Research funded by the National Institutes of Health (NIH) has demonstrated that SARS-CoV-2 is capable of directly infiltrating the tissues of coronary arteries. This could provide an explanation for the heightened risk of heart attacks and strokes observed in post-COVID-19 cases.
SARS-CoV-2 has been shown to infect the coronary arteries and escalate inflammation in arterial plaques. This lends insight into the virus’s role in elevating the risk of cardiac events such as heart attacks and strokes.
While COVID-19 is already identified as a factor that increases the risk of cardiac complications, it was previously uncertain whether the SARS-CoV-2 virus had a direct influence on blood vessels.
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Recent Insights into Vascular Infection
To investigate this, a research group led by Dr. Chiara Giannarelli of New York University School of Medicine, and supported by NIH funding, examined coronary artery tissues from eight individuals who succumbed to COVID-19 between May 2020 and May 2021. The results were subsequently published in the journal Nature Cardiovascular Research.
The researchers discovered the presence of SARS-CoV-2 RNA in the coronary artery tissues of all subjects. The viral RNA was more prevalent in arterial walls compared to adjacent adipose tissue. Macrophages, a specific type of white blood cell responsible for ingesting pathogens, were found to be frequently infected. Tissue samples that contained more macrophages also displayed elevated levels of viral RNA.
Atherosclerosis is characterized by the narrowing of arteries due to plaque accumulation, comprising fat, cholesterol, and other substances. The narrowing impedes blood flow, and rupture of these plaques can instigate blood clots, thus precipitating heart attacks or strokes. Risk factors include elevated blood pressure and tobacco use.
SARS-CoV-2 and Its Relationship with Atherosclerosis
Macrophages play a role in eliminating cholesterol from blood vessels. When these cells are engorged with cholesterol, they transform into foam cells. The accumulation of foam cells in arterial walls forms plaques, a defining feature of atherosclerosis. The study confirmed that SARS-CoV-2 can infect human macrophages as well as foam cells in vitro. Foam cells proved to be particularly susceptible to infection, which could account for the increased vulnerability of individuals with atherosclerosis to COVID-19.
In both cell types, the infection relied on the presence of a cellular surface protein known as neuropilin. Deactivating the gene responsible for neuropilin led to a reduced rate of infection, as did inhibiting the virus from binding to neuropilin.
Infection activated various inflammatory pathways in both macrophages and foam cells. These cells also released molecules known to contribute to heart attacks and strokes. In surgically extracted arterial plaques from patients, similar inflammatory responses to SARS-CoV-2 infection were observed.
Implications and Future Studies
The data indicates that SARS-CoV-2 may exacerbate the risk of cardiac events by infecting the tissues of arterial walls, including associated macrophages, thereby causing inflammation in atherosclerotic plaques, potentially leading to cardiac events such as heart attacks or strokes.
Dr. Giannarelli commented that these findings illuminate a potential link between preexisting cardiovascular issues and long-term COVID-19 symptoms. She noted that immune cells primarily involved in atherosclerosis could serve as a viral reservoir, allowing the virus to persist in the body.
Dr. Michelle Olive of NIH’s National Heart, Lung, and Blood Institute remarked, “From the onset of the pandemic, it has been clear that post-COVID-19 patients are at a heightened risk for cardiovascular complications up to one year following infection. We believe our research helps explain one of the underlying causes.”
The researchers intend to continue their exploration of the possible connection between arterial infection and long-term COVID-19 symptoms. They are also keen to examine whether their findings are applicable to newer variants of the SARS-CoV-2 virus.
For further information on this study, consult the publication titled “COVID-19 Infects Coronary Arteries and Increases Plaque Inflammation.”
Reference: “SARS-CoV-2 infection triggers pro-atherogenic inflammatory responses in human coronary vessels” by a list of authors, published on 28 September 2023 in Nature Cardiovascular Research. DOI: 10.1038/s44161-023-00336-5
Funding: This study received support from the National Institutes of Health’s National Heart, Lung, and Blood Institute, National Center for Advancing Translational Sciences, National Institute of Allergy and Infectious Diseases, and National Institute of Diabetes and Digestive and Kidney Diseases; as well as the American Heart Association, the Chan Zuckerberg Initiative, and New York University.
Frequently Asked Questions (FAQs) about SARS-CoV-2 and cardiovascular risk
What is the main focus of the NIH-funded research discussed in the article?
The research, funded by the National Institutes of Health, primarily aims to investigate whether SARS-CoV-2, the virus causing COVID-19, directly infects the tissues of coronary arteries. The study further explores how such infection could amplify the risks of heart attacks and strokes in individuals.
Who led the research team and where was the research conducted?
The research team was led by Dr. Chiara Giannarelli from the New York University School of Medicine. The research analyzed coronary artery tissue samples from individuals who died due to COVID-19 between May 2020 and May 2021.
What cells did the virus predominantly infect in the coronary arteries?
The virus predominantly infected macrophages, a type of white blood cell responsible for ingesting pathogens. The presence of more macrophages in tissue samples correlated with higher levels of viral RNA.
What is the relationship between SARS-CoV-2 and atherosclerosis according to the study?
The study confirms that SARS-CoV-2 can infect human macrophages and foam cells, which are macrophages laden with cholesterol. Foam cells contribute to the formation of plaques in arteries, a hallmark of atherosclerosis. Therefore, people with atherosclerosis may be more vulnerable to COVID-19.
How does the infection contribute to cardiovascular risks?
The infection activates various inflammatory pathways in macrophages and foam cells. These cells release molecules known to contribute to heart attacks and strokes. Inflammation in atherosclerotic plaques could potentially lead to cardiac events.
What are the implications for individuals with preexisting heart conditions?
The research suggests that immune cells primarily involved in atherosclerosis could serve as a reservoir for the SARS-CoV-2 virus, allowing it to persist in the body. This could establish a link between preexisting cardiovascular issues and long-term COVID-19 symptoms.
What are the future directions of this research?
The researchers plan to further investigate the potential connection between SARS-CoV-2 infection in the arteries and long-term COVID-19 symptoms. They also intend to examine whether their findings apply to newer variants of the virus.
Who funded the research?
The research received funding from various departments of the National Institutes of Health, including the National Heart, Lung, and Blood Institute, the National Center for Advancing Translational Sciences, the National Institute of Allergy
