Francis G S, McDonald K M, Cohn J N
Department of Medicine, University of Minnesota Medical School, Minneapolis.
Circulation. 1993 May;87(5 Suppl):IV90-6.
Congestive heart failure is often preceded by a latent or preclinical phase in which patients are relatively asymptomatic. During this period, there is neuroendocrine activation, left ventricular dysfunction, and remodeling of the heart. The extent to which these activities are interrelated is unclear, but it appears from experimental studies that myocardial damage is associated with chronic sympathetic nervous system activation, left ventricular hypertrophy, and a subsequent increase in left ventricular volume. The nondamaged myocardial tissue demonstrates enhanced messenger RNA for angiotensinogen and angiotensin converting enzyme activity. Angiotensin II along with other trophic signals may prime the cell for "growth." Alteration of left ventricular function may produce unusual loading conditions on the myocardium. Stretch of membrane-bound ion channels may impart mechanical signals that may be transduced and expressed as cellular hypertrophy. Interstitial collagenase may be activated, leading to disruption of the collagen-supporting network. Elongated cells (eccentric hypertrophy), cell slippage, and cell dropout may contribute to the dilatative process. The end product is cardiac dilatation, inefficient left ventricular performance, and congestive heart failure. We have observed that an increase in left ventricular mass is the initial morphological response to acute myocardial damage in a canine model. This occurs at 1 week and is followed by progressive activation of the sympathetic nervous system, left ventricular dilatation, and modest left ventricular dysfunction, a condition that mimics preclinical heart failure in patients. The remodeling process in the canine model, including the increase in mass and volume, may be blocked by angiotensin converting enzyme inhibitor.(ABSTRACT TRUNCATED AT 250 WORDS)
充血性心力衰竭通常之前会有一个潜伏或临床前期阶段，在此期间患者相对无症状。在此期间，会出现神经内分泌激活、左心室功能障碍和心脏重塑。这些活动之间的相互关联程度尚不清楚，但从实验研究来看，心肌损伤与慢性交感神经系统激活、左心室肥厚以及随后左心室容积增加有关。未受损的心肌组织显示血管紧张素原信使核糖核酸和血管紧张素转换酶活性增强。血管紧张素II与其他营养信号可能使细胞为“生长”做好准备。左心室功能的改变可能会给心肌带来异常的负荷条件。膜结合离子通道的拉伸可能传递机械信号，这些信号可能被转导并表现为细胞肥大。间质胶原酶可能被激活，导致胶原支持网络的破坏。拉长的细胞（离心性肥大）、细胞滑动和细胞脱失可能促成扩张过程。最终结果是心脏扩张、左心室功能低效和充血性心力衰竭。我们观察到，在犬模型中，左心室质量增加是对急性心肌损伤的最初形态学反应。这发生在1周时，随后是交感神经系统的逐渐激活、左心室扩张和轻度左心室功能障碍，这种情况类似于患者的临床前心力衰竭。犬模型中的重塑过程，包括质量和容积的增加，可能会被血管紧张素转换酶抑制剂阻断。（摘要截短至250字）
