The virus responsible for COVID-19 [le SRAS-CoV-2] can directly infect the coronary arteries and cause significant inflammation in the plaques that accumulate on their walls, warns a new American study.
This could explain why some patients affected by COVID-19 then have a higher risk of cardiovascular disease, or even why they develop more cardiac complications if the disease has already set in.
This new study adds to a scientific literature that is increasingly interested in the role that inflammation plays in coronary heart disease, said Dr.r Jean-Claude Tardif, of the Montreal Heart Institute.
“For many years, we thought that blocked arteries were only a problem of fat and cholesterol,” recalled Dr.r Late. Cholesterol is implicated in blockages, but there is a lot of emerging literature that shows inflammation in the arteries is probably just as important. That’s why you have all these studies in coronary heart disease that are now targeting inflammation. »
Researchers funded by the U.S. National Institutes of Health looked at older patients who died from COVID-19 and had atherosclerosis.
They found that SARS-CoV-2 is able to infect not only the cells of the coronary arteries, but also atherosclerotic plaques and two types of leukocytes ― macrophages and squamous cells ―, whose role is to clean the cholesterol circulating in the body.
Researchers then discovered that the virus most easily infects squamous cells (macrophages full of cholesterol). These then struggle to get rid of the virus, which could transform atherosclerotic plaques into reservoirs of SARS-CoV-2 and potentially lead to longer and more persistent COVID-19.
“We found a kind of reservoir of COVID virus in the macrophages of the artery of the heart, but it is possible that there are other reservoirs in other types of cells as well, so this raises important questions », recalled Doctor Tardif.
The role of inflammation
Researchers have finally documented that macrophages and squamous cells infected by SARS-CoV-2 release cytokines, a molecule that increases inflammation and promotes the formation of more new atherosclerotic plaques ― “and that says inflammation in a arterial wall means there is a risk of clinical events such as angina, heart attacks or strokes,” said Dr. Tardif.
The “cytokine storm” that sometimes accompanies SARS-CoV-2 infection was already well known, he said, but this study allows us to better understand the mechanism at play.
“It helps us understand why patients who are infected with the COVID virus are more at risk of having a heart problem, and if they already have a heart problem, then they are even more at risk,” explained Doctor Tardif.
This could indeed explain why patients who already have plaque accumulations present cardiovascular complications long after COVID-19, the American researchers indicated.
The study, Dr. Tardif said, 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 or even hypercholesterolemia is the inflammation they cause in the arteries. , recalled Doctor Tardif.
“We can perhaps better understand why diabetics have more complications after a COVID infection, for example, because there, you have two factors which act in an additive manner to increase inflammation in the arteries,” he said. -he explains. The most important message [de cette étude], is that inflammation in the arteries of the heart is an important phenomenon that must be targeted. »
The findings of this study were published by the medical journal Nature Cardiovascular Research.