SARS-CoV-2 infection can inflame heart arteries and increase the risk of heart attack and stroke. This study focused on older adults and provides insight into the increased cardiovascular risk in patients with COVID-19.
NIH-funded research revealed the following relationship: COVID-19 (new coronavirus infection) Infections and increased risk cardiovascular disease And a stroke.
SARS-CoV-2, virus According to research funded by It is said that it may increase the risk of National Institutes of Health.The survey results were published in a magazine Nature cardiovascular researchexplains why certain people with COVID-19 are more likely to develop cardiovascular disease or, if already infected, develop more heart-related complications. may be helpful.
In the study, researchers focused on older adults who developed fat deposits known as atherosclerotic plaques and died from COVID-19. However, the researchers found that the virus infects and replicates in the arteries regardless of plaque levels, so this finding could have broader implications for people infected with COVID-19.
“Since the early days of the pandemic, we have known that people infected with COVID-19 have an increased risk of cardiovascular disease and stroke up to a year after infection,” said Dr. said Dr. Michelle Olive. Basic and Early Translational Research Program of the National Heart, Lung, and Blood Institute (NHLBI), part of the NIH. “We believe that one of the reasons for this has been solved.”
Understanding the effects on arterial cells
Previous studies have shown that SARS-CoV-2 can directly infect tissues such as the brain and lungs, but less was known about its effects on coronary arteries. Researchers knew that once the virus reached cells, the body’s immune system sent in white blood cells known as macrophages to help remove the virus. In arteries, macrophages also help remove cholesterol, and when there is too much cholesterol, they transform into a special type of cell called a foam cell.
The researchers reasoned that if SARS-CoV-2 could directly infect arterial cells, normally free macrophages could increase inflammation in existing plaques, said Dr. explained Chiara Giannarelli, MD, PhD.Pathology new york universityGrossman School of Medicine and senior author of the study. To test their theory, Giannarelli and her team took tissue from the coronary arteries and plaques of people who died from COVID-19 and confirmed that the virus was present in those tissues. They then harvested arterial and plaque cells (including macrophages and foam cells) from healthy patients and infected them with SARS-CoV-2 in a laboratory dish. They discovered that the virus was also infecting those cells and tissues.
Further discoveries and suggestions
Additionally, the researchers found that when comparing the infection rates of SARS-CoV-2, the virus was shown to infect macrophages at a higher rate than other arterial cells. Foam cells, which contain a lot of cholesterol, are the most susceptible to infection and cannot easily remove viruses. This suggests that foam cells may serve as a reservoir for SARS-CoV-2 within atherosclerotic plaques. Higher plaque buildup and higher numbers of foam cells can increase the severity and duration of COVID-19 infection.
Next, the researchers looked at the inflammation they predicted could occur within the plaques after they were infected with the virus. They immediately recorded the release of molecules known as cytokines, which are known to increase inflammation and promote the formation of more plaques. Cytokines were released by infected macrophages and foam cells. Researchers say this may help explain why people who have underlying plaque buildup and subsequently become infected with COVID-19 may develop cardiovascular complications long after infection. He said it might be possible.
“This study is very important because it adds to a larger body of work to better understand COVID-19,” Olive said. “This is just another study demonstrating how the virus infects and causes inflammation in many cells and tissues throughout the body. This will provide useful information for future research on the virus.”
The findings conclusively show that SARS-CoV-2 can infect and replicate in macrophages in plaques and arterial cells, which were prevalent in New York City between May 2020 and May 2021. related only to the original strain of SARS-CoV-2. The study was conducted in a small cohort of older adults, all of whom had atherosclerosis or other medical conditions. Therefore, the results cannot be generalized to young, healthy people.
Reference: “SARS-CoV-2 infection causes a pro-atherogenic inflammatory response in human coronary vessels” Natalia Eberhardt, Maria Gabriela Noval, Ravneet Kaur, Letizia Amadri, Michael Gildea, Swathy Sajja, Dayasagar Das, Burak Cilhoroz, O ‘ Written by Jay Stewart, Dawn M. Fernandez, Rosa Chamailova, Andrea Vasquez Guillen, Sonia Jungura, Michael Schottsart, Jonathan D. Newman, Peter Fairies, Tomas Maldonado, Caron Rockman, Amy – Lapkiewicz, Kenneth A. Stapleford, Navneet Narula, Kathryn J. Moore, Chiara Giannarelli, September 28, 2023. Nature cardiovascular research.
DOI: 10.1038/s44161-023-00336-5
This research was funded by NIH/NHLBI grants 1R01HL165258, R01HL153712, R35HL135799, and R01HL084312. NIAID and NIDDK also provided funding.
