SARS-CoV-2 infection may increase risk of heart disease and stroke

What you need to know

Research has shown that SARS-CoV-2, the virus that causes COVID-19, can directly infect the brain, lungs and other tissues. Less is known about how it affects the arteries of the heart, and scientists don’t fully understand why people with COVID-19 are at higher risk for heart disease and stroke up to a year after infection.

In a study supported by the National Heart, Lung, and Blood Institute, the National Institute of Allergy and Infectious Diseases, and the National Institute of Diabetes and Digestive and Kidney Diseases, researchers found that SARS-CoV-2 can directly infect coronary arteries and cause intense inflammation in the fatty, or atherosclerotic, plaques inside, potentially increasing the risk of heart attack and stroke.

What did the researchers do?

In this study, the researchers focused on older adults who had fatty buildups called atherosclerotic plaques and who died from COVID-19. After the researchers confirmed the presence of SARS-CoV-2 in both the arteries and plaques of the heart, they took arterial and plaque cells from healthy patients (including virus-fighting, cholesterol-cleaning white blood cells called macrophages, and “foam cells,” which form when macrophages become overloaded with cholesterol) and infected the cells with SARS-CoV-2 in petri dishes in the lab. The virus also infected these cells and tissues.

The researchers found that the virus was more likely to infect macrophages than other arterial cells. Foam cells, which cannot easily clear plaque, were even more susceptible to infection. This suggests that foam cells may act as a reservoir for SARS-CoV-2 within atherosclerotic plaques. Increased plaque accumulation, and therefore more foam cells, may worsen or prolong COVID-19 symptoms.

When the researchers studied the inflamed plaques, they also found that infected macrophages and foam cells released cytokines – molecules that increase inflammation and cause more plaque to form.

Why is this research important?

These findings relate to the SARS-CoV-2 strain circulating in New York City between May 2020 and May 2021. Additionally, the study only included a small cohort of older adults with atherosclerosis, so the results cannot be generalized to younger, healthy individuals.

But because the virus can infect and grow in arteries regardless of plaque levels, the findings could have broader implications for people infected with COVID-19. They may also help explain why some people with COVID-19 are more likely to develop heart disease, or why those who already have heart disease may develop more advanced heart-related complications.

Ultimately, the researchers say this information will inform future studies of both acute COVID-19 infection and long COVID.

Where can I go to learn more?

Long-term COVID-19 study of older adults with chronic conditions

• Adults over 55 with chronic conditions have been disproportionately affected by COVID-19.

Inflammatory patterns in the brain may drive many long COVID symptoms

• SARS-CoV-2 can cause long-term organ damage as well as trigger patterns of inflammation in the brain that may be associated with long COVID symptoms.

COVID-19 Cell Atlas Mapping

• The two studies provide a clearer picture of what happens to the cells and tissues in the lungs, heart and other organs of patients with severe COVID-19.

source

Eberhardt, N., Noval, MG, Kaur, R., Amadori, L., Gildea, M., Sajia S., Das, D., Cilhoroz, B., Stewart, O., Fernandez, DM, Shamailova, R., Guillen, AV, Jangra, S., Schotsaert, M., Newman, JD, Faries, P, Maldonado, T., Rockman, C., Rapkiewicz, A., Stapleford, KA, . . . Giannarelli, C. (2023). SARS-CoV-2 infection induces a proatherogenic inflammatory response in human coronary arteries. Nature Cardiovascular Research, 2899–916. https://www.nature.com/articles/s44161-023-00336-5