BIPHASIC COURSE OF LEFT-VENTRICULAR DYSFU NCTION IN A 22-YEAR-OLD WOMAN WITH ACUTE MYOCARDITIS

History and clinical findings: Two days before admission a 22-year-old woman developed general fatigue, nausea, headache and retrosternal pa in. Physical examination was unremarkable. Investigations: Erythrocyte sedimentation rate was increased to 20/48, C-reactive protein to 3.3 mg/dl, and there was evidence of myocardial damage (creatine kinase 60 9 U/I, creatine kinase-MB 42 U/I, troponine T 8.39 ng/ml); ST-segment elevations in I, II, III, aVF and V-V6 of the ECC. Echocardiography re vealed clearly thickened myocardium, moderate but haemodynamically not significant pericardial effusion, as well as impaired left ventricula r function. Antimyosin scintigraphy was very abnormal. Cardiac cathete rization confirmed the left ventricular dysfunction, rise of left vent ricular enddiastolic pressure to 17 mm Hg, and a markedly reduced card iac output of 2.4 l/min. Myocardial biopsy showed severe myocarditis w ith marked myocytolysis and considerable lymphocytic infiltrations. En teroviral RNA was demonstrated in the myocardium by polymerase chain r eaction. Treatment and course: The haemodynamics became normal within only 3 days. Myocardial biopsy after 6 months was unremarkable histolo gically and immunohistologically, and left ventricular function was al so normal. However, while after a further 12 months myocardial biopsy remained normal and no virus was demonstrated, there was definite, tho ugh moderate, impairment in left ventricular function, indicating a di lated cardiomyopathy. Interpretation: Even when histological and immun ohistological evidence of healing of an acute viral myocarditis has be en achieved, with complete normalization of left ventricular function, a dilated cardiomyopathy may subsequently develop. The pathophysiolog ical mechanism of this occurrence remains unknown.