Viral cardiomyopathy is a dilated heart muscle dysfunction that is the result of myocarditis (inflammation) of the ventricles (lower chambers of the heart) that leads to deterioration of cardiac function and causes the ventricle to change shape and enlarge. There are several causes of myocarditis, but viruses play a predominant role.
Several viruses have been shown to cause myocarditis. These viruses have different mechanisms in which they cause myocarditis:
- Cardiotropic – the virus directly infects the heart cells
- Vasculotropic – the virus infects heart cells through blood vessels
- Lymphotropic – the virus indirectly damages heart cells through immune cells
These mechanisms above ultimately lead to an inflammatory process where the body's immune cells damage and destroy the heart cells. These inflammatory processes can occur acutely (over less than one month) or chronically (over several months). When the heart cells are damaged, they can remodel and dilate the heart, causing dilated cardiomyopathy. This can lead to a reduction in the ability of the heart to pump blood forward to the tissues that need them, causing heart failure with reduced pump function. The natural history of viral myocarditis and those who develop viral cardiomyopathy is often unpredictable. About 50% of the patients who develop viral cardiomyopathy regain normal heart function. However, 25% have some permanent damage, and the other 25% of patients go on to require advanced heart failure therapies (such as transplants or durable ventricular assist devices) or pass away. In patients with active myocarditis, there is also a small risk of sudden cardiac death related to ventricular arrhythmias (abnormal rhythms starting in the ventricles).