Effects of statins on myocarditis: A review of underlying molecular mechanisms.
Myocarditis refers to the clinical and histological characteristics of a diverse range of inflammatory cellular pathophysiological conditions which result in cardiac dysfunction. Myocarditis is a major cause of mortality in individuals less than 40 years of age and accounts for approximately 20% of cardiovascular disease (CVD) events. Myocarditis contributes to dilated cardiomyopathy in 30% of patients and can progress to cardiac arrest, which has a poor prognosis of <40% survival over 10 years. Myocarditis has also been documented after infection with SARS-CoV-2. The most commonly used lipid-lowering therapies, HMG-CoA reductase inhibitors (statins), decrease CVD-related morbidity and mortality. In addition to their lipid-lowering effects, increasing evidence supports the existence of several additional beneficial, 'pleiotropic' effects of statins. Recently, several studies have indicated that statins may attenuate myocarditis. Statins modify the lipid oxidation, inflammation, immunomodulation, and endothelial activity of the pathophysiology and have been recommended as adjuvant treatment. In this review, we focus on the mechanisms of action of statins and their effects on myocarditis, SARS-CoV-2 and CVD.
['Parsamanesh|Negin|N|', 'Karami-Zarandi|Morteza|M|', 'Banach|Maciej|M|', 'Penson|Peter E|PE|', 'Sahebkar|Amirhossein|A|']
D000893:Anti-Inflammatory Agents D000086382:COVID-19 D002318:Cardiovascular Diseases D006801:Humans D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors D015394:Molecular Structure D009205:Myocarditis
Myocarditis SARS-CoV-2 Inflammation HMG-CoA inhibitors RhoA