Coronavirus infects coronary arteries, increases risk of heart attack and stroke: NIH funded study - Video

Recent research funded by the National Institutes of Health (NIH) has uncovered a concerning revelation: SARS-CoV-2, the virus responsible for COVID-19, can directly infect the arteries of the heart. This infection prompts inflammation in the fatty plaque lining the arteries, significantly elevating the risk of heart attacks and strokes.

The researchers believed that if SARS-CoV-2 could directly infect arterial cells, the unleashed macrophages might contribute to increased inflammation within existing plaque. To test this hypothesis, the team analyzed tissue samples from the coronary arteries and plaque of individuals who had died from COVID-19. They confirmed the presence of the virus in these tissues. Subsequently, the researchers infected arterial and plaque cells, including macrophages and foam cells, from healthy individuals with SARS-CoV-2 in a laboratory setting. The virus successfully infected these cells and tissues.

Furthermore, the study highlighted that SARS-CoV-2 has a higher infection rate in macrophages compared to other arterial cells. Notably, cholesterol-laden foam cells proved the most susceptible to infection and struggled to clear the virus effectively. This observation suggested that foam cells might serve as a reservoir for SARS-CoV-2 within atherosclerotic plaque. Consequently, a more extensive plaque buildup, accompanied by a higher number of foam cells, could exacerbate the severity and persistence of COVID-19.

The researchers then investigated the inflammation within plaque following viral infection. They quickly identified the release of molecules known as cytokines, recognized for increasing inflammation and fostering further plaque formation. These cytokines were primarily released by infected macrophages and foam cells.

Reference: Eberhardt, N., Noval, M.G., Kaur, R. et al. SARS-CoV-2 infection triggers pro-atherogenic inflammatory responses in human coronary vessels. Nat Cardiovasc Res (2023). https://doi.org/10.1038/s44161-023-00336-5