A Study Has Been Conducted to Shed Light on The Correlation Between COVID-19 & An Increased Susceptibility To Heart Attacks and Strokes

A recent study has revealed that infection with the pandemic virus SARS-CoV-2 can elicit a perilous immune response in calcified atherosclerotic plaques that line the major blood vessels of the heart in certain patients.

The results of the study are predicated on the immune system of the human body, which has evolved to eliminate invading microbes but can also trigger disease when activated in an inappropriate context. This activation leads to a series of responses known as inflammation, which includes swelling resulting from immune cells and signaling proteins homing in on infection sites. The authors assert that misplaced inflammation can result in both immediate and long-term heart issues, such as the disintegration of artery-clogging plaques, and may contribute to the collection of symptoms referred to as "long COVID."

For a year following infection, COVID-19 has been observed by experts to increase the likelihood of heart attack or stroke, particularly for those with pre-existing heart conditions. However, the specific mechanisms that account for these risks have remained unclear until now. The study, led by researchers at NYU Grossman School of Medicine, investigated how the coronavirus behaves in individuals with atherosclerosis, a disease characterized by the accumulation of plaque in major arteries, which prompts chronic inflammation.

As part of the findings, published online on September 28 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. In addition to colonizing arterial heart tissue, the coronavirus was also observed inside local immune cells known as macrophages, which typically protect the heart by "swallowing" and disposing of excess fat molecules in arteries.

The experiments conducted further demonstrated that in response to the infection, the macrophages released cytokines, which are inflammatory signaling proteins that promote a chronic immune response. It is noteworthy that two of these identified cytokines, namely interleukin-1 beta and interleukin-6, have already been associated with heart attacks.

According to Natalia Eberhardt, PhD, the lead author of the study and a postdoctoral fellow in the Department of Medicine at NYU Langone Health, "Our findings establish, for the first time, a direct mechanistic connection between COVID-19 infection and the cardiac complications it triggers. The virus creates an intensely inflammatory environment that could facilitate the growth, rupture, and obstruction of plaque in the heart, brain, and other vital organs."

Previous research has indicated that the coronavirus elicits a widespread immune response throughout the entire body. Dr. Eberhardt suggests that this cytokine storm may contribute to heart problems. However, the objective of this new study was to uncover more direct mechanisms that may also be involved.

To conduct the analysis, the research team obtained 27 samples of artery tissue from autopsies of patients who had succumbed to severe COVID-19 between May 2020 and May 2021. All of these individuals had previously been diagnosed with heart disease. Subsequently, the authors trained an artificial intelligence (AI) computer program to quantify the levels of the coronavirus in plaque cells. They observed that while viral genetic material was detected using fluorescent dyes and examined under a microscope, the program was capable of quantifying thousands of viral features on a cell-by-cell basis.

The team also analyzed samples of plaque-covered tissue obtained from patients who had undergone surgery to remove the fatty deposits from their arteries. By utilizing a novel laboratory technique that enabled the examination of live tissue infected with the coronavirus, the researchers demonstrated that exposure of plaque to the virus leads to an increase in inflammation levels within blood vessels.

Collectively, the experimental findings unveiled that macrophages containing a higher amount of engulfed fat were more frequently and for longer durations invaded by the virus compared to those with lower fat content. According to the researchers, this indicates that individuals with substantial plaque buildup in their arteries are more susceptible to COVID-19, thereby partially explaining why those with atherosclerosis are at a heightened risk.

Study senior author and cardiologist Chiara Giannarelli, MD, PhD, stated, "These findings provide insight into a potential association between preexisting cardiovascular conditions and persistent COVID-19 symptoms." She further added, "It appears that the immune cells primarily involved in atherosclerosis may act as a reservoir for the virus, allowing it to persist within the body for an extended period."

Consequently, the research team intends to further investigate the potential correlation between the behavior of the coronavirus during atherosclerosis and long COVID, which encompasses symptoms such as heart palpitations, chest pain, and fatigue, among others.

Dr. Giannarelli, an associate professor in the Departments of Medicine and Pathology at NYU Langone, states that the current investigation focused on analyzing tissue infected with viral strains that spread throughout New York City early in the pandemic. The authors intend to replicate the study in individuals exposed to newer variants.

The study received funding from the National Institutes of Health grants R01HL165258 and R01HL153712. Additional funding was provided by the American Heart Association grant 20SFRN35210252 and a Chan Zuckerberg Initiative grant.

Apart from Dr. Eberhardt and Dr. Giannarelli, other investigators from NYU Langone involved in the study include Maria Gabriela Noval, PhD; Ravneet Kaur, MS; Letizia Amadori, PhD; Michael Gildea, PhD; Swathy Sajja, MS; Dayasagar Das, PhD; Burak Cilhoroz, MS; Roza Shamailova, BA; Andrea Vasquez Guillen, AS; Jonathan Newman, MD, MPH; Thomas Maldonado, MD; Caron B. Rockman, MD; Amy V. Rapkiewicz, MD; Kenneth A. Stapleford, PhD; Navneet Narula, MD; and Kathryn J. Moore, PhD. The study also includes O’Jay Stewart, BSc; Dawn Fernandez, PhD; Sonia Jangra, PhD; Michael Schotsaert, PhD; and Peter Faries, MD, from the Icahn School of Medicine at Mount Sinai in New York City.