Feature | Coronavirus (COVID-19) | July 23, 2020

Autopsies Reveal Surprising Cardiac Changes in COVID-19 Patients

COVID causes a unique pattern of cell death scattered in individual myocytes

Figure B — Top panel, neutrophils noted in collections within small vessels (blue arrow), plump endothelial cells (yellow arrowhead) and a single perivascular dying myocyte (blue arrowhead). Bottom panel, single myocyte undergoing degeneration (blue arrowhead) and plump endothelial cell (yellow arrowhead). Figure C — Electron microscopy, showing particles of SARS-CoV-2 virus present within a cardiac endothelial cell (blue arrowheads), but not present in neighboring cardiac myocyte. #COVID19

Figure B — Top panel, neutrophils noted in collections within small vessels (blue arrow), plump endothelial cells (yellow arrowhead) and a single perivascular dying myocyte (blue arrowhead). Bottom panel, single myocyte undergoing degeneration (blue arrowhead) and plump endothelial cell (yellow arrowhead). Figure C — Electron microscopy, showing particles of SARS-CoV-2 virus present within a cardiac endothelial cell (blue arrowheads), but not present in neighboring cardiac myocyte (left side of image). Images from Circulation.

July 23, 2020 - A series of autopsies conducted by Louisiana State University (LSU) Health New Orleans pathologists shows the damage to the hearts of COVID-19 (SARS-CoV-2) patients is not the expected typical inflammation of the heart muscle associated with myocarditis, but rather a unique pattern of cell death in scattered individual heart muscle cells. They report the findings of a detailed study of hearts from 22 deaths confirmed due to COVID-19 in a research letter published in Circulation.[1]

"We identified key gross and microscopic changes that challenge the notion that typical myocarditis is present in severe SARS-CoV-2 infection," explained Richard Vander Heide, M.D., Ph.D., professor and director of pathology research at LSU Health New Orleans School of Medicine. "While the mechanism of cardiac injury in COVID-19 is unknown, we propose several theories that bear further investigation that will lead to greater understanding and potential treatment interventions."

The team of LSU Health pathologists led by Vander Heide, an experienced cardiovascular pathologist, also found that unlike the first SARS coronavirus, SARS-CoV-2 was not present in heart muscle cells. Nor were there occluding blood clots in the coronary arteries.

Their previously reported results revealed diffuse alveolar damage (DAD) - damage to the small airspaces of the lung where gas exchange occurs - along with blood clots and bleeding in the small blood vessels and capillaries of the lung, were the major contributors to death.

"These findings, along with severely enlarged right ventricles, may indicate extreme stress on the heart secondary to acute pulmonary disease," adds Sharon Fox, M.D., Ph.D., associate director of research and development in the Department of Pathology at LSU Health New Orleans School of Medicine.

The autopsies, believed to be some of the first reported from the U.S., were conducted on 22 patients who died of COVID-19 at University Medical Center in New Orleans. The majority were African American. The 10 male and 12 female patients ranged in age from 44-79. Although there were other underlying conditions, the majority had high blood pressure, half had insulin-treated type 2 diabetes, and about 41 percent had obesity.

The LSU Health New Orleans pathologists, as have others, also found viral infection of some of the cells in the lining of the smaller blood vessels (endothelium). Although at low levels, it may be enough to cause dysfunction leading to individual cell death. The effects of the so-called "cytokine storm" (severe overreaction of the immune system cells fighting the infection) associated with COVID may also play a role.

"Given that inflammatory cells can pass through the heart without being present in the tissue proper, a role for cytokine-induced endothelial damage cannot be ruled out," Vander Heide explained.

In addition to Vander Heide and Fox, the LSU Health New Orleans team included Pathology residents Aibek Akmatbekov, M.D.; Fernanda S. Lameira, M.D..; and Jack L. Harbert, M.D. Guang Li, and J. Quincy Brown from Tulane, also participated.

This was the second publication by this team on autopsy COVID-19 findings. In May, they had a paper published in The Lancet that examined the pulmonary and cardiac pathology in African American patients with COVID-19.[2] Important findings included presence of thrombosis and micro-angiopathy in the small vessels and capillaries of the lungs, with associated hemorrhage, that significantly contributed to death. Features of diffuse alveolar damage, including hyaline membranes, were also present, even in patients who had not been ventilated. 

Cardiac findings included individual cell necrosis without lymphocytic myocarditis. There was no evidence of secondary pulmonary infection by micro-organisms. 

 

Related Cardiac COVID-19 Content:

The Cardiovascular Impact of COVID-19

2018 ACC/AHA/HRS Guideline on the Evaluation and Management of Patients with Bradycardia and Cardiac Conduction Delay: A Report from the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society

How Cardiology Dealt With the COVID-19 Surge in New York City

Kawasaki-like Inflammatory Disease Affects Children With COVID-19 

New Research Highlights Blood Clot Dangers of COVID-19

 

 

Reference: 

1. Sharon E. Fox, Guang Li, Aibek Akmatbekov, Jack L. Harbert, Fernanda S. Lameira, J. Quincy Brown, and Richard S. Vander Heide. Unexpected Features of Cardiac Pathology in COVID-19 Infection. Circulation. Originally published 21 July 2020. https://doi.org/10.1161/CIRCULATIONAHA.120.049465.

2. Sharon E Fox, Aibek Akmatbekov, Jack L Harbert, Guang Li, J Quincy Brown, Richard S Vander Heide. Pulmonary and cardiac pathology in African American patients with COVID-19: an autopsy series from New Orleans. The Lancet. Published May 27, 2020. DOI:https://doi.org/10.1016/S2213-2600(20)30243-5.

 

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