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ID 63815
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Tsuji, Masahiro Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
Kawai, Yusuke Department of Cardiovascular Medicine, Okayama City Hospital
Miyoshi, Toru Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences ORCID Kaken ID publons
Saito, Eisuke Department of Cardiovascular Medicine, Okayama City Hospital
Kawamura, Kohei Department of Cardiovascular Medicine, Okayama City Hospital
Ono, Tamaki Department of Cardiovascular Medicine, Okayama City Hospital
Tokioka, Koji Department of Cardiovascular Medicine, Okayama City Hospital
Ohe, Tohru Department of Cardiovascular Medicine, Okayama City Hospital
Nakamura, Kazufumi Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences Kaken ID publons researchmap
Ito, Hiroshi Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences Kaken ID
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).
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).
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.
Keywords
Myocardial infarction
Left ventricular remodelling
Platelet reactivity
Inflammation
Reverse remodelling
Prasugrel
Published Date
2022-07-31
Publication Title
ESC Heart Failure
Publisher
Wiley Periodicals, Inc
ISSN
2055-5822
Content Type
Journal Article
language
English
OAI-PMH Set
岡山大学
Copyright Holders
© 2022 The Authors.
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DOI
Web of Science KeyUT
Related Url
isVersionOf https://doi.org/10.1002/ehf2.14100
License
https://creativecommons.org/licenses/by-nc/4.0/
Funder Name
Japan Society for the Promotion of Science
助成番号
19K08558