COVID-19 can leave consequences that lead to other long-term health problems, and experts had already observed that this disease increases the chances of suffering from cardiovascular problems up to a year after infection. However, it was not known exactly why this occurred and a new study led by researchers at New York University Grossman School of Medicine has now analyzed how the coronavirus behaves in people with atherosclerosisa disease characterized by the accumulation of plaque in the arteries and causing chronic inflammation.
Researchers have found that, in some patients, SARS-CoV-2 infection can trigger a dangerous immune response in hardened fatty deposits (plaques) that line the largest blood vessels of the heart. The findings have been published in Nature Cardiovascular Research and are based on the body’s immune system, which has evolved to eliminate invading pathogens, but also triggers diseases when activated in the wrong situation.
This misactivation of the immune system triggers a series of inflammatory responses, including swelling, which occurs when immune cells and signaling proteins concentrate at sites of infection. Misplaced inflammation can lead to immediate and longer-lasting heart problems, such as the rupture of artery-clogging plaques, and can contribute to group of symptoms known as “long COVID”as the authors have explained.
“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.”
The researchers detected the virus inside the arteriess of eight men and women with a history of atherosclerosis who had died of COVID-19, and found that in addition to colonizing the arterial tissue of the heart, SARS-CoV-2 was also found in local immune cells called macrophages, which normally protect the heart “swallowing” and eliminating excess fat molecules in the arteries.
They also found that, in response to infection, macrophages released inflammatory signaling proteins called cytokines that induce a chronic immune response. Specifically, two of the identified cytokines, interleukin-1 beta and interluekin-6have already been linked to heart attacks.
Connection between pre-existing heart problems and long COVID
“Our findings provide for the first time a direct mechanistic link between COVID-19 infection and the cardiac complications it causes,” said the lead author of the study, 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.”
It was already known that the coronavirus causes a massive immune response throughout the body that has been called cytokine storm, and is suspected of contributing to heart problems, says Dr. Eberhardt. However, the new study was designed to uncover more direct mechanisms that could also play a role.
The researchers collected 27 autopsy arterial tissue samples from patients who had died of COVID-19 between May 2020 and May 2021. All had previously been diagnosed with heart disease. The authors then trained an artificial intelligence (AI) computer program to measure coronavirus levels in the cells in the dish and observed that while viral genetic material was detected using fluorescent dyes viewed under a microscope, the program was able to count thousands of viral characteristics in each cell.
They also examined samples of plaque-covered tissue that came from patients who had surgery to remove fatty buildup in their arteries. Using a new technique that allowed them to study coronavirus infection of living tissue in the laboratory, the researchers showed that exposing plaque to the virus increases levels of inflammation in blood vessels.
The findings from these experiments 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 has an easier time thriving in people who already have large amounts of plaque buildup in their arteries, which partly explains why people with atherosclerosis are more vulnerable to COVID-19.
“These results shed light on a possible connection between pre-existing heart problems and long COVID symptoms,” said the study’s lead author and cardiologist, Dr. Dr. Chiara Giannarelli. “It seems that the Immune cells most involved in atherosclerosis may serve as a reservoir for the virusgiving it the opportunity to persist in the body over time.”
The group of researchers intends to further analyze this potential link between the behavior of the coronavirus during atherosclerosis and long COVID, which includes heart palpitations, chest pain and fatigue, among other health problems.