Optimizing care of heart failure after acute MI with an aldosterone receptor antagonist

被引:18
作者
Verma A.
Solomon S.D. [1 ,2 ]
机构
[1] Department of Medicine, Harvard Medical School, Boston, MA 02115
关键词
Aldosterone; Chronic Heart Failure; Sudden Cardiac Death; Mineralocorticoid Receptor; Ventricular Remodel;
D O I
10.1007/s11897-007-0011-8
中图分类号
学科分类号
摘要
The presence of heart failure or left ventricular systolic dysfunction in the setting of acute myocardial infarction is associated with poor prognosis. Aldosterone is an important downstream mediator of the renin-angiotensin- aldosterone system that promotes myocardial collagen deposition, myocardial fibrosis, apoptosis, ventricular remodeling, and endothelial dysfunction. It may play an important role in the increased morbidity and mortality and the development and progression of heart failure after acute myocardial infarction. Extending the findings from the Randomized Aldactone Evaluation Study (RALES) in patients with chronic heart failure, the Eplerenone Post-Acute Myocardial Infarction Heart Failure Efficacy and Survival Study (EPHESUS) demonstrated that the selective aldosterone blocker eplerenone offered a significant survival benefit, attenuation of progression of heart failure, and prevention of sudden cardiac death when used in addition to optimal medical therapy. The current evidence-based guidelines now suggest that aldosterone blockade should be an integral component of heart failure therapy to improve outcomes in this high-risk population. Copyright © 2007 by Current Medicine Group LLC.
引用
收藏
页码:183 / 189
页数:6
相关论文
共 26 条
  • [1] Guidry U.C., Evans J.C., Larson M.G., Et al., Temporal trends in event rates after Q-wave myocardial infarction: The Framingham Heart Study, Circulation, 100, pp. 2054-2059, (1999)
  • [2] Pitt B., Zannad F., Remme W.J., Et al., The effect of spironolactone on morbidity and mortality in patients with severe heart failure. Randomized Aldactone Evaluation Study Investigators, N Engl J Med, 341, pp. 709-717, (1999)
  • [3] Weber K.T., Sun Y., Recruitable ACE and tissue repair in the infarcted heart, J Renin Angiotensin Aldosterone Syst, 1, pp. 295-303, (2000)
  • [4] Weber K.T., Brilla C.G., Campbell S.E., Et al., Myocardial fibrosis: Role of angiotensin II and aldosterone, Basic Res Cardiol, 88, SUPPL. 1, pp. 107-124, (1993)
  • [5] Swedberg K., Cleland J., Dargie H., Et al., Guidelines for the diagnosis and treatment of chronic heart failure: Executive summary (update 2005), Eur Heart J, 26, pp. 1115-1140, (2005)
  • [6] Struthers A.D., Aldosterone blockade in cardiovascular disease, Heart, 90, pp. 1229-1234, (2004)
  • [7] Opie L.H., Commerford P.J., Gersh B.J., Pfeffer M.A., Controversies in ventricular remodelling, Lancet, 367, pp. 356-367, (2006)
  • [8] Delcayre C., Silvestre J.S., Garnier A., Et al., Cardiac aldosterone production and ventricular remodeling, Kidney Int, 57, pp. 1346-1351, (2000)
  • [9] Silvestre J.S., Heymes C., Oubenaissa A., Et al., Activation of cardiac aldosterone production in rat myocardial infarction: Effect of angiotensin II receptor blockade and role in cardiac fibrosis, Circulation, 99, pp. 2694-2701, (1999)
  • [10] Hayashi M., Tsutamoto T., Wada A., Et al., Relationship between transcardiac extraction of aldosterone and left ventricular remodeling in patients with first acute myocardial infarction: Extracting aldosterone through the heart promotes ventricular remodeling after acute myocardial infarction, J Am Coll Cardiol, 38, pp. 1375-1382, (2001)