Clinical study
Viral myocarditis mimicking acute myocardial infarction

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Abstract

Anecdotal reports have shown that myocarditis can mimic acute myocardial infarction with chest pain, electrocardiographic (ECG) abnormalities, serum creatine kinase elevation and hemodynamic instability. Thirty-four patients with clinical signs and symptoms consistent with acute myocardial infarction underwent right ventricular endomyocardial biopsy during a 6.5-year period after angiographic identification of normal coronary anatomy. Myocarditis was found on histologic study in 11 of these 34 patients. Cardiogenic shock requiring intraaortic balloon support developed within 6 h of admission in three (27%) of the patients with myocarditis.

The mean age of the group with myocarditis was 42 ± 5 years. A preceding viral illness had been present in six patients (54%). The ECG abnormalities were varied and included ST segment elevation (n = 6), T wave inversions (n = 3), ST segment depression (n = 2) and pathologic Q waves (n = 2). The ECG abnormalities were typically seen in the anterior precordial leads but were diffusely evident in three patients. Left ventricular function was normal in six patients and globally decreased in the remaining five patients, whose ejection fraction ranged from 14% to 45%. Lymphocytic myocarditis was diagnosed in 10 patients, and giant cell myocarditis was detected in the remaining patient. Four patients with impaired left ventricular function received immunosuppressive therapy with prednisone and either azathioprine (n = 2) or cyclosporine (n = 2).

All six patients whose left ventricular function was normal on admission remain alive in functional class I. Of the five patients with impaired systolic function, ejection fraction normalized in three of the four patients who received immonosuppressive therapy within 3 months of treatment and in the one patient who received only supportive therapy. All patients who required intraaortic balloon pump support survived to discharge. One death, due to progressive heart failure, occurred at 18 months in the patient with giant cell myocarditis.

Myocarditis should be clinically suspected in patients with an ischemic chest pain syndrome, particularly when ECG abnormalities are present beyond a single vascular distribution, segmental wall motion abnormalities are lacking or global left ventricular hypokinesia is present on ventriculography. The subsequent demonstration of normal coronary anatomy should prompt consideration of right ventricular endomyocardial biopsy, because those patients with myocarditis have an excellent long-term prognosis and do not require anti-ischemic therapy.

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This work was presented in part at the 62nd Annual Scientific Sessions of the American Heart Association, New Orleans, Louisiana, November 1989.