Is SARS-CoV-2 Directly Responsible for Cardiac Injury? Clinical Aspects and Postmortem Histopathologic and Immunohistochemical Analysis

Abstract

Myocardial injury in patients with SARS-CoV-2 infection may be attributed to the presence of the virus at the cellular level, however, it may also be secondary to other diseases, playing an essential role in the evolution of the disease. We evaluated 16 patients who died because of SARS-CoV-2 infection and analyzed the group from both clinical and pathological points of view. All autopsies were conducted in the Sibiu County morgue, taking into consideration all the national protocols for COVID-19 patients. Of the 16 autopsies we performed, two were complete, including an extensive examination of the cranial cavity. In our study, the cardiac injury was primarily cumulative. Chronic cardiac injuries included fatty infiltration of the myocardium in five cases, fibrosis in 11 cases, and coronary atherosclerosis in two cases. Among the cases with evidence of acute cardiovascular injuries, inflammatory lymphocytic infiltrate was observed in nine cases, subepicardial or visceral pericardial neutrophil-rich vascular congestion in five cases, and venous thrombosis in three cases. Acute ischemia or myocytic distress was identified by vacuolar degeneration in four cases; areas of undulated and/or fragmented myocardial fibers, with eosinophilia and nuclear pyknosis with or without enucleation of the myocytes in nine cases; and in one case, we observed a large area of myocardial necrosis. Immunohistochemical criteria confirmed the presence of the SARS-CoV-2 antigen at the level of the myocardium in only two cases. Comorbidities existing prior to SARS-CoV-2 infection associated with systemic and local inflammatory, thrombotic, hypoxic, or immunological phenomena influence the development of cardiac lesions, leading to death.