Research shows “direct mechanistic link” between COVID-19 infection and heart attack, stroke


A new study has shed fresh light on the potential connection between pre-existing heart issues and symptoms of ‘long-COVID’. According to researchers from New York University (NYU) Langone Health in New York City, USA, being infected with the pandemic virus SARS-CoV-2 can trigger a dangerous immune response in plaques lining the heart’s largest blood vessels in some patients.

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 remained unclear until now.

As part of their findings, published online on 28 September in the journal Nature Cardiovascular Research, a team at the NYU Grossman School of Medicine 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 released inflammatory signalling proteins called cytokines that promote a chronic immune response. Notably, the researchers say, two of the identified cytokines—interleukin-1 beta and interluekin-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 study lead author Natalia Eberhard (NYU Langone Health, New York City, USA). “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.”

Past research has revealed that the coronavirus stirs up a “massive immune response” referred to as a ‘cytokine storm’ throughout the entire body, which is suspected to contribute to heart issues, according to Eberhardt. However, this new study was designed to uncover more direct mechanisms that could be at play as well.

For their 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. Next, the authors trained an artificial intelligence (AI) computer programme to measure coronavirus levels in plaque cells, noting that—while viral genetic material was detected using fluorescent dyes viewed under a microscope—the programme 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 build-up 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, these 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 build-up in their arteries—explaining, in part, why those with atherosclerosis are more vulnerable to COVID-19.

“These results shed light onto a possible connection between pre-existing heart issues and long-COVID symptoms,” said study senior author Chiara Giannarelli (NYU Langone Health, New York City, USA). “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.”

As a result, the research team now plans to more closely explore this potential link between the coronavirus’ behaviour during atherosclerosis and long-COVID, which includes heart palpitations, chest pain, and fatigue, among other issues. Giannarelli added that, because the current investigation analysed tissue infected with viral strains that spread throughout New York City early on in the pandemic, the authors intend to repeat the study in those exposed to newer variants as well.


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