How is viral myocarditis treated?

Updated: Nov 28, 2018
  • Author: Vinh Q Nguyen, MD, FACC; Chief Editor: Gyanendra K Sharma, MD, FACC, FASE  more...
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Answer

The exact mechanism for myocardial injury in viral cardiomyopathy is controversial. Several mechanisms have been proposed based on animal models. Viruses affect myocardiocytes by direct cytotoxic effects and by cell-mediated (T-helper cells) destruction of myofibers. Other mechanisms include disturbances in cellular metabolism, vascular supply of myocytes, and other immunologic mechanisms.

Viral myocarditis may resolve over several months during the treatment of left ventricular systolic dysfunction. However, it can progress to a chronic cardiomyopathy. The main issue in recovery is ventricular size. Reduction of ventricular size is associated with long-term improvement; otherwise, the course of the disease is characterized by progressive dilation.

Because of an immunologic mechanism of myocyte destruction, several trials have investigated the use of immunomodulatory medications. According to Mason et al in 1995, the Myocarditis Treatment Trial demonstrated no survival benefit with prednisone plus cyclosporine or azathioprine in patients with viral (lymphocytic) myocarditis. [5]

A randomized study by McNamara et al (Intervention in Myocarditis and Acute Cardiomyopathy [IMAC]) did not show IVIG-treatment–related improvement in left ventricular ejection fraction (LVEF) at 6 and 12 months over placebo. Both groups had similar improvement in LVEF over the study period. [6]  In contrast, in a small group of 21 pediatric patients with acute myocarditis, IVIG treatment showed a smaller LV end-diastolic dimension and higher fractional shortening at 12 months. Those treated with IVIG were also more likely to achieve normal LV function and had a higher probability of survival compared to placebo. Although IVIG and immunosuppression are used commonly in myocarditis, a review of studies on immunosuppression in the pediatric population concluded that there was insufficient date for its routine use due to small sample sizes, lack of control group, and differences in medical regimens. [7, 8]


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