A new study has shed fresh light on the potential connection between pre-existing heart issues and symptoms of ‘long-COVID’. According to researchers from New York University (NYU) Langone Health in New York City, USA, being infected with the pandemic virus SARS-CoV-2 can trigger a dangerous immune response in plaques lining the heart’s largest blood vessels in some patients.
Experts have long observed that the COVID-19 coronavirus increases the likelihood of having a heart attack or stroke for up to a year after infection, particularly for those who already have underlying heart conditions. However, the specific mechanisms that account for these risks had remained unclear until now.
As part of their findings, published online on 28 September in the journal Nature Cardiovascular Research, a team at the NYU Grossman School of Medicine detected the virus within the arteries of eight men and women with a history of atherosclerosis who had died of COVID-19. Besides colonising arterial heart tissue itself, the coronavirus was also spotted inside local immune cells called macrophages, which normally protect the heart by ‘swallowing’ and disposing of excess fat molecules in arteries.
The experiments further showed that, in response to the infection, the macrophages released inflammatory signalling proteins called cytokines that promote a chronic immune response. Notably, the researchers say, two of the identified cytokines—interleukin-1 beta and interluekin-6—have already been linked to heart attacks.
“Our findings provide, for the first time, a direct mechanistic link between COVID-19 infection and the heart complications it provokes,” said study lead author Natalia Eberhard (NYU Langone Health, New York City, USA). “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.”
Past research has revealed that the coronavirus stirs up a “massive immune response” referred to as a ‘cytokine storm’ throughout the entire body, which is suspected to contribute to heart issues, according to Eberhardt. However, this new study was designed to uncover more direct mechanisms that could be at play as well.
For their analysis, the research team collected 27 artery tissue samples from autopsies of patients who had died of severe COVID-19 between May 2020 and May 2021. All had been previously diagnosed with heart disease. Next, the authors trained an artificial intelligence (AI) computer programme to measure coronavirus levels in plaque cells, noting that—while viral genetic material was detected using fluorescent dyes viewed under a microscope—the programme was able to count thousands of viral features on a cell-by-cell basis.