Suppression of the renin-angiotensin-aldosterone system in chronic heart failure: choice of agents and clinical impact.
Suppression of the renin-angiotensin-aldosterone system in chronic heart failure: choice of agents and clinical impact.
复制标题
DOI：
10.1097/01.crd.0000201550.94389.50
复制
发表时间：
2006-03-01
影响因子：
2.1
通讯作者：
Jorde, Ulrich P
中科院分区：
文献类型：
--
作者：
Jorde, Ulrich P
慢性心力衰竭（CHF）在美国已成为流行病，每年约有550，000例新发病例。随着过去20年来靶向神经激素通路的药物治疗的发展，纽约心脏协会（NYHA）IV级受试者的年死亡率从开创性CONSENSUS试验的52%显著改善至最近CHF试验的20%以下。在几项大规模的CHF试验中，已经证明用各种血管紧张素转换酶（ACE）抑制剂抑制肾素-血管紧张素系统（RAS）可以挽救生命，并且所有这些药物都可以在临床试验中测试的剂量下使用，没有明显的偏好。在ACE抑制剂不耐受的情况下，血管紧张素受体阻滞剂（ARB）可用于替代ACE抑制剂，结果相当。然而，ARB的试验之间存在一些不一致性，并且不确定临床试验中检测的ARB是否提供了相当的临床获益，无论是替代ACE抑制剂还是与ACE抑制剂联合使用。一旦开始ACE抑制，所有症状性CHF受试者应遵循β受体阻滞。三重神经激素阻滞可以通过加入醛固酮受体或ARB来完成。无论使用哪种药物或开始的顺序如何，仔细监测神经激素阻滞的至关重要性都不能被夸大。肾功能衰竭和高钾血症是抑制肾素-血管紧张素-醛固酮系统（RAAS）的最重要并发症，RALES试验发表后，高钾血症的住院和死亡人数增加，说明了"随意"使用神经激素阻滞剂的危险。鉴于神经激素阻滞的巨大益处，这些数据的唯一结论是根据相应临床试验中测试的安全性预防措施开始使用RAAS阻滞剂。
Chronic heart failure (CHF) has taken on epidemic proportions in the United States, with approximately 550,000 new cases annually. With the evolution of pharmacotherapy targeting neurohormonal pathways over the past 2 decades, the annual mortality in subjects with New York Heart Association (NYHA) class IV has dramatically improved from 52% in the seminal CONSENSUS trial to less than 20% in more recent trials in CHF. Suppression of the renin-angiotensin system (RAS) with various angiotensin-converting enzyme (ACE) inhibitors has been proven to save lives in several large-scale trials of CHF, and all of them can be used at doses tested in clinical trials without clear preference of one over another. Angiotensin receptor blockers (ARBs) can be used in place of ACE inhibitors in the case of ACE inhibitor intolerance with comparable results. However, some inconsistencies exist between trials with ARBs, and it is uncertain if the ARBs tested in clinical trials provide comparable clinical benefit whether used in place of or in combination with ACE inhibitors. Once ACE inhibition has been started, beta blockade should follow for all subjects with symptomatic CHF. Triple neurohormonal blockade can then be accomplished with the addition of an aldosterone receptor or ARB. Regardless of the exact agent used or sequence of initiation, the critical importance of careful monitoring of neurohormonal blockade cannot be overstated. Renal failure and hyperkalemia are the most important complications of suppression of the renin-angiotensin-aldosterone system (RAAS), and an increase in hospital admissions and death from hyperkalemia after publication of the RALES trial illustrates the danger of "casual" use of neurohormonal blockers. In light of the tremendous benefits of neurohormonal blockade, the only conclusion from these data is to initiate RAAS-blocking agents following the safety precautions tested in the respective clinical trials.