Patients with damage of the mitral, aortic and tricuspid valves and systolic myocardial dysfunction associated with previous SARS-CoV-2 infection are described. The diagnosis of acquired defect was established in 4 patients based on medical history, electrocardiography, echocardiography, magnetic resonance imaging of the heart, endomyocardial or intraoperative myocardial biopsy, and in one case, autopsy. The study of the myocardium included H&E, Van Gieson staining, immunohistochemical (IHC) study with antibodies to CD3, CD20, CD45, CD68, to the nucleocapsid and Spike proteins of SARS-CoV-2. Previous valve diseases (prolapse, bicuspid aortic valve) served as a background for the development of the defect in 2 patients. In all cases, IHC studies revealed coronavirus proteins, lymphocytic endocarditis and myocarditis, moderate fibrosis, and signs of connective tissue disorganization. High titers of anticardiac antibodies indicated an autoimmune mechanism for carditis. No signs of infective endocarditis or thromboembolic complications were identified in any case. In patients with an unclear nature of valvular heart defects, a previous new coronavirus infection should be identified and taken into account as a possible etiological factor. The simultaneous development of lymphocytic myocarditis significantly increases the risk of surgical intervention on the valves and requires an integrated approach to treatment.

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http://dx.doi.org/10.17116/patol20238506152DOI Listing

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Patients with damage of the mitral, aortic and tricuspid valves and systolic myocardial dysfunction associated with previous SARS-CoV-2 infection are described. The diagnosis of acquired defect was established in 4 patients based on medical history, electrocardiography, echocardiography, magnetic resonance imaging of the heart, endomyocardial or intraoperative myocardial biopsy, and in one case, autopsy. The study of the myocardium included H&E, Van Gieson staining, immunohistochemical (IHC) study with antibodies to CD3, CD20, CD45, CD68, to the nucleocapsid and Spike proteins of SARS-CoV-2.

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