Electron microscopic study of cardiac lesions induced in rats by isoproterenol and by repeated stress. With suggestion that idiopathic cardiomyopathy may be a "disease of adaptation".

An electron microscopic study of cardiac lesions induced in rats by isoproterenol and by repeated stress is described, and a possible pathogenetic mechanism of idiopathic cardiomyopathy is proposed. Three types of cardiac cells could be roughly differentiated according to the structure and arrangement of myofibrils: 1) normo-type with normal structure and normal arrangement of myofibrils, 2) nondestroyed-degenerated-type in which myofibrils show normal structure and abnormal arrangement, and 3) destroyed-degenerated-type with destroyed myofibrils. Various degrees and frequency of mitochondrial changes (accumulation, variation of size, swelling, loss of cristae and myelin figure), increase of glycogen granules, dilation of sarcoplasmic reticulum or T-tubules and nuclear changes were seen in every type. These 3 types seemed to correlate well with the degree of myocardial beta-adrenergic stimulation by isoproterenol or repeated stress. Normo-types were extensively observed in hearts exposed to mild myocardial beta-adrenergic stimulation. Nondestroyed-degenerated-types and destroyed-degenerated-types were frequently observed in hearts exposed to excessive myocardial beta-adrenergic stimulation. These results show a similarity between cardiac lesions induced in rats by isoproterenol or repeated stress and those seen in human idiopathic cardiomyopathy, and suggest the possibility that idiopathic cardiomyopathy is a "Disease of Adaptation."