Researchers from New York University have uncovered an explanation for why infection with the virus that causes COVID-19 can increase the risk of heart attacks and strokes: it triggers an immune response in fatty plaques.
These plaques are fat deposits within the arteries, which accumulate over time, reduce blood flow and lead to complications like coronary heart disease and atherosclerosis.
Since the pandemic, health researchers have warned of the potential connection between COVID-19 and several inflammatory heart problems including myocarditis and pericarditis, and heightened risk of heart attack and stroke for a year after infection.
The researchers from NYU’s Grossman School of Medicine have now learnt how this increased risk occurs within certain COVID-19 patients, though they also note their research only applies to those versions of SARS-CoV-2 in circulation in New York from May 2020-21.
The researchers took tissue samples from the arteries of eight people who died from severe COVID-19 in the first year of the pandemic – each with previously diagnosed heart disease and three or more cardiovascular risk factors such as high blood pressure – they used an AI program and microscope analysis to detect sites of viral infection.
They found the virus infects both arterial cells and macrophages (a type of white blood cell) involved in guarding against excess plaque within the heart. Macrophages surrounded by plaque were more likely to attract the virus than those that weren’t, and infection caused them to release a range of cytokines – inflammatory proteins that facilitate the body’s immune response – including interleukins previously linked to heart attacks.
With fat-laden macrophages unable to perform their job, the risk of further plaque build-up risks prolonging the effects of COVID-19 and cardiovascular complications.
“The virus creates a highly inflammatory environment that could make it easier for plaque to grow, rupture, and block blood flow to the heart, brain, and other key organs,” says Dr Natalia Eberhardt, an immunologist at NYU Langone Health who led the study published in Nature Cardiovascular. “Our findings provide for the first time a direct mechanistic link between COVID-19 infection and the heart complications it provokes.”
Eberhardt and her colleagues highlight how SARS-CoV-2 can infect a range of cells in the body to cause inflammation and elicit an immune response. Severe inflammatory responses dubbed ‘cytokine storms’ occur when a flood of cytokines creates an extreme immune response that attacks the body’s healthy tissues as well as clearing away infections.