Hedrich Olaf, Patten Richard D, Denofrio David
Cardiac Transplantation Program and Cardiomyopathy Center, Department of Medicine, Division of Cardiology, Tufts-New England Medical Center, 750 Washington Street, Box #5931, Boston, MA 02111, USA.
Curr Treat Options Cardiovasc Med. 2005 May;7(1):3-13. doi: 10.1007/s11936-005-0001-7.
Heart failure (HF) is highly prevalent in our society and its incidence is increasing in concert with the growing aged population. Experimental and clinical studies have consistently shown that HF is ameliorated by inhibition of the renin-angiotensin-aldosterone system (RAAS). Acknowledging that heightened activation of the RAAS contributes significantly to HF progression has led to the development of pharmacologic antagonists of RAAS components that have greatly improved both symptoms and prognosis of patients suffering from this syndrome. Angiotensin-converting enzyme (ACE) inhibitors represent the first developed agents that block the production of angiotensin II, and have been shown to be effective across a broad spectrum of patients with HF, including those with asymptomatic left ventricular dysfunction to overt HF. Initiation of ACE inhibitors prior to the onset of symptoms in those with left ventricular systolic dysfunction, and as early as feasible following a myocardial infarction, has been shown to reduce mortality and the development of overt HF in several clinical trials. Clinical data also support the use of angiotensin II receptor antagonists as an alternative to ACE inhibitors in patients who are allergic to, or intolerant of, ACE inhibitors. Agents that antagonize aldosterone via blockade of mineralocorticoid receptors improve clinical outcomes in patients with advanced HF or those with reduced ejection fraction and HF following an acute myocardial infarction. Maximally inhibiting the RAAS, in conjunction with other neurohormonal systems (eg, the sympathetic nervous system by b-adrenergic blockade), leads to improved clinical outcomes in HF, a highly prevalent and costly disease in our society.
心力衰竭(HF)在我们的社会中非常普遍,并且随着老年人口的增加,其发病率也在上升。实验和临床研究一致表明,抑制肾素-血管紧张素-醛固酮系统(RAAS)可改善HF。认识到RAAS的过度激活对HF进展有显著影响,促使人们开发了RAAS组分的药理拮抗剂,这些拮抗剂极大地改善了患有该综合征患者的症状和预后。血管紧张素转换酶(ACE)抑制剂是最早开发的阻断血管紧张素II产生的药物,已被证明对广泛的HF患者有效,包括那些无症状左心室功能障碍至明显HF的患者。在左心室收缩功能障碍患者出现症状之前,以及在心肌梗死后尽早开始使用ACE抑制剂,已在多项临床试验中显示可降低死亡率和明显HF的发生。临床数据也支持在对ACE抑制剂过敏或不耐受的患者中使用血管紧张素II受体拮抗剂作为ACE抑制剂的替代药物。通过阻断盐皮质激素受体拮抗醛固酮的药物可改善晚期HF患者或急性心肌梗死后射血分数降低和HF患者的临床结局。最大限度地抑制RAAS,结合其他神经激素系统(例如,通过β-肾上腺素能阻滞剂抑制交感神经系统),可改善HF的临床结局,HF是我们社会中一种非常普遍且代价高昂的疾病。