Trevi G, Sheiban I, Gorni R
Cattedra di Cardiologia, Università di Torino.
G Ital Cardiol. 1995 Oct;25(10):1331-8.
Myocardial hypertrophy in different cardiac diseases is considered to be an adaptive mechanism to the increase of hemodynamic load which might restore to normal radius/wall thickness ratio and consequently to normalize wall stress. However, it has been widely demonstrated that beside the hemodynamic load, other factors contribute to the development of myocardial hypertrophy. It has been shown that in hypertensive patients, functional abnormalities (increased contribution of atrial systole to total diastolic filling, increased isovolumic relaxation period, prolonged diastolic duration, slowed ventricular filling and altered diastolic distensibility) precede the development of myocardial hypertrophy. Thus, in hypertensive patients, sign and symptoms of heart failure could be manifested in absence of myocardial hypertrophy, and might be exclusively due to diastolic dysfunction (with normal systolic function). Systolic function might be involved and compromised late when focal myocardial cell death and fibrosis occur and consequently ¿adequate¿ hypertrophy is shifted to ¿inadequate¿. This evolution is accompanied by morphological and functional changes of the myocardium similar to those encountered in dilated cardiomyopathy. Impairment of systolic function in ¿inadequate¿ hypertrophy is also due to structural changes; altered ratio between sarcomers and mitochondria, increased intercapillary distance, sarcoplasmatic reticulum dysfunction, increase of collagene component with a consequent increment of wall rigidity, hypertrophy of arterial tunica media, which alters coronary flow and coronary reserve. The progression of these morpho-functional abnormalities is a very slow process, in which adaptive mechanism mediated by several enzymes and contractile protein, contribute to maintain myocardial viability. However, over the long course, disseminated focal myocardial cell necrosis and fibrosis, which is an evolving process, is considered to be the main responsible factor for the irreversible myocardial damage and systolic dysfunction in advanced myocardial inadequate hypertrophy.
不同心脏疾病中的心肌肥厚被认为是对血流动力学负荷增加的一种适应性机制，这可能会使半径/壁厚比恢复正常，从而使壁应力正常化。然而，大量研究表明，除了血流动力学负荷外，其他因素也会导致心肌肥厚的发生。研究显示，在高血压患者中，功能异常（心房收缩对总舒张期充盈的贡献增加、等容舒张期延长、舒张期持续时间延长、心室充盈减慢以及舒张期扩张性改变）在心肌肥厚发生之前就已出现。因此，在高血压患者中，心力衰竭的体征和症状可能在没有心肌肥厚的情况下就已出现，并且可能完全是由于舒张功能障碍（收缩功能正常）所致。当局部心肌细胞死亡和纤维化发生，进而使“适当的”肥厚转变为“不适当的”肥厚时，收缩功能可能会在后期受到影响并受损。这种演变伴随着心肌的形态和功能变化，类似于扩张型心肌病中所见到的变化。“不适当的”肥厚中收缩功能的损害也归因于结构改变；肌节与线粒体的比例改变、毛细血管间距增加、肌浆网功能障碍、胶原成分增加导致壁僵硬度增加、动脉中膜肥厚，从而改变冠状动脉血流和冠状动脉储备。这些形态功能异常的进展是一个非常缓慢的过程，在此过程中，由多种酶和收缩蛋白介导的适应性机制有助于维持心肌的活力。然而，从长远来看，弥漫性局灶性心肌细胞坏死和纤维化这一不断发展的过程，被认为是晚期心肌不适当肥厚中不可逆心肌损伤和收缩功能障碍的主要责任因素。
