Neurohormonal activation in heart failure with reduced ejection fraction

被引:464
作者
Hartupee, Justin [1 ]
Mann, Douglas L. [1 ]
机构
[1] Washington Univ, Sch Med, Dept Med, Ctr Cardiovasc Res,Div Cardiol, St Louis, MO 63110 USA
关键词
LEFT-VENTRICULAR DYSFUNCTION; CHANNEL RYANODINE RECEPTOR; CARDIAC MYOCYTE APOPTOSIS; FAILING HUMAN HEART; MYOCARDIAL-INFARCTION; GENE-EXPRESSION; ANGIOTENSIN-II; BETA(1)-ADRENERGIC RECEPTOR; SIGNAL-TRANSDUCTION; TRANSGENIC MICE;
D O I
10.1038/nrcardio.2016.163
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Heart failure with reduced ejection fraction (HFrEF) develops when cardiac output falls as a result of cardiac injury. The most well-recognized of the compensatory homeostatic responses to a fall in cardiac output are activation of the sympathetic nervous system and the renin-angiotensinaldosterone system (RAAS). In the short term, these 'neurohormonal' systems induce a number of changes in the heart, kidneys, and vasculature that are designed to maintain cardiovascular homeostasis. However, with chronic activation, these responses result in haemodynamic stress and exert deleterious effects on the heart and the circulation. Neurohormonal activation is now known to be one of the most important mechanisms underlying the progression of heart failure, and therapeutic antagonism of neurohormonal systems has become the cornerstone of contemporary pharmacotherapy for heart failure. In this Review, we discuss the effects of neurohormonal activation in HFrEF and highlight the mechanisms by which these systems contribute to disease progression.
引用
收藏
页码:30 / 38
页数:9
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