Díez J, Fortuño M A, Ravassa S
Vascular Pathophysiology Unit, School of Medicine, University of Navarra, Pamplona, Spain.
Curr Opin Cardiol. 1998 Sep;13(5):317-25. doi: 10.1097/00001573-199809000-00005.
Numerous hypotheses have been considered to explain the fundamental mechanism(s) for the development of systolic dysfunction and heart failure in animals and humans with arterial hypertension. Besides contractile disturbances of cardiomyocytes and interstitial and perivascular fibrosis, cardiomyocyte loss is now being considered as one of the determinants of the maladaptive processes implicated in the transition from compensated to decompensated left ventricular hypertrophy. A number of experimental evidence suggest that exaggerated apoptosis may account for the loss of cardiomyocytes in the hypertensive left ventricle. Furthermore, some factors intrinsic and extrinsic to the cardiomyocyte emerge as potential candidates to trigger apoptosis. The elucidation of the possible interactions between these factors may be of major interest to prevent the progression to heart failure in patients with hypertensive heart disease.
人们已经考虑了许多假说来解释患有动脉高血压的动物和人类发生收缩功能障碍和心力衰竭的基本机制。除了心肌细胞的收缩紊乱以及间质和血管周围纤维化外，心肌细胞丢失现在被认为是参与从代偿性左心室肥厚向失代偿性左心室肥厚转变的适应不良过程的决定因素之一。大量实验证据表明，过度凋亡可能是高血压左心室中心肌细胞丢失的原因。此外，心肌细胞内在和外在的一些因素成为触发凋亡的潜在候选因素。阐明这些因素之间可能的相互作用对于预防高血压心脏病患者进展为心力衰竭可能具有重要意义。
