Key result
This review highlights the pathophysiological role of inflammation and cell-mediated autoimmunity in the progression from viral myocarditis to dilated cardiomyopathy.
Why the study?
A progression from viral myocarditis to DCM has long been hypothesized, and the role of myocardial inflammation in heart failure pathogenesis has been increasingly recognized.
This review highlights the critical role of inflammation and cell-mediated autoimmunity in the progression from viral myocarditis to dilated cardiomyopathy.
Supports immunomodulatory trials in viral myocarditis; leaves open whether they alter progression to dilated cardiomyopathy.
Dilated cardiomyopathy (DCM) is a heterogeneous group of myocardial diseases clinically defined by the presence of left ventricular dilatation and contractile dysfunction. Among various causes of DCM, a progression from viral myocarditis to DCM has long been hypothesized. Supporting this possibility, studies by endomyocardial biopsy, the only method to obtain a definite diagnosis of myocarditis at present, have provided evidence of inflammation in the myocardium in DCM patients. A number of experimental studies have elucidated a cell-mediated autoimmune mechanism triggered by viral infection in the progression of myocarditis to DCM. In addition, the important role of inflammation in the pathogenesis of heart failure has been recognized, and many terms including myocarditis, inflammatory cardiomyopathy, and inflammatory DCM have been used for myocardial diseases associated with inflammation. This review discusses the pathophysiology of inflammation in the myocardium, and refers to diagnosis and treatment based on these concepts.
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Kyoko Imanaka‐Yoshida (2019) conducted a review in Dilated cardiomyopathy and myocarditis. Inflammation was evaluated. This review highlights the pathophysiological role of inflammation and cell-mediated autoimmunity in the progression from viral myocarditis to dilated cardiomyopathy.
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