Impact of persistent endothelial dysfunction in an infarct-related coronary artery on future major adverse cardiovascula
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ORIGINAL ARTICLE
Impact of persistent endothelial dysfunction in an infarct‑related coronary artery on future major adverse cardiovascular event occurrence in STEMI survivors Takeo Horikoshi1 · Takamitsu Nakamura1 · Toru Yoshizaki1 · Yosuke Watanabe1 · Manabu Uematsu1 · Tsuyoshi Kobayashi1 · Kazuto Nakamura1 · Yukio Saito1 · Jun‑ei Obata1 · Kiyotaka Kugiyama1 Received: 16 July 2020 / Accepted: 30 October 2020 © Springer Japan KK, part of Springer Nature 2020
Abstract Although coronary endothelial vasomotor dysfunction predicts future coronary events, few human studies have shown the relationship between persistent endothelial vasomotor dysfunction and major adverse cardiovascular events (MACE) using serial assessments in the same coronary artery. This study examined whether persistent endothelial vasomotor dysfunction is related to MACE occurrence in the infarct-related coronary artery (IRA) of ST-segment elevation myocardial infarction (STEMI) survivors using serial assessments of the coronary vasomotor response to acetylcholine (ACh). This study included 169 consecutive patients with a first acute STEMI due to left anterior descending coronary artery (LAD) occlusion and successful reperfusion therapy with percutaneous coronary intervention. Vasomotor response to ACh in the LAD was measured within 2 weeks of acute myocardial infarction (AMI) (first test) and repeated 6 months (second test) after AMI under optimal anti-atherosclerotic therapy. MACE was defined as the composite of all-cause death, non-fatal MI, angina recurrence requiring percutaneous intervention or surgical bypass, and hospitalization for heart failure. We followed up 126 patients for a period of ≤ 60 months until MACE occurrence after second test. Nineteen MACEs occurred during the follow-up. The logrank test, Kaplan–Meier curves and univariate Cox proportional hazards regression analysis showed that MACE occurrence was significantly associated with the persistent impairment of epicardial coronary artery dilation and coronary blood flow increases in response to ACh (log-rank test, p 30% in the LAD. The exclusion criteria were as follows: (1) previous PCI in the LAD; (2) previous coronary artery bypass surgery; (3) organic stenosis ≥ 30% in the LAD at either 1–2 weeks (first test) or 6 months (second test) after acute MI (AMI); (4) cardiovascular events during the 6-month follow-up period between the first and second tests after AMI; (5) epicardial coronary constriction degree > 30% in the LAD in response to ACh; (6) presence of collaterals to the LAD with Rentrop grade ≥ 2; (7) congestive heart failure (New York Heart Association classification IV) at 1 week after AMI; (8) persistent atrial fibrillation and a paced rhythm; (9) age > 80 years; (10) presence of valvular heart diseases (aortic stenosis [aortic valve area 2.0 mg/dL), or other serious disease. After the application of the exclusion criteria, this study included 169 patients at admission (Fig. 1). Written informed consent was obtained from all patients before the study. The study w
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