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急性心肌梗死合并心力衰竭后的醛固酮受体阻断

[Aldosterone receptor blockade after acute myocardial infarction with heart failure].

作者信息

Bauersachs Johann, Ertl Georg

机构信息

Medizinische Klinik I, Universitätsklinikum, Josef-Schneider-Strasse 2, 97080 Würzburg.

出版信息

Med Klin (Munich). 2006 Jun 15;101(6):458-66. doi: 10.1007/s00063-006-1063-3.

DOI:10.1007/s00063-006-1063-3
PMID:16767569
Abstract

BACKGROUND

Based on the RALES study, in patients with moderate to severe chronic heart failure and reduced left ventricular function, the nonselective aldosterone antagonist spironolactone has a well-established role in combination with ACE inhibition, beta-blockade and diuretics. This indication was recently reinforced by the guideline for chronic heart failure therapy of the German Cardiac Society, although there is no formal approval for spironolactone for this indication in Germany.

NEW CLINICAL STUDIES

Heart failure after acute myocardial infarction represents a new indication for aldosterone receptor blockade. In the EPHESUS trial of patients with acute myocardial infarction, reduced ejection fraction, and clinical signs of heart failure, the selective aldosterone antagonist eplerenone in combination with ACE inhibition and beta-blockade significantly reduced mortality. The best benefit was achieved by early treatment, i. e., starting 3-7 days post myocardial infarction. In addition, as early as after 30 days, eplerenone-treated patients had significantly reduced mortality and hospitalization. Eplerenone was approved for the indication heart failure after acute myocardial infarction in late 2004 in Germany.

PURPOSE OF THIS STUDY

The present review summarizes the pathophysiological basis, the experimental and clinical trials that constitute the rationale for therapy with aldosterone antagonists in patients with acute myocardial infarction and heart failure. Tips for use in clinical practice are given which allow to profit from the effective potential for mortality and morbidity reduction of aldosterone receptor blockade and to minimize the risk of serious hyperkalemia.

摘要

背景

基于RALES研究,对于中重度慢性心力衰竭且左心室功能降低的患者,非选择性醛固酮拮抗剂螺内酯在与ACE抑制剂、β受体阻滞剂及利尿剂联合使用时具有明确的作用。德国心脏病学会慢性心力衰竭治疗指南最近强化了这一适应证,尽管在德国螺内酯尚未获得该适应证的正式批准。

新的临床研究

急性心肌梗死后心力衰竭是醛固酮受体阻滞剂的一个新适应证。在针对急性心肌梗死、射血分数降低且有心力衰竭临床体征患者的EPHESUS试验中,选择性醛固酮拮抗剂依普利酮与ACE抑制剂及β受体阻滞剂联合使用可显著降低死亡率。早期治疗(即心肌梗死后3 - 7天开始治疗)效果最佳。此外,早在30天后,接受依普利酮治疗的患者死亡率及住院率显著降低。依普利酮于2004年末在德国被批准用于急性心肌梗死后心力衰竭这一适应证。

本研究的目的

本综述总结了病理生理基础、构成急性心肌梗死合并心力衰竭患者使用醛固酮拮抗剂治疗理论依据的实验及临床试验。给出了临床实践中的使用建议,以便从醛固酮受体阻滞剂降低死亡率和发病率的有效潜力中获益,并将严重高钾血症的风险降至最低。

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1
[Aldosterone receptor blockade after acute myocardial infarction with heart failure].急性心肌梗死合并心力衰竭后的醛固酮受体阻断
Med Klin (Munich). 2006 Jun 15;101(6):458-66. doi: 10.1007/s00063-006-1063-3.
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Eplerenone: new drug. Recent myocardial infarction with heart failure: a spironolactone me too.依普利酮:新药。近期心肌梗死伴心力衰竭:一种螺内酯的仿制药。
Prescrire Int. 2006 Apr;15(82):46-9.
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Serum potassium and clinical outcomes in the Eplerenone Post-Acute Myocardial Infarction Heart Failure Efficacy and Survival Study (EPHESUS).依普利酮急性心肌梗死后心力衰竭疗效和生存研究(EPHESUS)中的血清钾与临床结局
Circulation. 2008 Oct 14;118(16):1643-50. doi: 10.1161/CIRCULATIONAHA.108.778811. Epub 2008 Sep 29.
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Cost effectiveness of eplerenone in patients with heart failure after acute myocardial infarction who were taking both ACE inhibitors and beta-blockers: subanalysis of the EPHESUS.依普利酮用于急性心肌梗死后同时服用血管紧张素转换酶抑制剂和β受体阻滞剂的心力衰竭患者的成本效果:EPHESUS 的亚组分析。
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A systematic review and economic evaluation of the clinical effectiveness and cost-effectiveness of aldosterone antagonists for postmyocardial infarction heart failure.心肌梗死后心力衰竭中醛固酮拮抗剂的临床疗效和成本效果的系统评价和经济评估。
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Eplerenone, a selective aldosterone blocker, in patients with left ventricular dysfunction after myocardial infarction.依普利酮,一种选择性醛固酮阻滞剂,用于心肌梗死后左心室功能不全的患者。
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Optimizing care of heart failure after acute MI with an aldosterone receptor antagonist.使用醛固酮受体拮抗剂优化急性心肌梗死后心力衰竭的治疗。
Curr Heart Fail Rep. 2007 Dec;4(4):183-9. doi: 10.1007/s11897-007-0011-8.
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Integrating traditional and emerging treatment options in heart failure.整合心力衰竭的传统和新型治疗方案。
Am J Health Syst Pharm. 2004 May 1;61 Suppl 2:S14-22. doi: 10.1093/ajhp/61.suppl_2.S14.