IIn some patients, infection with the pandemic virus SARS-CoV-2 can trigger a dangerous immune response in hardened fatty deposits (plaques) that line the heart’s largest blood vessels, new research suggests. research has shown.
The findings are based on the body’s immune system, which evolved to destroy invading microorganisms, but can also cause disease if triggered in the wrong circumstances. Doing so triggers a series of reactions called inflammation, including swelling, which causes immune cells and signaling proteins to return to the site of infection. Inappropriate inflammation can cause immediate and long-term heart problems, including the breakdown of artery-clogging plaque, and may contribute to a cluster of symptoms called ‘long-term coronavirus.’ say the authors.
Experts have long observed that COVID-19 increases the likelihood of a heart attack or stroke for up to a year after infection, especially for people with pre-existing heart disease. However, the specific mechanisms explaining these risks have remained unclear until now. The study, led by researchers at New York University’s Grossman School of Medicine, investigated how the coronavirus acts in patients with atherosclerosis, a disease in which plaque builds up in major arteries and causes chronic inflammation.
As part of the findings, published online on September 28 in the journal Nature cardiovascular research, the team detected the virus in the arteries of eight men and women with a history of atherosclerosis who died from COVID-19. In addition to colonizing the arterial heart tissue itself, the coronavirus was also found within local immune cells called macrophages. Macrophages normally protect the heart by “engulfing” and disposing of excess fat molecules in the arteries.
Experiments also showed that in response to infection, macrophages release inflammatory signaling proteins called cytokines that promote chronic immune responses. Notably, researchers say two of the cytokines identified, interleukin-1 beta and interleukin-6, have already been linked to heart attacks.
“Our findings reveal for the first time a direct mechanistic link between COVID-19 infection and the cardiac complications it causes,” said lead study author and postdoctoral fellow at NYU Langone Health School of Medicine. said Dr. Natalia Everhart. She says, “Viruses create a highly inflammatory environment that can make it easier for plaques to grow, rupture, and block blood flow to the heart, brain, and other vital organs.”
Previous studies have shown that coronaviruses cause a massive immune response throughout the body. This cytokine storm, so-called a cytokine storm, is suspected to be a contributing factor to heart disease, Dr. Eberhardt says. However, the new study was designed to uncover a more direct mechanism that may be at work as well.
For analysis, the research team collected 27 arterial tissue samples from autopsies of patients who died from severe COVID-19 infection 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 within plaque cells, and while the virus’ genetic material was detected using a fluorescent dye viewed under a microscope, the program noted that thousands of viral signatures can be counted on a cell-by-cell basis.
The researchers also examined samples of plaque-covered tissue taken from patients who underwent surgery to remove fat buildup from their arteries. Using a new technique that allows them to study coronavirus infections in living tissue in the lab, researchers have shown that exposing plaques to the virus increases levels of inflammation in blood vessels.
Together, the experimental results revealed that engulfed fat-enriched macrophages invaded more frequently and for a longer period of time than fat-poor macrophages. According to the researchers, this suggests that the coronavirus multiplies more easily in people who already have large amounts of plaque buildup in their arteries, making it more likely that people with atherosclerosis will develop a new coronavirus infection. This explains in part why they are more vulnerable to
“These results highlight a possible link between pre-existing heart disease and long-term symptoms of COVID-19,” said study lead author and cardiologist Chiara Giannarelli, MD. . “It appears that the immune cells most involved in atherosclerosis may act as a reservoir for the virus, giving it an opportunity to persist in the body for long periods of time.”
As a result, the research team then further investigated the potential link between coronavirus behavior during atherosclerosis and long-term COVID-19 infections, including problems such as heart palpitations, chest pain, and fatigue, among others. We plan to conduct a detailed investigation.
Dr. Giannarelli, an associate professor in the Department of Medicine and Pathology at New York University Langone, said the current study analyzed tissue infected with a strain of the virus that spread throughout New York City early in the pandemic, so the authors were able to identify He added that he plans to repeat the study. To the new variant.
Funding for this research was provided by National Institutes of Health grants R01HL165258 and R01HL153712. Additional funding was provided by American Heart Association Grant 20SFRN35210252 and Chan Zuckerberg Initiative Grant.
In addition to Dr. Eberhardt and Dr. Giannarelli, other NYU Langone researchers involved in this study are Dr. Maria Gabriela Noval; Ravneet Kaur, Mississippi. Dr. Leticia Amadori. Dr. Michael Gildea. Swathy Sajja, Mississippi. Dr. Dayasagar Das; Burak Shilhoros, Mississippi. Rosa Chamailova, BA; Andrea Vázquez Guillen, AS; Jonathan Newman, MD, MPH. Dr. Thomas Maldonado. Caron B. Rockman, MD. Amy V. Lapkiewicz, MD. Dr. Kenneth A. Stapleford. Navneet Narula, Maryland. and Dr. Katherine J. Moore. Other study authors include Ojay Stewart, B.S.; Dr. Dawn Fernandez. Dr. Sonia Jangla. Dr. Michael Schottsaert; and Dr. Peter Fairlies of the Icahn School of Medicine at Mount Sinai in New York City.
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