SARS-CoV-2 can infect coronary arteries and cause inflammation
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SARS-CoV-2 can infect coronary arteries and cause inflammation

MONTREAL — The virus responsible for COVID-19 can directly infect coronary arteries and cause significant inflammation in the plaques that accumulate on their walls, warns a new American study.

This may explain why some patients with COVID-19 have an increased risk of heart disease, or even why they develop more heart complications once the disease has already begun.

“This new study adds to the scientific literature that is increasingly interested in the role of inflammation in coronary heart disease,” said Dr. Jean-Claude Tardif of the Montreal Heart Institute.

“For years, we thought that clogged arteries were just a problem of fat and cholesterol,” recalls Dr. Tardif. Cholesterol is involved in the blockage, but a lot of new literature is emerging that shows that inflammation in the arteries is probably just as important. That’s why there are all these studies on coronary heart disease that are now targeting inflammation.”

Researchers funded by the US National Institutes of Health studied older patients who died from COVID-19 and had atherosclerosis.

They found that SARS-CoV-2 is able to infect not only coronary artery cells, but also atherosclerotic plaques and two types of white blood cells – macrophages and squamous cells, whose role is to clear cholesterol circulating in the body.

The researchers then discovered that the virus most easily infects squamous cells (macrophages full of cholesterol). They then scramble to get rid of the virus, which can turn atherosclerotic plaques into reservoirs for SARS-CoV-2 and potentially lead to longer, more persistent COVID-19 disease.

“We found a reservoir of sorts for the COVID virus in cardiac artery macrophages, but it is possible that there are other reservoirs in other cell types, so this raises important questions,” Dr. Tardif recalled.

Researchers have finally documented that macrophages and squamous cells infected with SARS-CoV-2 release cytokines, molecules that increase inflammation and promote the formation of new atherosclerotic plaques. events such as angina, heart attacks or strokes,” Dr. Tardif said.

The “cytokine storm” that sometimes accompanies SARS-CoV-2 infection is already well known, but this study allows us to better understand the mechanism of action, he said.

“This helps us understand why patients infected with the COVID virus are at greater risk for heart problems, and if they already have heart problems, they are at even greater risk,” Dr. Tardif explained.

This may indeed explain why patients who already have plaque accumulations experience cardiovascular complications long after contracting COVID-19, US researchers point out.

The study, according to Dr. Tardif, helps to better understand not only COVID-19, but also the role of inflammation in coronary heart disease.

The classic risk factors for coronary heart disease are well known, but the common denominator of smoking, diabetes, obesity, hypertension and even high cholesterol is the inflammation they cause in the arteries,” Dr. Tardif recalled.

“We may be able to better understand why diabetics experience more complications after, for example, contracting COVID, because there are two factors that act additively to increase inflammation in the arteries,” he said. The most important conclusion (from this study) is that inflammation in the arteries of the heart is an important phenomenon that needs to be addressed.

The results of this study were published in the medical journal Nature Cardioglass Research.

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