A study conducted by NYU Langone Health has determined why COVID-19 leads to an increased risk of heart complications following infection. The study's lead author, Natalia Eberhardt, PhD, a postdoctoral fellow at NYU Langone Health, highlights that their research establishes a direct mechanistic connection between COVID-19 infection and the inflammatory environment it triggers, potentially facilitating plaque formation and blockages in crucial organs, including the heart and brain.
According to NYU Langone's recent study, it has been revealed that in certain patients, infection with the SARS-CoV-2 virus responsible for the COVID-19 pandemic can initiate a harmful immune response within the hardened fatty deposits (plaques) lining the major blood vessels of the heart. This immune response, triggered inappropriately by the body's immune system designed to combat invading pathogens, can result in inflammation, including swelling, and potentially lead to immediate and persistent heart problems, including the disruption of plaque build-up in arteries. Additionally, the study suggests that this misplaced inflammation might contribute to the development of symptoms commonly associated with "long COVID."
Previous research has shown that the coronavirus triggers a significant immune response throughout the body, referred to as a cytokine storm, which is suspected to contribute to heart problems, according to Eberhardt, study lead author. However, this new study aimed to uncover more direct mechanisms that might be involved. In this study, the research team obtained 27 samples of artery tissue from autopsies of individuals who had died from severe COVID-19 between May 2020 and May 2021, all of whom had previously been diagnosed with heart disease. They then used an artificial intelligence computer program to measure the levels of the coronavirus in plaque cells. This program was capable of counting thousands of viral features on a cell-by-cell basis, even though viral genetic material had been detected using fluorescent dyes observed under a microscope.
The research team also investigated tissue samples covered in plaque collected from patients who had undergone surgery to remove the fatty deposits from their arteries. Using a new laboratory technique that allowed them to study how the virus infects live tissue, they found that when plaque is exposed to the coronavirus, it increases inflammation in blood vessels. The experimental results showed that immune cells called macrophages, which are rich in fat, were more frequently invaded by the virus and for longer durations compared to those with less fat. This suggests that the coronavirus is more likely to thrive in individuals with significant plaque build-up in their arteries, which partly explains why people with atherosclerosis are at a higher risk of severe COVID-19.
Natalia Eberhardt, PhD, commented on the study's findings, stating, "Our findings provide for the first time a direct mechanistic link between COVID-19 infection and the heart complications it provokes. 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."
This study sheds light on the underlying mechanisms that contribute to the increased risk of heart complications in COVID-19 patients. Understanding these mechanisms may help in developing targeted treatments and interventions to mitigate the risk and improve outcomes for individuals with COVID-19.
