A 19-year-old student was admitted for orthopnea. He had been a badminton player having no experience of serious diseases until he became aware of exertional epigastralgia ten days before admission. On examination, blood pressure was 102/70 mmHg, heart rate 148, and respiration 34. A third sound and moist rales were heard. The liver was enlarged and palpable at 8 cm below the right costal margin. The titers of the virus neutralizing antibodies determined on admission were all less than 32-fold. Chest roentgenogram as compared with that taken six months before admission showed a marked increase in the cardiothoracic ratio and pulmonary venous congestion. Echocardiogram showed a markedly dilated cavity of the left ventricule (LV) (LV diastolic diameter = 74 mm) compared with the cavity of the right ventricule (RV) (RV diastolic diameter = 20 mm) and diffusely impaired wall motion of the LV (fractional shortening = 9%). He died of intractable congestive heart failure two weeks after admission. Heart weight was 620 g. The LV cavity was markedly dilated, but the thickness of the LV free wall was within normal limits. Microscopy of the both atria, the RV, and the basal ventricular septum showed acute and chronic-staged inflammation. However, microscopy of the free wall of the LV showed only slight interstitial fibrosis without necrosis of the myocytes. The marked dilatation of the LV cavity would be due to either the same mechanism as that of dilated cardiomyopathy or excessive exercise after infection with myocarditis. This case showed that LV dilatation without myocardial necrosis/degeneration could develop among patients with myocarditis.