Vogt M, Strauer B E
Medical Clinic, Heinrich-Hèine-University of Düsseldorf, Germany.
Am J Cardiol. 1995 Nov 2;76(13):48D-53D. doi: 10.1016/s0002-9149(99)80492-5.
Left ventricular hypertrophy in arterial hypertension is characterized by myocyte hypertrophy, myocardial fibrosis, and structural changes of the intramural coronary arteries. Hypertensives with or without left ventricular hypertrophy have a reduced coronary vasodilator reserve due to alterations of the coronary microcirculation. The impairment in coronary vasodilator reserve is likely to initiate a process of malperfusion and malnutrition concomitant with increased metabolic demands. Further, malperfusion is supported by an increase in diastolic filling pressure, which will enhance the extravascular component of coronary resistance. The sum of interactions of these structural alterations of myocardium, interstitium, and coronary vasculature are likely to initiate and maintain a process of myocardial malperfusion and malnutrition, which can provoke functional depression of the myocardial performance, a loss of contractile proteins, an increase in interstitial fibrosis, and, not least, an overall decrease in contractile function in long-standing cardiac hypertrophy. Finally, the reversal of these processes by adequate antihypertensive treatment may contribute to renormalization of cardiac function and to prevention of late cardiac failure in hypertensive heart disease.
动脉高血压所致的左心室肥厚的特征为心肌细胞肥大、心肌纤维化以及壁内冠状动脉的结构改变。无论有无左心室肥厚，高血压患者由于冠状动脉微循环的改变，其冠状动脉舒张储备均会降低。冠状动脉舒张储备受损可能会引发灌注不良和营养障碍过程，同时代谢需求增加。此外，舒张期充盈压升高会加重冠状动脉阻力的血管外成分，从而加重灌注不良。心肌、间质和冠状血管的这些结构改变相互作用，可能会引发并维持心肌灌注不良和营养障碍过程，进而导致心肌功能抑制、收缩蛋白丢失、间质纤维化增加，长期心脏肥大时还会导致收缩功能全面下降。最后，通过适当的抗高血压治疗逆转这些过程，可能有助于使心脏功能恢复正常，并预防高血压性心脏病晚期心力衰竭。
