Scientists have found that SARS-CoV-2, the virus behind Covid-19, triggers a dangerous immune response in hardened fatty deposits (plaques) lining the heart's largest blood vessels, leading to the risk of heart attack, stroke.
Experts have long observed that the Covid-19 coronavirus increases the likelihood of having a heart attack or stroke for up to a year after infection, particularly for those who already have underlying heart conditions.
However, the specific mechanisms that account for these risks had until now remained unclear.
Researchers at New York University’s (NYU) Grossman School of Medicine in the US explored how the coronavirus behaves in those with atherosclerosis -- a disease in which plaque collects in major arteries and prompts chronic inflammation.
For the study, published online in the journal Nature Cardiovascular Research, the team detected the virus within the arteries of eight men and women with a history of atherosclerosis who had died of Covid-19.
Besides colonising arterial heart tissue itself, the coronavirus was also spotted inside local immune cells called macrophages, which normally protect the heart by "swallowing" and disposing of excess fat molecules in arteries.
The experiments further showed that in response to the infection, the macrophages release inflammatory signalling proteins called cytokines that promote a chronic immune response. Notably, the researchers said, two of the identified cytokines, interleukin-1 beta and interleukin-6, have already been linked to heart attacks.
"Our findings provide for the first time a direct mechanistic link between Covid-19 infection and the heart complications it provokes," said lead author Natalia Eberhardt, Postdoctoral fellow in the Department of Medicine at NYU Langone Health.
"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 collected 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 heart disease.
They team trained an artificial intelligence (AI) computer programme to measure coronavirus levels in plaque cells. It was able to count thousands of viral features on a cell-by-cell basis.
The team also examined samples of plaque-covered tissue collected from patients who had received surgery to remove the fatty buildup from their arteries. Using a new technique that allowed them to study coronavirus infection of live tissue in the lab, the researchers showed that exposing plaque to the virus boosts inflammation levels in blood vessels.
Together the experimental findings revealed that macrophages rich in engulfed fat were invaded more frequently and for longer periods than those containing less fat.
According to the researchers, this suggests that the coronavirus flourishes more easily in people who already have large amounts of plaque buildup in their arteries, explaining in part why those with atherosclerosis are more vulnerable to Covid-19.
The research team next plans to more closely explore this potential link between the coronavirus's behaviour during atherosclerosis and long Covid, which includes heart palpitations, chest pain, and fatigue, among other issues.
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