Ultrastructural alterations of the myocardium in Coxsackie B-3 virus myocarditis in mice. 18 Month follow-up study by transmission and analytical electron microscopy.

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Abstract
In a series of studies on experimental coxasackie virus B-3 myocarditis, ultrastructural changes of the myocardium in mice were observed for 18 mo. On the 5th day, a number of necrotic myocardial cells were connected with apparently intact cells at intercalated discs in multiple myocardial lesions. In the necrotic cells, myofibrils underwent lysis and mitochondria contained very electron-dense spicular or granular inclusions and moderately electron-dense amorphous ones. X-ray analytical EM proved that the former type of inclusions contained Ca. Macrophages phagocytosed cell debris and many calcified mitochondria which were aggregated into large masses in the cytoplasm. As the macrophages were disorganized, calcified masses remained naked in the interstitial space and were identifiable by light microscopy. On the 9th day, a crystalloid structure of virus was identified in degenerated myocardial cells. On the 21st day, acute inflammatory reaction was rare in the myocardium. In the 3rd mo., some myocardial cells degenerated near fibrotic or calcified foci. In the 12th and 18th mo., calcified foci remained and interstitial fibrosis was extensive in some animals; some myocardial cells showed various degenerative changes including myofibrillar disorientation and lysis, numerous spherical microparticles adjacent to the sarcolemma, amorphous mitochondrial inclusions and thickening of the basement membrane. Adjacent to fibrotic or calcified foci, some myocardial cells were hypertrophied or atrophied. The hypertrophied cells occasionally possessed multiple intercalated discs and extensive side-to-side junctions. Except for the calcified foci, most myocardial changes in the late chronic phase resembled those in myocardial biopsies obtained from patients with various heart diseases including cardiomyopathies and were assumed to be nonspecific in nature.