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临床环境中的心脏保护:J-WIND 研究的启示。

Cardioprotection in the clinical setting-lessons from J-WIND studies.

机构信息

Department of Clinical Research, National Cerebral and Cardiovascular Center, 5-7-1 Fujishirodai, Suita, 565-8565, Japan.

出版信息

Cardiovasc Drugs Ther. 2010 Jun;24(3):289-95. doi: 10.1007/s10557-010-6253-9.

Abstract

INTRODUCTION

Both prevention and attenuation of ischemic heart disease are important issues, and there are three different strategies to save patients from the deleterious sequelae of ischemic injury. The first strategy is to remove the causes of ischemic heart disease; the second is to attenuate on-going ischemic and reperfusion injury; the third is to prevent the progression of cardiac remodeling and chronic heart failure following ischemic injury.

EVIDENCE AND DISCUSSION

For prevention of acute myocardial infarction, it is widely accepted to treat high risk patients with aspirin and/or statins. On the other hand, several medications such as angiotensin converting enzyme inhibitors, aldosterone receptor antagonists and beta blockers have been used for the prevention of post-infarction heart failure in patients who have suffered from an acute myocardial infarction. However, at present we do not have an adjunctive drug therapy to reduce infarct size in the acute phase in patients with myocardial infarction. Recently, the J-WIND trials suggested that an infusion of human atrial natriuretic peptide in the acute phase and oral administration of nicorandil in the chronic phase of infarction result in a better outcome in patients with a myocardial infarction. In this article we propose potential mechanisms for cardioprotection in patients with an acute myocardial infarction.

摘要

简介

预防和减轻缺血性心脏病都很重要,有三种不同的策略可以使患者免受缺血性损伤的不良后果。第一种策略是消除缺血性心脏病的病因;第二种策略是减轻正在进行的缺血和再灌注损伤;第三种策略是预防缺血损伤后心脏重构和慢性心力衰竭的进展。

证据和讨论

对于急性心肌梗死的预防,广泛接受的方法是用阿司匹林和/或他汀类药物治疗高危患者。另一方面,几种药物如血管紧张素转换酶抑制剂、醛固酮受体拮抗剂和β受体阻滞剂已被用于预防急性心肌梗死后心力衰竭的发生。然而,目前我们没有辅助药物治疗来减少急性心肌梗死患者的梗死面积。最近,J-WIND 试验表明,在急性心肌梗死患者中,急性时程给予人心房利钠肽输注,慢性时程给予尼可地尔口服,可以改善患者的预后。在本文中,我们提出了急性心肌梗死后患者心脏保护的潜在机制。

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