Factors associated with myocardial SARS-CoV-2 infection, myocarditis, and cardiac inflammation in patients with COVID-19

Abstract

COVID-19 has been associated with cardiac injury and dysfunction. While both myocardial inflammatory cell infiltration and myocarditis with myocyte injury have been reported in patients with fatal COVID-19, clinical-pathologic correlations remain limited. The objective was to determine the relationships between cardiac pathological changes in patients dying from COVID-19 and cardiac infection by SARS-CoV-2, laboratory measurements, clinical features, and treatments. In a retrospective study, 41 consecutive autopsies of patients with fatal COVID-19 were analyzed for the associations between cardiac inflammation, myocarditis, cardiac infection by SARS-CoV-2, clinical features, laboratory measurements, and treatments. Cardiac infection was assessed by in situ hybridization and NanoString transcriptomic profiling. Cardiac infection by SARS-CoV-2 was present in 30/41 cases: virus + with myocarditis (n = 4), virus + without myocarditis (n = 26), and viruswithout myocarditis (n = 11). In the cases with cardiac infection, SARS-CoV-2 + cells in the myocardium were rare, with a median density of 1 cell/cm 2. Virus + cases showed higher densities of myocardial CD68 + macrophages and CD3 + lymphocytes, as well as more electrocardiographic changes (23/27 vs 4/10; P = 0.01). Myocarditis was more prevalent with IL-6 blockade than with nonbiologic immunosuppression, primarily glucocorticoids (2/3 vs 0/14; P = 0.02). Overall, SARS-CoV-2 cardiac infection was less prevalent in patients treated with nonbiologic immunosuppression (7/14 vs 21/24; P = 0.02). Myocardial macrophage and lymphocyte densities overall were positively correlated with the duration of symptoms but not with underlying comorbidities. In summary, cardiac infection with SARS-CoV-2 is common among patients dying from COVID-19 but often with only rare infected cells. Cardiac infection by SARS-CoV-2 is associated with more cardiac inflammation and electrocardiographic changes. Nonbiologic immunosuppression is associated with lower incidences of myocarditis and cardiac infection by SARS-CoV-2.

Cardiac pathology in COVID-19: a single center autopsy experience

“…Despite concern for myocarditis in both non-critical and critically ill patients, biopsy proven myocarditis remains rare and inconsistent across autopsy reports. [ 7 , 8 , 9 , 10 , 11 , 12 , 13 , 14 , 17 , 18 , 19 , 20 , 21 , 34 ] In this cohort, only two (4.0%) patients met criteria for a focal myocarditis – with the cause of death in these patients attributed to COVID-19 pneumonia with bacterial coinfection and COVID-19 pneumonia with pulmonary embolism. In the two patients in which the cause of death was listed as a dilated cardiomyopathy, neither patient exhibited a lymphocytic inflammatory infiltrate within the heart, and findings were most consistent with chronic hypertensive and atherosclerotic cardiovascular disease.…”

Longitudinal monitoring of laboratory markers characterizes hospitalized and ambulatory COVID-19 patients

“…Myocardial injury may play a significant role in predicting poor outcomes in patients without a known history of chronic coronary syndromes 35 . However, a very recent study shows abundant evidence of heart damage in COVID-19 patients 36 . This retrospective study that examined 41 autopsies of COVID-19 patients concluded that cardiac tissues of the 30/41 cases harboured the SARS-CoV-2 virus in their hearts, while others have experienced inflammation of the sac surrounding the heart 36 .…”

Coronary Microvascular Dysfunction is Common in Patients Hospitalized with COVID-19 Infection

“…Sars-COV-2 gains access to cells by binding to the ACE2 receptor, which is expressed ubiquitously is many tissues (21,22). There is histopathologic evidence to suggest that Sars-COV-2 infects endothelial cells and possibly inducing endothelial dysfunction (23,24). There is also a well-known tendency towards thrombosis in patients with moderate-to-severe COVID-19 infection.…”