JaLCDOI 10.18926/AMO/31817
FullText URL fulltext.pdf
Author Ito, Hiroshi|
Abstract <p>For patients with acute myocardial infarction (MI), the immediate therapeutic goal is to establish the patency of the infarct-related artery. Prolonged myocardial ischemia, however, often breaks down the coronary microvasculature, and the flow to the infarct myocardium may be markedly reduced. This is called the no-reflow phenomenon. This phenomenon is important not solely because it correlates with infarct size but because it provides additional prognostic information. With recent advances in imaging modalities, the no-reflow phenomenon is observed more frequently than when clinical judgment alone is used. Patients with this phenomenon are associated with poor functional and clinical outcomes. Now, the no-reflow phenomenon can be a parameter with which to predict high-risk patients. The focus of reperfusion therapy has shifted toward the improvement of myocardial perfusion. The improvement of myocardial perfusion could promote the functional recovery of viable muscle and reduce infarct expansion, which is associated with favorable clinical outcomes. For this purpose, pharmacological interventions and catheter-based devices to retrieve embolic materials have been proposed. Advances in our understanding of the pathophysiology of microvascular dysfunction would aid the development of therapeutic strategies for its prevention and treatment.</p>
Keywords cardiac function coronary intervention microcirculation myocardial infarction reperfusion
Amo Type Review
Published Date 2009-08
Publication Title Acta Medica Okayama
Volume volume63
Issue issue4
Publisher Okayama University Medical School
Start Page 161
End Page 168
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language 英語
File Version publisher
Refereed True
PubMed ID 19727200
Web of Sience KeyUT 000269228400001
Author Ito, Hiroshi|
Published Date 2009-08-03
Publication Title 岡山医学会雑誌
Volume volume121
Issue issue2
Content Type Journal Article
Author Nakamura, Kazufumi| Ito, Hiroshi|
Published Date 2012-04-01
Publication Title 岡山医学会雑誌
Volume volume124
Issue issue1
Content Type Journal Article
Author Dan, Kazuhiro| Miyoshi, Toru| Ueeda, Masayuki| Ohtsuka, Hiroaki| Ugawa, Satoko| Ohnishi, Nobuhiko| Takaishi, Atsushi| Nakamura, Kazufumi| Kusano, Kengo| Ito, Hiroshi|
Published Date 2012-09
Publication Title Circulation Journal
Volume volume76
Issue issue9
Content Type Journal Article
Author Wada, Tadashi| Nakahama, Makoto| Toda, Hironobu| Watanabe, Atsuyuki| Hashimoto, Katsushi| Terasaka, Ritsuko| Nakamura, Kazufumi| Yamada, Nobuyuki| Ito, Hiroshi|
Published Date 2013
Publication Title ISRN Cardiology
Volume volume2013
Content Type Journal Article
Author Kitagawa, Masashi| Sugiyama, Hitoshi| Morinaga, Hiroshi| Inoue, Tatsuyuki| Takiue, Keiichi| Ogawa, Ayu| Yamanari, Toshio| Kikumoto, Yoko| Uchida, Haruhito Adam| Kitamura, Shinji| Maeshima, Yohei| Nakamura, Kazufumi| Ito, Hiroshi| Makino, Hirofumi|
Published Date 2013-02-19
Publication Title PLoS ONE
Volume volume8
Issue issue2
Content Type Journal Article
Author Nosaka, Kazumasa| Nakamura, Kazufumi| Kusano, Kengo| Toh, Norihisa| Tada, Takeshi| Miyoshi, Toru| Doi, Masayuki| Kohno, Kunihisa| Morita, Hiroshi| Ito, Hiroshi|
Published Date 2013-08
Publication Title Congestive Heart Failure
Volume volume19
Issue issue4
Content Type Journal Article
Author Mizoguchi, Hiroki| Ogawa, Aiko| Munemasa, Mitsuru| Mikouchi, Hiroshi| Ito, Hiroshi| Matsubara, Hiromi|
Published Date 2013-12-02
Publication Title 岡山医学会雑誌
Volume volume125
Issue issue3
Content Type Journal Article
Author Tokioka, Koji| Kusano, Kengo F.| Morita, Hiroshi| Miura, Daiji| Nishii, Nobuhiro| Nagase, Satoshi| Nakamura, Kazufumi| Kohno, Kunihisa| Ito, Hiroshi| Ohe, Tohru|
Published Date 2014-05-27
Publication Title Journal of the American College of Cardiology
Volume volume63
Issue issue20
Content Type Journal Article
Author Kobayashi, Junko| Yoshida, Masashi| Tarui, Suguru| Hirata, Masataka| Nagai, Yusuke| Kasahara, Shingo| Naruse, Keiji| Ito, Hiroshi| Sano, Shunji| Oh, Hidemasa|
Published Date 2014-07-22
Publication Title PLoS ONE
Volume volume9
Issue issue7
Content Type Journal Article
JaLCDOI 10.18926/AMO/53519
FullText URL 69_3_129.pdf
Author Akagi, Satoshi| Nakamura, Kazufumi| Matsubara, Hiromi| Ogawa, Aiko| Sarashina, Toshihiro| Ejiri, Kentaro| Ito, Hiroshi|
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.
Keywords pulmonary arterial hypertension epoprostenol high-dose complications side effects
Amo Type Review
Published Date 2015-06
Publication Title Acta Medica Okayama
Volume volume69
Issue issue3
Publisher Okayama University Medical School
Start Page 129
End Page 136
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language 英語
Copyright Holders CopyrightⒸ 2015 by Okayama University Medical School
File Version publisher
Refereed True
PubMed ID 26101188
Web of Sience KeyUT 000356903000001
JaLCDOI 10.18926/AMO/54600
FullText URL 70_5_397.pdf
Author Akagi, Satoshi| Nakamura, Kazufumi| Akagi, Teiji| Nakagawa, Koji| Takaya, Yoichi| Sarashina, Toshihiro| Ejiri, Kentaro| Ito, Hiroshi|
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.
Keywords pulmonary hypertension atrial septal defect repair and treat transcatheter closure
Amo Type Clinical Study Protocols
Published Date 2016-10
Publication Title Acta Medica Okayama
Volume volume70
Issue issue5
Publisher Okayama University Medical School
Start Page 397
End Page 400
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language 英語
Copyright Holders CopyrightⒸ 2016 by Okayama University Medical School
File Version publisher
Refereed True
PubMed ID 27777434
Web of Sience KeyUT 000388098700011