Schwartzkopff B, Mundhenke M, Strauer B E
Medical Clinic, Heinrich-Heine-University Düsseldorf, Germany.
Eur Heart J. 1995 Aug;16 Suppl I:82-6. doi: 10.1093/eurheartj/16.suppl_i.82.
The heart in pressure overload is threatened by the development of diastolic and systolic dysfunction even in the absence of coronary heart disease. In pressure overload, systolic wall stress leads to an increase in left ventricular mass through hypertrophy of myocytes. An activation of myocytic as well as non-myocytic cells is present. An increase in interstitial collagen accompanies hypertrophy of the myocytes. Thus, myocytic hypertrophy and fibrosis cause diastolic dysfunction early on, even when systolic function is still well preserved. In hypertensive heart disease, the coronary microcirculation is remodelled by thickening of the walls of intramyocardial arterioles in relation to their lumen and by an increase in periarteriolar fibrosis. This remodelling of the intramyocardial vasculature is combined with a reduction in coronary vasodilator reserve that may lead to malnutrition and malperfusion of the hypertrophied myocytes. The combined processes of myocytic hypertrophy, vascular remodelling and increased fibrosis may be important in the process of ventricular dilatation and failure in hypertensive heart disease.
即使在没有冠心病的情况下，压力超负荷的心脏也会受到舒张功能和收缩功能障碍发展的威胁。在压力超负荷时，收缩期壁应力通过心肌细胞肥大导致左心室质量增加。心肌细胞以及非心肌细胞被激活。间质胶原增加伴随心肌细胞肥大。因此，即使收缩功能仍保持良好，心肌细胞肥大和纤维化也会早期导致舒张功能障碍。在高血压性心脏病中，心肌内小动脉壁相对于其管腔增厚以及动脉周围纤维化增加，导致冠状动脉微循环重塑。心肌内血管系统的这种重塑与冠状动脉扩张储备减少相结合，这可能导致肥大心肌细胞的营养不足和灌注不良。心肌细胞肥大、血管重塑和纤维化增加的联合过程在高血压性心脏病的心室扩张和衰竭过程中可能很重要。
