Eichhorn E J, Bristow M R
Department of Internal Medicine (Cardiology Division), University of Texas Southwestern, USA.
Circulation. 1996 Nov 1;94(9):2285-96. doi: 10.1161/01.cir.94.9.2285.
Myocardial failure has been considered to be an irreversible and progressive process characterized by ventricular enlargement, chamber geometric alterations, and diminished pump performance. However, more recent evidence has suggested that certain types of medical therapy may lead to retardation and even reversal of the cardiomyopathic process. In the failing heart, long-term neurohormonal/autocrine-paracrine activation results in abnormalities in myocyte growth, energy production and utilization, calcium flux, and receptor regulation that produce a progressively dysfunctional, mechanically inefficient heart. Interventions such as ACE inhibition and beta-blockade result in a reduction in the harmful long-term consequences of neurohormonal/autocrine-paracrine effects and retard the progression of left ventricular dysfunction or ventricular remodeling. Furthermore, in subjects with idiopathic dilated or ischemic cardiomyopathy, antiadrenergic therapy with beta-blocking agents appears to be able to partially reverse systolic dysfunction and ventricular remodeling. Although the precise mechanisms underlying this latter effect have not yet been elucidated, the general mechanism appears to be via improvement in the biological function of the cardiac myocyte. Such an improvement in the intrinsic defect(s) responsible for myocardial failure will likely translate into important clinical benefits.
心肌衰竭一直被认为是一个不可逆的渐进过程,其特征为心室扩大、腔室几何形状改变以及泵功能减弱。然而,最近的证据表明,某些类型的药物治疗可能会导致心肌病进程的延缓甚至逆转。在衰竭心脏中,长期的神经激素/自分泌 - 旁分泌激活会导致心肌细胞生长、能量产生与利用、钙通量以及受体调节异常,进而产生一个功能逐渐失调、机械效率低下的心脏。诸如血管紧张素转换酶(ACE)抑制和β受体阻滞剂等干预措施可减少神经激素/自分泌 - 旁分泌效应的有害长期后果,并延缓左心室功能障碍或心室重塑的进展。此外,在患有特发性扩张型或缺血性心肌病的患者中,使用β受体阻滞剂进行抗肾上腺素能治疗似乎能够部分逆转收缩功能障碍和心室重塑。尽管这种后期效应的确切机制尚未阐明,但总体机制似乎是通过改善心肌细胞的生物学功能。心肌衰竭内在缺陷的这种改善可能会转化为重要的临床益处。