Bleifeld W, Pop T
Klin Wochenschr. 1975 Jan;53(1):29-37. doi: 10.1007/BF01466854.
The effect of chronic coronary insufficiency on the hemodynamics, the geometry and muscle mass of the left ventricle were studied in 30 patients and compared to 13 controls. In these patients the cardiac output was normal in spite of impaired contractility and left ventricular wall movement. The impaired cardiac performance was compensated by 1. hypertrophy and 2. dialatation of the left ventricle. In one-vessel disease of the the coronary arteries left ventricular muscle mass was modestly, but not significant increased. Hypertrophy decreased from +20% in one vessel disease to +10% in three vessel disease. In contrast, left ventricular dilatation increased from +23% in one vessel disease to 43% in two vessel disease and to 70% in patients with sclerotic lesions in three vessels. Left ventricular dilatation seems to be the main hemodynamic compensatory mechnism resulting in a relative increase of the pump function of the heart compared to non dilated hearts. However, dilatation leads in the end-phase to left ventricular failure. By increased wall tension in the presence of impaired coronary blood flow dilatation bears the risk of deterioration of left ventricular function.
对30例慢性冠状动脉供血不足患者的左心室血流动力学、几何形状和肌肉质量进行了研究，并与13例对照者进行了比较。尽管这些患者的心肌收缩力和左心室壁运动受损，但心输出量仍正常。心脏功能受损通过以下两种方式得到代偿：1. 左心室肥厚；2. 左心室扩张。在冠状动脉单支病变中，左心室肌肉质量有一定程度增加，但无统计学意义。肥厚程度从单支病变时的+20%降至三支病变时的+10%。相反，左心室扩张程度从单支病变时的+23%增至双支病变时的43%，在三支血管有硬化病变的患者中增至70%。与未扩张的心脏相比，左心室扩张似乎是导致心脏泵功能相对增加的主要血流动力学代偿机制。然而，扩张最终会导致左心室衰竭。在冠状动脉血流受损的情况下，由于壁张力增加，扩张会带来左心室功能恶化的风险。
