Scientists Gain Insight Into How COVID Harms the Heart
MONDAY, Oct. 2, 2023 (HealthDay News) -- New research shows the COVID-19 virus can directly infect coronary arteries, inflaming fatty plaque inside them, which can increase the risk of heart disease and stroke.
This may explain why some people who get COVID-19 have a greater chance of developing heart disease. It also may shed light on why those who already have heart trouble develop more heart-related complications.
“Since the early days of the pandemic, we have known that people who had COVID-19 have an increased risk for cardiovascular disease or stroke up to one year after infection,” said Michelle Olive, acting associate director of the Basic and Early Translational Research Program at the U.S. National Heart, Lung, and Blood Institute (NHLBI).
“We believe we have uncovered one of the reasons why,” said Olive, who was not involved with the study.
While the researchers focused on older people with fatty plaques in the arteries who died from COVID-19, the findings could have broader implications for anybody who gets the virus.
Previous research had shown that COVID-19 could directly infect tissues such as the brain and lungs.
Once the virus reaches the cells, researchers knew that the immune system sends in white blood cells known as macrophages to help clear the virus.
These macrophages also help remove cholesterol in the arteries. But when macrophages become overloaded with cholesterol, they morph into a specialized type of cell called foam cells, according to the study authors.
The investigators theorized that if SARS-CoV-2 could infect arterial cells, the macrophages might increase inflammation in the existing plaque, explained senior author Dr. Chiara Giannarelli. She is an associate professor of medicine and pathology at New York University’s Grossman School of Medicine, in New York City.
The researchers tested the theory with tissue from the coronary arteries and plaque of people who had died from COVID-19. They were able to confirm the virus was in those tissues.
After that, they took arterial and plaque cells, including these macrophages and foam cells, from healthy patients. When researchers infected those cells in a lab dish, they found that the virus had infected them, too.
The findings showed that the virus infects macrophages at a higher rate than other arterial cells. Foam cells filled with cholesterol were the most susceptible to infection.
These foam cells may act as a reservoir of virus in the atherosclerotic plaque, the team reported. COVID-19 infection could be more severe or persistent in those with more plaque build-up.
The researchers also documented the release of cytokines, known to increase inflammation and promote plaque. This may help explain why people who have underlying plaque buildup and then get COVID may have heart-related complications long after, they suggested.
“This study is incredibly important as it adds to the larger body of work to better understand COVID-19,” Olive said in an NHLBI news release. “This is just one more study that demonstrates how the virus both infects and causes inflammation in many cells and tissues throughout the body. Ultimately, this is information that will inform future research on both acute and long COVID.”
The study was conducted in a small group of older individuals and in the original virus strains that circulated between May 2020 and May 2021 in New York City. So, it can’t be generalized to other strains of the virus or to younger, healthy individuals, the researchers noted.
This work was funded by the U.S. National Institutes of Health. The report was published online Sept. 28 in Nature Cardiovascular Research.
The U.S. Centers for Disease Control and Prevention has more on COVID-19.
SOURCE: U.S. National Heart, Lung, and Blood Institute, news release, Sept. 28, 2023