A series of autopsies conducted by pathologists at the Louisiana State University (LSU) Health New Orleans show that heart damage in patients with COVID-19 is not the typical inflammation of the heart muscle associated with myocarditis, but rather a particular pattern of cell death of individual cardiac myocytes. The results come from a detailed study of the hearts of 22 patients who died from COVID-19.
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"We have identified the major macroscopic and microscopic changes that challenge the idea that typical myocarditis is associated with severe SARS-CoV-2 infection," says Prof. Richard Vander Heide. "Although the mechanism of cardiac damage in COVID-19 is unknown, we propose several theories that need further investigation to arrive at a better understanding and potential therapeutic interventions” he adds.
The LSU Health Sciences Center's team of pathologists led by Dr. Vander Heide, an experienced cardiovascular pathologist, also discovered that, unlike the coronavirus responsible for SARS, the SARS-CoV-2 virus was not present in heart muscle cells. Nor were there clots in the coronary arteries.
The results of their previous research had revealed that widespread alveolar damage together with thrombus formation and bleeding in pulmonary microcirculation was the major cause of death in COVID-19 patients. "These findings, together with evidence of right ventricular enlargement, may indicate extreme heart stress secondary to acute lung disease," adds Dr. Sharon Fox, Associate Director of Research and Development in the Department of Pathology at LSU Health New Orleans School of Medicine.
Autopsies were conducted at the University Medical Center in New Orleans on 22 patients who died of COVID-19. Most were African-American. The ten male and twelve female patients were aged between 44 and 79 years. Although there were other underlying pathological conditions, the majority had high blood pressure, half had type-2 diabetes treated with insulin and about 41% had obesity.
LSU Health New Orleans pathologists, like others, also found viral infection damage to endothelial cells. Although minimal, this endothelial damage may be sufficient to cause organ dysfunction due to the death of individual cells. The effects of the so-called "cytokine storm" associated with COVID-19 may also play a role in the evolution of the disease. "Since inflammatory cells can pass through the heart without necessarily being present in the actual cardiac tissue, it cannot be excluded that this plays a role in the genesis of cytokine-induced endothelial damage," says Dr. Vander Heide.
Fox SE, Li G, Akmatbekov A, et al. Unexpected Features of Cardiac Pathology in COVID-19 Infection [published online ahead of print, 2020 Jul 21]. Circulation. 2020;10.1161/CIRCULATIONAHA.120.049465. doi:10.1161/CIRCULATIONAHA.120.049465