key: cord-0826273-jx70owzh
authors: Parmar, Mr Dilen; Gandhi, Tanaya; Ahmad, Dr Mahmood; Kirresh, Dr Ali; Seligmann, Mr George
title: Letter to the Editor in Response to Buja et al. 2020
date: 2020-08-29
journal: Cardiovasc Pathol
DOI: 10.1016/j.carpath.2020.107269
sha: e037af71a63e68b79b38aeb00e1a57b2c6124a9e
doc_id: 826273
cord_uid: jx70owzh

nan

Letter to the Editor in Response to Buja Fox et al. 4 carried out autopsies on ten African American patients who tested positive for SARS-CoV-2, with the aim of investigating the pathogenesis of SARS-CoV-2 on different organs. They remarked that the myocardium showed areas of dispersed myocyte necrosis, a finding that was demonstrated by Buja et al. 1 Fox et al. 4 also observed a rise in cardiac troponin I in 6/10 cases (60%), supporting Buja et al.'s 1 finding that a rise in troponin levels correlates to cardiomyocyte damage. However, it should be noted that Fox et al. 4 did not find lymphocytic infiltrates or significant evidence of viral myocarditis. While Buja et al. 1 alerted us to the comorbidities that each patient possessed, we were only given further information about the cardiovascular history and function of the second case from Houston, which included their left ventricular ejection fraction and electrocardiogram reports. This makes it difficult to discern whether the cardiac necrosis present was due to COVID-19 or other causes. While it was not possible for Buja et al. 1 to provide information on the cardiovascular function of each patient before they contracted COVID-19, it would be of benefit for future studies to include these data and describe the course of disease in patients with fewer comorbidities.

Schaller et al. 5 conducted autopsies on 10 patients in Germany with proven COVID-19 infection, with an emphasis on discerning the cardiopulmonary effects. These autopsies demonstrated mild lymphocytic myocarditis in 4/10 (40%) cases and signs of epicarditis in 2/10 (20%) cases. While this supports the findings by Buja et al. 1 , it is important to note that Schaller et al. 5 could not attribute these myoepicardial changes to myocarditis rather than systemic inflammation. Therefore, looking for markers of systemic inflammation in their cohort may be of benefit.

In conclusion, further research is required to elucidate the cardiac involvement in patients with COVID-19. The establishment of rigorous safety protocols has paved the way for additional studies to be carried out and data from larger sample sizes is necessary to further understanding of the pathogenesis of COVID-19.

The emerging spectrum of cardiopulmonary pathology of the coronavirus disease 2019 (COVID-19): Report of 3 autopsies from Houston, Texas, and review of autopsy findings from other United States cities

Dying with SARS-CoV-2 infection-an autopsy study of the first consecutive

Cardiac troponin I in patients with coronavirus disease 2019 (COVID-19): Evidence from a meta-analysis', Progress in cardiovascular diseases. 2020/03/10

Pulmonary and cardiac pathology in African American patients with COVID-19: an autopsy series from New Orleans', The Lancet Respiratory Medicine

Postmortem Examination of Patients with COVID-19