Cardiomyopathy occurs when viral infections cause myocarditis with a resulting thickening of the myocardium and dilation of the ventricles.
These viruses include Coxsackie B and adenovirus, echoviruses, influenza H1N1, Epstein–Barr virus, rubella (German measles virus), varicella (chickenpox virus), mumps, measles, cytomegalovirus, parvoviruses, yellow fever, dengue fever, polio, rabies and the viruses that cause hepatitis A and C, as well as COVID-19.
Myocarditis may result from a direct viral infection of the myocardium.
Cardiovascular biomarkers like troponin, lactate dehydrogenase, high sensitivity amino-terminal B-type natriuretic peptide, creatinine kinase, and creatinine kinase myocardial band, which indicate myocardial damage, increase in concentration in response to viral infections.
It is suspected that viruses enter cardiac myocytes through a transmembrane receptor, with necrosis, apoptosis, and activation of innate immunity within 1 to 7 days.
Subsequent viral replication and activation of acquired immune responses, with T cell infiltration and autoantibodies occur with either viral clearance or evolution to dilated cardiomyopathy months to years later.