PMC:7543426 / 24779-26093 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7543426","sourcedb":"PMC","sourceid":"7543426","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7543426","text":"Several publications have shown an association of the severity of the clinical expression of COVID-19 with the number of comorbidities present. Cardiac involvement in severe COVID-19 pathogenesis has been well documented [23], and cardiac risk factors have been identified as risk factors for increased mortality [24]. In our study of the macroscopic and microscopic features of hearts we found several differences between patients with and without comorbidities. The 4 cases without comorbidities showed pronounced pericarditis and inflammatory cells infiltrating adventitia, indicating that the heart can be compromised irrespective of previous cardiovascular disease. Kidney injury has been reported in nearly 30% of COVID-19 patients [25]. We found that histopathological changes in kidney in patients without comorbidities appeared more severe that those with comorbidities. Patients without comorbidities also showed greater hepatic injury. Whether these findings represent liver or kidney damage caused directly by SARS-CoV-2 itself or are a reflection of the consequences of an abnormal and excessive inflammatory response, requires definition [26]. Studies of other viral infections of the respiratory tract have shown that liver injury may be immune mediated or a result of direct cytopathic damage 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