Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) was present in the myocardia of patients who died of COVID-19, but this was not associated with an increased inflammatory response, according to the results of a new autopsy study.
Myocardial injury is common in patients with COVID-19. Numerous etiologies are implicated, including acute coronary syndromes, myocarditis, heart failure, stress cardiomyopathy, pulmonary embolism, tachycardia and sepsis. However, fulminant myocarditis with COVID-19 appears to be rare.
Diana Lindner, PhD, of University Heart and Vascular Centre, Germany, and co-investigators, investigated myocardial infection through autopsies of 39 consecutive patients who died of COVID-19 in Hamburg, Germany, in April. Their findings were published online Monday in JAMA Cardiology.
Myocardial tissue was collected from patents, with median postmortem intervals of 3 days. Patients were distributed into two cohorts depending on the presence of a viral load above 1000 copies per μg RNA. The authors then analyzed the samples for six pro-inflammatory genes (tumor necrosis growth factor alpha, interferon gamma, C-C chemokine ligand 5, interleukin [IL]-6, IL-8, IL-18) and for three markers of leukocyte infiltration and presence (cluster of differentiation [CD]3, CD45RO, CD68).
Patients in this study had a mean age of 85 years, and 59% were women. The authors found that of the 39 patients examined, 16 had a viral load above 1000 copies per μg RNA, eight had a viral load below 1000 copies per μg RNA, and the remaining 15 did not have any viral load presence within the myocardium. Gene expression data of a cytokine response panel (tumor necrosis growth factor alpha, interferon gamma, C-C chemokine ligand 5, IL-6, IL-8, IL-18) demonstrated an increase of cytokine presence in patients with viral load above 1000 in comparison with patients with non-infected myocardia. However, immunohistochemistry staining for leukocyte presence (CD3, CD45RO, CD68), did not reveal a difference in patients with infected myocardia versus those without infected myocardia.
This study was limited by its design as an autopsy study. It is possible that in non-autopsy studies, the incidence of viral infection could be different. However, this information is not readily available. Obtaining endomyocardial tissue from patients with active COVID-19 is not feasible in large enough numbers amid this healthcare crisis. Additionally, advanced age in this study, in particular, may have influenced the results, the authors acknowledged.
Despite case reports of clinical myocarditis in patients with COVID-19 in the literature, data from this study suggest that the presence of COVID-19 in myocardial tissue did not necessarily result in the typical inflammatory response consistent with fulminant myocarditis. The authors conclude that the long-term consequences of cardiac involvement requires further investigation.
Lindner D, Fitzek A, Bräuninger H, et al. Association of Cardiac Infection With SARS-CoV-2 in Confirmed COVID-19 Autopsy Cases. JAMA Cardiol 2020 Jul 27. DOI: 10.1001/jamacardio.2020.3551