 patients with BS and 16 patients with ABS. The maximum amplitudes at J0, J20, J40 and J60 were compared between the 2 groups, as were 3-dimensional maps. The maximum amplitudes at J0, J20 and J60 under control conditions were larger in patients with BS than in patients with ABS (P < 0.05). A three-dimensional map of the ST segments under control conditions in patients with BS showed a higher peak of ST elevation in the median precordium compared to that for patients with ABS. Increases in ST elevation at J20, J40 and J60 following drug administration were greater in patients with BS than in patients with ABS (P < 0.05). Evaluation of the change in amplitude of the ST segment at E5 caused by Ic drug administration was also useful for differentiating between the 2 groups. In conclusion, BSM was useful for differentiating patients with BS from those with ABS.</p>
en-copyright=
kn-copyright=

en-aut-name=HisamatsuKenichi
en-aut-sei=Hisamatsu
en-aut-mei=Kenichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KusanoKengo Fukushima
en-aut-sei=Kusano
en-aut-mei=Kengo Fukushima
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=MoritaHiroshi
en-aut-sei=Morita
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TakenakaShiho
en-aut-sei=Takenaka
en-aut-mei=Shiho
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=NagaseSatoshi
en-aut-sei=Nagase
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=NakamuraKazufumi
en-aut-sei=Nakamura
en-aut-mei=Kazufumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=EmoriTetsuro
en-aut-sei=Emori
en-aut-mei=Tetsuro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=MatsubaraHiromi
en-aut-sei=Matsubara
en-aut-mei=Hiromi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=OheTohru
en-aut-sei=Ohe
en-aut-mei=Tohru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

affil-num=1
en-affil=
kn-affil=Okayama University

affil-num=2
en-affil=
kn-affil=Okayama University

affil-num=3
en-affil=
kn-affil=Okayama University

affil-num=4
en-affil=
kn-affil=Okayama University

affil-num=5
en-affil=
kn-affil=Okayama University

affil-num=6
en-affil=
kn-affil=Okayama University

affil-num=7
en-affil=
kn-affil=Okayama University

affil-num=8
en-affil=
kn-affil=Okayama University

affil-num=9
en-affil=
kn-affil=Okayama University
en-keyword=body surface map
kn-keyword=body surface map
en-keyword=Brugada syndrome
kn-keyword=Brugada syndrome
en-keyword=asymptomatic Brugada syndrome
kn-keyword=asymptomatic Brugada syndrome
en-keyword=Ic antiarrhythmic drugs
kn-keyword=Ic antiarrhythmic drugs
END

start-ver=1.4
cd-journal=joma
no-vol=59
cd-vols=
no-issue=3
article-no=
start-page=73
end-page=78
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2005
dt-pub=200506
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Hepatocyte growth factor gene therapy reduces ventricular arrhythmia in animal models of myocardial ischemia.
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=<p>It was recently reported that gene therapy using hepatocyte growth factor (HGF) has the potential to preserve cardiac function after myocardial ischemia. We speculated that this HGF gene therapy could also prevent ventricular arrhythmia. To investigate this possibility, we examined the antiarrhythmic effect of HGF gene therapy in rat acute and old myocardial infarction models. Myocardial ischemia was induced by ligation of the left descending coronary artery. Hemagglutinating virus of Japan (HVJ)-coated liposome containing HGF genes were injected directly into the myocardium fourteen days before programmed pacing. Ventricular fibrillation (VF)was induced by programmed pacing. The VF duration was reduced and the VF threshold increased after HGF gene therapy ( p&#60; 0.01). Histological analyses revealed that the number of vessels in the ischemic border zone was greatly increased after HGF gene injection. These findings revealed that HGF gene therapy has an anti-arrhythmic effect after myocardial ischemia.</p>

