Mudd James O, Kass David A
Johns Hopkins Medical Institutions, Division of Cardiology, Department of Medicine, Baltimore, MD, USA.
Expert Rev Cardiovasc Ther. 2007 May;5(3):585-98. doi: 10.1586/14779072.5.3.585.
Chronic heart failure is a debilitating condition with significant morbidity, mortality and an increasing economic burden. The past 20 years have witnessed great strides in both medical and device-based therapies for heart failure. Central to these developments has been the ability to favorably reverse the chronic processes by which the failing heart remodels. In addition to pharmacotherapies, such as beta-blockade, and inhibition of the renin-angiotensin-aldosterone system, surgical remodeling, containment devices and new methods to restore synchronous contraction have been added to the armamentarium, in some instances, providing clear improvement to both symptoms and mortality. In more advanced stages of heart failure, left ventricular-assist devices provide marked unloading of the failing ventricle and such therapy has provided unique insights into the molecular and cellular mechanisms underlying reverse remodeling, given the immediate access to cardiac tissue. Genetic and cellular approaches, as well as new small molecule targets, may provide future avenues for reverse remodeling of the failing heart, improving symptoms and disease outcome.
慢性心力衰竭是一种使人衰弱的疾病，具有显著的发病率、死亡率且经济负担日益加重。在过去20年里，心力衰竭的药物治疗和器械治疗均取得了巨大进展。这些进展的核心在于能够有效地逆转衰竭心脏重塑的慢性过程。除了诸如β受体阻滞剂以及抑制肾素-血管紧张素-醛固酮系统等药物治疗外，手术重塑、限制装置以及恢复同步收缩的新方法也已被纳入治疗手段，在某些情况下，这些方法对症状和死亡率均有明显改善。在心力衰竭的更晚期阶段，左心室辅助装置可显著减轻衰竭心室的负荷，鉴于能够直接获取心脏组织，这种治疗为逆向重塑背后的分子和细胞机制提供了独特的见解。基因和细胞方法以及新的小分子靶点可能为衰竭心脏的逆向重塑提供未来途径，改善症状和疾病结局。
