This case report highlights the potential for restrictive cardiomyopathy to develop as a sequela of acute myocarditis following an upper respiratory infection.
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May link acute myocarditis to later restrictive cardiomyopathy; hypothesis-generating case report that leaves open frequency and surveillance needs.
A fifty-five-year-old man developed intractable heart failure four weeks after upper respiratory infection. His central venous pressure was as high as 300 mmH2O. Two-dimensional echocardiogram revealed no muscular hypertrophy of the ventricles, no pericardial thickness, and no pericardial effusion. On catheterization, hemodynamic data were compatible with restrictive cardiomyopathy. Transvenous endomyocardial biopsy of the left ventricle was performed. Histologic examination strongly suggested that cardiomyopathy developed after acute myocarditis.
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Katayama et al. (1990) studied this question.
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