Development of necrosis and its sequelae in the myocardium of polymyopathic hamsters (BIO 8262). An electron microscopic study.

Beginning about 30 days after birth, polymyopathic Syrian hamsters of the strain BIO 8262 develop calcifying myocardial necrosis. In the final stage the resorptive granulation tissue is followed by scars with multi-nucleated giant cells containing huge amorphous calcium plaques. The ultrastructural findings reveal the importance of myocardial mitochondria as starting points for calcification. The pattern of cell damage shows marked similarity to the changes observed in the myocardiocytes of magnesium-deficient rats. However, it is different from the alterations described in degenerating myocardiocytes of dehydrotachysterol-treated animals. Spicular electron-dense inclusions are the first and only kind of intramitochondrial calcification. Granular and annular-granular inclusions, as observed in ischaemic and infarcted canine myocardium, could not be detected, indicating that different pathogenetic mechanisms operate. The increased intracellular calcium level triggering myocardial necrosis is regarded as a secondary phenomenon, based on a genetic abnormality.