Anversa P, Kajstura J, Olivetti G
New York Medical College, Department of Medicine, Valhalla 10595, USA.
Curr Opin Cardiol. 1996 May;11(3):245-51. doi: 10.1097/00001573-199605000-00004.
Decompensated eccentric ventricular hypertrophy characterizes the transition from compensated pressure or volume over-load hypertrophy to myocardial dysfunction and failure. Myocyte loss is the major etiologic factor of wall thinning and chamber dilation and may condition the progression of the cardiac myopathy. Myocyte death can occur by apoptosis or necrosis, but the activation of the suicide program of myocytes exceeds necrotic cell death in the pathologic heart of ischemic origin. Whether reactive fibrosis constitutes a primary event in the initiation of ventricular dysfunction or a secondary reaction to myocyte death is an important unanswered question.
失代偿性离心性心室肥厚是从代偿性压力或容量超负荷肥厚向心肌功能障碍和衰竭转变的特征。心肌细胞丢失是心室壁变薄和心腔扩张的主要病因，可能决定心肌病的进展。心肌细胞死亡可通过凋亡或坏死发生，但在缺血性起源的病理性心脏中，心肌细胞自杀程序的激活超过坏死性细胞死亡。反应性纤维化是心室功能障碍起始的原发性事件还是对心肌细胞死亡的继发性反应，是一个重要的未解决问题。
