Calcific aortic valve stenosis and COVID-19: clinical management, valvular damage, and pathophysiological mechanisms

Abstract

Patients with corona virus disease (COVID)-19 are prone to a variety of myocardial and vascular complications. Recent studies suggest that cardiac valves are also potential targets for the Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2). Calcific aortic valve stenosis (CAVS) is the most common valvular heart disease. Severe COVID-19 has been associated with main risk factors for CAVS, including male sex, older age, cardiovascular co-morbidities, obesity, hypertension, diabetes, and chronic kidney disease. Prognostic implications for concomitant CAVS and SARS-CoV-2 infection have been reported. Changes in CAVS diagnostic, interventional, and follow-up clinical processes have occurred during the COVID-19 pandemic. SARS-CoV-2 may damage aortic valves via both direct injury and indirect mechanisms that include hyperinflammation, oxidative stress, and valve thrombosis. The injury is often acute but may be irreversible and thus favor future CAVS development. Rheumatic heart disease, which develops as a sequel of rheumatic fever, is one example of a possible relation between an acute infection and chronic valvular heart disease. A persistent prothrombotic state, prolonged endothelial dysfunction, and incomplete resolution of inflammation after COVID-19 convalescence may expose the aortic valves to chronic stimulation toward CAVS. Priority of CAVS management in COVID-19 includes avoiding treatment delay and managing underlying pathophysiological state that promotes CAVS.