Werner Christian M, Böhm Michael
Kardiologische Forschung Kardiologie, Angiologie und Internistische Intensivmedizin Innere Medizin - Universitätsklinikum des Saarlandes Kirrberger Str. D-66421 Homburg, Germany.
Ther Adv Cardiovasc Dis. 2008 Jun;2(3):167-77. doi: 10.1177/1753944708091777.
Cardiovascular disease represents a continuum that starts with risk factors such as hypertension and progresses to atherosclerosis, end-organ damage, and ultimately to chronic heart failure (CHF) and premature death. Renin-angiotensin system (RAS) blockade with angiotensin converting enzyme (ACE) inhibitors and/or angiotensin II type 1 receptor blockers (ARBs) has turned out to be beneficial at all stages of this continuum. Several mechanisms govern the progression of structural myocardial damage to end-stage CHF. Chronic neuroendocrine activation fosters left ventricular remodeling and dilatation and leads to clinical symptoms of CHF via forward/backward failure. RAS inhibition is a cornerstone of neuroendocrine blockade in CHF patients, and combined RAS blockade is especially effective in patients presenting with repetitive cardiac decompensations. This review focuses on the therapeutic role of inhibitors of different RAS components in chronic heart failure caused by systolic left ventricular dysfunction.
心血管疾病呈现出一个连续的过程,始于高血压等危险因素,进而发展为动脉粥样硬化、终末器官损害,最终导致慢性心力衰竭(CHF)和过早死亡。使用血管紧张素转换酶(ACE)抑制剂和/或1型血管紧张素II受体阻滞剂(ARB)阻断肾素-血管紧张素系统(RAS)在这一连续过程的各个阶段都已证明是有益的。有几种机制控制着结构性心肌损伤发展至终末期CHF。慢性神经内分泌激活促进左心室重构和扩张,并通过前向/后向衰竭导致CHF的临床症状。RAS抑制是CHF患者神经内分泌阻断的基石,联合RAS阻断在反复发生心脏失代偿的患者中尤其有效。本综述重点关注不同RAS组分抑制剂在收缩性左心室功能障碍所致慢性心力衰竭中的治疗作用。