en-copyright=
kn-copyright=

en-aut-name=YumotoAkihisa
en-aut-sei=Yumoto
en-aut-mei=Akihisa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KusanoKengo Fukushima
en-aut-sei=Kusano
en-aut-mei=Kengo Fukushima
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=NakamuraKazufumi
en-aut-sei=Nakamura
en-aut-mei=Kazufumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=HashimotoKatsushi
en-aut-sei=Hashimoto
en-aut-mei=Katsushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=AokiMotokuni
en-aut-sei=Aoki
en-aut-mei=Motokuni
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=MorishitaRyuichi
en-aut-sei=Morishita
en-aut-mei=Ryuichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=KanedaYasufumi
en-aut-sei=Kaneda
en-aut-mei=Yasufumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=OheTohru
en-aut-sei=Ohe
en-aut-mei=Tohru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

affil-num=1
en-affil=
kn-affil=Okayama University

affil-num=2
en-affil=
kn-affil=Okayama University

affil-num=3
en-affil=
kn-affil=Okayama University

affil-num=4
en-affil=
kn-affil=Okayama University

affil-num=5
en-affil=
kn-affil=&#65279;Geriatric Medicine	 

affil-num=6
en-affil=
kn-affil=Okayama University

affil-num=7
en-affil=
kn-affil=Okayama University

affil-num=8
en-affil=
kn-affil=Okayama University
en-keyword=ventricular arrhythmia
kn-keyword=ventricular arrhythmia
en-keyword= HGF (hepatocyte growth factor)
kn-keyword= HGF (hepatocyte growth factor)
en-keyword=ischemia
kn-keyword=ischemia
en-keyword= HVJ (hemagglutinating virus of Japan)
kn-keyword= HVJ (hemagglutinating virus of Japan)
END

start-ver=1.4
cd-journal=joma
no-vol=116
cd-vols=
no-issue=1
article-no=
start-page=9
end-page=16
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2004
dt-pub=20040531
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=心不全における酸化ストレスの関与：基礎的ならびに臨床的検討 ―岡山大学医学賞（結城賞）を受賞して―
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=心不全患者において血中の過酸化脂質の上昇などが報告され，活性酸素による酸化ストレスの関与が示唆されている．そこで，心筋が実際に活性酸素を発生するかどうかを，活性酸素を検出する蛍光プローブを用いてラットの培養心筋細胞において検討した．心不全増悪因子であるアンジオテンシンIIおよびtumor necrosis factor(TNF)-alphaを加えると心筋細胞で濃度依存性に活性酸素が発生した．さらにヒトの不全心筋においても実際に酸化ストレスの発生が増強しているかを検討した．過酸化脂質の代謝産物で，有害なアルデヒドである4-Hydroxy-2-nonenal(HNE)によって修飾された蛋白質を免疫染色にて調べたところ，拡張型心筋症患者の心筋において正常心機能者に比べ5倍以上増加していた．さらにβ遮断薬(Carvedilol)により治療を行ったところ心機能の改善とともに，HNE修飾蛋白質が40%低下した．以上の一連の研究により，
活性酸素による酸化ストレスの発生が不全心筋において増強しており，その抑制が心不全治療のターゲットの一つになりうることを明らかにした．
en-copyright=
kn-copyright=

en-aut-name=
en-aut-sei=
en-aut-mei=
kn-aut-name=中村一文
kn-aut-sei=中村
kn-aut-mei=一文
aut-affil-num=1
ORCID=

en-aut-name=
en-aut-sei=
en-aut-mei=
kn-aut-name=草野研吾
kn-aut-sei=草野
kn-aut-mei=研吾
aut-affil-num=2
ORCID=

en-aut-name=
en-aut-sei=
en-aut-mei=
kn-aut-name=垣下幹夫
kn-aut-sei=垣下
kn-aut-mei=幹夫
aut-affil-num=3
ORCID=

en-aut-name=
en-aut-sei=
en-aut-mei=
kn-aut-name=三浦綾
kn-aut-sei=三浦
kn-aut-mei=綾
aut-affil-num=4
ORCID=

en-aut-name=
en-aut-sei=
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