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Viral 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, parvoviruses, yellow fever, dengue fever, polio, rabies, and the ...
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Empiric IV glucocorticoids are indicated in acute myocarditis with cardiogenic shock, heart failure, ventricular arrhythmias or high degree AV block that is suspected due to auto-immune disease; but the European Society of Cardiology also recommends subsequent viral genome testing of endomyocardial biopsy specimens due to risk of viral ...
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Viral-induced dilated cardiomyopathy can be characterized using different methods. A 2011 study showed in coxsackievirus infected heart proteome , increased levels of fibrotic extracellular matrix proteins and reduced amounts of energy-producing enzymes can be observed suggesting they could be characteristic in enteroviral cardiomyopathy.
Coxsackie B is a group of six serotypes of coxsackievirus (CVB1-CVB6), a pathogenic enterovirus, that trigger illnesses ranging from a mild febrile rash to full-fledged pericarditis and myocarditis (coxsackievirus-induced cardiomyopathy). [1] [2] The genome of Coxsackie B virus consists of approximately 7,400 base pairs. [3]
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In 2015 cardiomyopathy and myocarditis affected 2.5 million people. [6] Hypertrophic cardiomyopathy affects about 1 in 500 people while dilated cardiomyopathy affects 1 in 2,500. [3] [10] They resulted in 354,000 deaths up from 294,000 in 1990. [7] [11] Arrhythmogenic right ventricular dysplasia is more common in young people. [2]
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