Ertl G, Gaudron P, Neubauer S, Bauer B, Horn M, Hu K, Tian R
Medizinische Klinik, Universität Würzburg, Germany.
Eur Heart J. 1993 Jul;14 Suppl A:33-7. doi: 10.1093/eurheartj/14.suppl_a.33.
A major consequence of chronic cardiac dysfunction is chronic overload of contractile myocardium. Various aetiologies, in reaction to this, may induce compensatory mechanisms consisting of excentric (dilatation) and concentric hypertrophy. Chronic left ventricular dysfunction is caused most frequently by myocardial infarction. Left ventricular dilatation and hypertrophy occurs in patients with extensive infarction. Dilatation may at first be compensatory, restoring stroke volume within 4 weeks of the infarct. However, as dilatation progresses, left ventricular ejection fraction and stroke volume deteriorate during exercise and at rest, and finally pulmonary capillary wedge pressure increases and patients become symptomatic 1.5-3 years after the infarct. Major determinants of progressive left ventricular dilatation and deterioration of haemodynamics are a depressed left ventricular ejection fraction, angiographically determined infarct size, stroke volume early (4 days) after myocardial infarction, infarct location (anterior/inferior) and the grade (TIMI) of perfusion of the infarct-associated coronary artery. Chronic loading and unloading may accelerate or decelerate this process. Efficiency and energy reserve (phosphocreatine) of the dilated ventricles is reduced. Further intrinsic changes in surviving myocardium include morphological and functional disturbance of coronary microcirculation.
慢性心功能不全的一个主要后果是收缩性心肌长期负荷过重。针对这一情况，多种病因可能会诱发包括离心性（扩张）和向心性肥厚在内的代偿机制。慢性左心室功能不全最常见的病因是心肌梗死。广泛梗死的患者会出现左心室扩张和肥厚。起初，扩张可能具有代偿作用，在梗死4周内恢复每搏输出量。然而，随着扩张的进展，运动和静息时左心室射血分数和每搏输出量会恶化，最终肺毛细血管楔压升高，患者在梗死后1.5至3年出现症状。左心室进行性扩张和血流动力学恶化的主要决定因素包括左心室射血分数降低、血管造影确定的梗死面积、心肌梗死后早期（4天）的每搏输出量、梗死部位（前壁/下壁）以及梗死相关冠状动脉的灌注分级（TIMI）。长期的负荷增加和减少可能会加速或减缓这一过程。扩张心室的效率和能量储备（磷酸肌酸）会降低。存活心肌的进一步内在变化包括冠状动脉微循环的形态和功能紊乱。
