2023-09-29 14:59:00
Research funded by the National Institutes of Health has highlighted the relationship between Covid-19 infection and an increased risk of cardiovascular disease and stroke.
The Coronavirus may directly infect the arteries of the heart and cause severe inflammation as a result of fatty deposits in the arteries, which increases the risk of heart attack or stroke, according to the study conducted by the National Institutes of Health.
These findings, published in the journal Nature Cardiovascular Research, help understand and explain why some people who become infected with Covid-19 are more likely to develop cardiovascular disease, or, if they do become infected, to develop heart-related complications.
During the study, the researchers focused on elderly people who suffer from fat accumulation, also known as atherosclerosis, and who died due to Covid-19. Note that the researchers found that the virus infects the arteries and affects them regardless of the level of fat in the arteries, which means that the results may have effects on anyone who has been infected with the virus.
Acting Assistant Director of the Institute, Dr. Michel Olive, said: “Since the early days of the pandemic, we have known that people who have been infected with Covid-19 have an increased risk of developing cardiovascular disease or stroke for up to a year after infection. We have discovered one of the reasons responsible for this.”
Although previous studies have shown that the virus directly infects brain and lung tissue, we know little about its effect on the coronary arteries. The researchers learned that after the virus reaches the cells, the body’s immune system sends white blood cells known as “macrophages” that help get rid of the virus.
Macrophages in the arteries also help get rid of cholesterol and remove it, but when they become overloaded with cholesterol, they turn into a specialized type of cell called “foam cells.”
The researchers explained that if SARS-CoV-2 can infect arterial cells, the eliminated macrophages may increase inflammation in the existing plaque.
As explained by Chiara Giannarelli, MD, associate professor in the departments of medicine and surgery, and an infectious disease scientist at Grossman University of Medicine in New York and senior author of the study. To test her theory, Giannarelli and her team took tissue from the coronary arteries and plaques of patients who died from Covid-19, and were able to find the virus in those tissues.
The researchers then took arterial and plaque cells, including macrophages and foam cells, from patients who had recovered from SARS-CoV-2. They were able to discover that the virus had infected those cells and tissues as well.
In addition, when comparing infection rates with SARS-CoV-2, researchers discovered that the virus infects macrophages at the same rate as other arterial cells.
The cholesterol-laden foam cells were the most susceptible to infection and unable to eliminate the virus easily. This suggests that foam cells may act as a reservoir for the SARS-CoV-2 virus to atherosclerosis. Therefore, more accumulation in the mineral sheet produces a greater number of foam cells, which can increase the severity or persistence of COVID-19.
The researchers were intrigued by the fact that the inflammation they expected to occur in the plaque after it was infected with the virus led to the release of molecules, known as cytokines, that increase inflammation and promote the formation of more plaques.
Cytokines are released by infected macrophages and foam cells. The researchers reported that this would help explain why people who suffer from an accumulation of essential minerals that cause them to become infected with Covid-19, leading to complications in the heart and blood vessels long after infection.
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