In a recent publication in Nature Cardiovascular Research, researchers presented findings from a National Institutes of Health (NIH) study that explored the effects of COVID-19 infection on the heart. The study led by New York University (NYU) Grossman School of Medicine researchers examined how the coronavirus acts in patients with atherosclerosis.

The authors wrote, “Patients with coronavirus disease 2019 (COVID-19) present increased risk for ischemic cardiovascular complications up to 1 year after infection. Although the systemic inflammatory response to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection likely contributes to this increased cardiovascular risk, whether SARS-CoV-2 directly infects the coronary vasculature and attendant atherosclerotic plaques remains unknown.”

In a press release on the NYU Langone Health website, lead author Natalia Eberhardt, PhD, a postdoctoral fellow in the department of medicine at NYU Langone Health, stated, “Our findings provide for the first time a direct mechanistic link between COVID-19 infection and the heart complications it provokes. The virus creates a highly inflammatory environment that could make it easier for plaque to grow, rupture, and block blood flow to the heart, brain, and other key organs.”

For the analysis, the research team gathered 27 artery tissue samples from autopsies of patients who had died of severe COVID-19 between May 2020 and May 2021. All had been previously diagnosed with cardiovascular disease.

The research team indicated that “Next, the authors trained an artificial intelligence (AI) computer program to measure coronavirus levels in plaque cells, noting that while viral genetic material was detected using fluorescent dyes viewed under a microscope, the program was able to count thousands of viral features on a cell-by-cell basis.”

The researchers discovered the COVID-19 virus within the arteries of eight men and women with a history of atherosclerosis who had died of COVID-19.

With regard to their findings, the authors wrote, “SARS-CoV-2 viral RNA is detectable and replicates in coronary lesions taken at autopsy from severe COVID-19 cases. SARS-CoV-2 targeted plaque macrophages and exhibited a stronger tropism for arterial lesions than adjacent perivascular fat, correlating with macrophage infiltration levels. SARS-CoV-2 entry was increased in cholesterol-loaded primary macrophages and dependent, in part, on neuropilin-1. SARS-CoV-2 induced a robust inflammatory response in cultured macrophages and human atherosclerotic vascular explants with secretion of cytokines known to trigger cardiovascular events.”

The authors also indicated that their study “highlights the hyperinflammatory response orchestrated by SARS-CoV-2-infected plaque macrophages and foam cells as a mechanistic link between infection of atherosclerotic coronary vessels and acute cardiovascular complications of COVID-19.”

“These results shed light onto a possible connection between preexisting heart issues and long COVID symptoms,” stated study senior author and cardiologist Chiara Giannarelli, MD, PhD. “It appears that the immune cells most involved in atherosclerosis may serve as a reservoir for the virus, giving it the opportunity to persist in the body over time.”

Due to their findings, the researchers plan to continue examining the potential correlation between the coronavirus’s behavior during atherosclerosis and long-term COVID-19, including heart palpitations, chest pain, and fatigue, among other issues.

In a press release from the NIH, Michelle Olive, PhD, acting associate director of the Basic and Early Translational Research Program at the National Heart, Lung, and Blood Institute, “This study is incredibly important as it adds to the larger body of work to better understand COVID-19. This is just one more study that demonstrates how the virus both infects and causes inflammation in many cells and tissues throughout the body. Ultimately, this is information that will inform future research on both acute and Long COVID.”

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