Enteroviruses are the most common agents of myocarditis and have been implicates in the pathogenesis of dilated cardiopmyopathy. There are still discrepancies in the association of enterovirus and myocardial disease, partially due to lack of data on detection of virus antigen or viral culture in the tissue. For the treatment of fulminant myocarditis, aggressive hemodynamic support is warranted because of its excellent long-term prognosis. This 16 year-old girl was admitted because of anterior chest pain for a day. She had flu-like symptoms such as fever, sore throat and cough at 2 weeks ago. Electrocardiogram showed sinus tachycardia and ST segment elevations in lead II, III, aVF and V1-V4. Troponin T was positive and creatinine phosphokinase was elevated (1323 IU/L) at emergency room. On emergency echocardiogram, inferior wall motion was decreased and the ejection fraction (EF) was 70%. Coronary angiogram showed no thrombus and no significant stenosis in coronary artery, and spasm was not induced with ergonovine. Conventional treatment for congestive heart failure with digoxin (0.25 mg daily) and furosemide (20 mg t.i.d) was started under the impression of myocarditis. On the first hospital day, pulmonary edema and signs of shock were developed. The whole left ventricular(LV) wall motion were markedly decreased and EF was less than 20% on echocardiogram. Despite of intra-aortic balloon pump (IABP) for 4 hours, shock and pulmonary edema was progressed. Mechanical circulatory support was started with left ventricular assist device (LVAD, Bio-pump, Medtronic Bio-Medicus, USA). At the time of operation, central venous pressure was 24cmH20, systolic blood pressure was 75mmHg, left atrium(LA) and LV was dilated and the whole wall of LV showed almost akinesia , and LA appendage was biopsied. After 126 hours of LVAD, LV wall motion was restored and EF was 79% on echocardiogram. LVAD was removed 10 days after operation and she was discharged on 23 days of hospitalization without any heart failure symptoms. Immunohistochemistry of LA showed enteroviral VP1 capsid protein (primary antibody; NoVo Castra Laboratory, UK) over the entire LA wall. Her serum neutralized coxsackievirus B3 (CVB3, H3 variant of Woodruff strain) in neutralization test using horse anti-CVB3 (Nancy strain) antibody (ATCC, V030-501-560) as a positive control. The titer of neutralization Ab in her serum of 21 days increased more than 4 times than that of 2 days.