Covert Threat to Cardiovascular Health: SARS-CoV-2 Inflames Heart Arteries and Heightens Inflammation in Plaque
Infection with SARS-CoV-2 can lead to inflammation in the coronary arteries, thereby raising the chances of heart attacks and strokes. This research, which predominantly focuses on an older demographic, offers important understanding of the escalated cardiovascular risks present in COVID-19 patients.
Research financially supported by the National Institutes of Health illuminates the relationship between COVID-19 infection and a heightened susceptibility to cardiovascular diseases and strokes.
According to a study sponsored by the National Institutes of Health and published in the scientific journal Nature Cardiovascular Research, SARS-CoV-2, the virus responsible for COVID-19, has the ability to directly infect heart arteries. This leads to an acute inflammatory response in the atherosclerotic plaque within these arteries, thereby escalating the likelihood of heart attacks and strokes. This data could elucidate why individuals infected with COVID-19 are at an elevated risk for cardiovascular diseases and further complications if they already have pre-existing heart conditions.
The research centered on older individuals with accumulated fatty deposits known as atherosclerotic plaque, who succumbed to COVID-19. Nevertheless, the study revealed that the virus has the capability to infect and propagate in the arteries regardless of the plaque levels, suggesting implications that could extend to the general population affected by COVID-19.
Michelle Olive, Ph.D., the acting associate director of the Basic and Early Translational Research Program at the National Heart, Lung, and Blood Institute (NHLBI), a branch of the NIH, stated, “From the pandemic’s onset, it has been established that individuals who contract COVID-19 are at a higher risk of cardiovascular disease or stroke for up to a year following infection. We think we have discovered one of the underlying causes.”
Understanding Cellular Impacts on Arteries
While prior studies have confirmed that SARS-CoV-2 can directly infect various organs such as the brain and lungs, the impact on coronary arteries was less understood. Scientists were aware that upon viral entry into cells, macrophages—a type of white blood cell—get activated by the immune system to eliminate the virus. In the context of arteries, macrophages also function to clear cholesterol. When overwhelmed by cholesterol, these cells transform into specialized cells known as foam cells.
Chiara Giannarelli, M.D., Ph.D., an associate professor in the departments of medicine and pathology at New York University’s Grossman School of Medicine, who is the senior author of the study, theorized that if SARS-CoV-2 could infect arterial cells directly, then activated macrophages might exacerbate inflammation in the pre-existing plaque. To verify this, her team examined tissues from coronary arteries and plaque from individuals who had died due to COVID-19 and confirmed the presence of the virus. Subsequently, they infected arterial and plaque cells, including macrophages and foam cells, from healthy individuals with SARS-CoV-2 in a controlled laboratory setting. The virus was found to have infected those cells as well.
Additional Findings and Implications
Moreover, the study found that macrophages were more susceptible to SARS-CoV-2 infection compared to other arterial cells. Foam cells loaded with cholesterol were particularly prone to infection and demonstrated difficulty in clearing the virus, suggesting they might serve as a viral reservoir within atherosclerotic plaques. An increased plaque build-up, and thereby a larger number of foam cells, could amplify the severity or persistence of COVID-19.
The research team then focused on the inflammation they hypothesized would occur in the plaque upon infection. They observed the swift release of cytokines, molecules known to augment inflammation and promote further plaque formation. This release was initiated by infected macrophages and foam cells, providing a potential explanation for long-term cardiovascular complications in individuals with underlying plaque who contract COVID-19.
Michelle Olive commented, “This research is of monumental importance as it adds to a growing body of knowledge aimed at comprehending COVID-19 more fully. It is yet another study that elucidates how the virus infects and induces inflammation in diverse cells and tissues throughout the human body. This information will guide future investigations into both acute and long-term effects of COVID-19.”
While the study does definitively demonstrate that SARS-CoV-2 can infect and multiply in arterial plaque macrophages, it should be noted that the findings are specific to the original strains of SARS-CoV-2 that were prevalent in New York City between May 2020 and May 2021. The study was conducted with a small group of older individuals with pre-existing atherosclerosis and other medical conditions, making it inappropriate to extrapolate these findings to younger, healthier populations.
References
The study was published under the title “SARS-CoV-2 infection triggers pro-atherogenic inflammatory responses in human coronary vessels” authored by an extensive list of researchers and was dated September 28, 2023, in Nature Cardiovascular Research. The research was funded by multiple grants from NIH/NHLBI, NIAID, and NIDDK.
