Scientists at New York University’s Grossman School of Medicine have uncovered a significant finding regarding the relationship between SARS-CoV-2, the virus responsible for Covid-19, and the heightened risk of heart attack and stroke. Their research sheds light on how the virus triggers a dangerous immune response within fatty deposits lining the heart’s major blood vessels, potentially leading to severe cardiovascular complications.

Increased Risk Among Covid-19 Patients

Medical experts have long noted an increased likelihood of heart attacks and strokes among individuals infected with the Covid-19 coronavirus, particularly those with pre-existing heart conditions. However, the precise mechanisms underlying these risks have remained elusive until now.

Insights from Research

The study, published in the journal Nature Cardiovascular Research, delved into how SARS-CoV-2 behaves in individuals with atherosclerosis, a condition characterized by the accumulation of plaque in major arteries and the subsequent onset of chronic inflammation.

Examining arterial tissue samples from eight individuals with a history of atherosclerosis who succumbed to Covid-19, researchers detected the presence of the virus within the arteries. Additionally, the virus was identified within macrophages, immune cells responsible for clearing excess fat molecules from arteries.

Inflammatory Response and Cardiovascular Complications

The study revealed that upon infection, macrophages release inflammatory signaling proteins called cytokines, which perpetuate chronic immune activation. Notably, two cytokines—interleukin-1 beta and interleukin-6—previously linked to heart attacks, were identified.

Lead author Natalia Eberhardt emphasized the direct mechanistic link between Covid-19 infection and its associated heart complications. The virus induces a highly inflammatory environment that may facilitate plaque growth, rupture, and subsequent blockage of blood flow to critical organs such as the heart and brain.

Experimental Findings and Future Directions

Utilizing an artificial intelligence (AI) computer program, researchers quantified coronavirus levels within plaque cells, providing insights into viral behavior. Experiments conducted on live tissue samples demonstrated that exposure to the virus enhances inflammation levels in blood vessels, particularly in macrophages laden with engulfed fat.

The research team’s next objective is to explore the potential connection between the virus’s behavior during atherosclerosis and long Covid, a condition characterized by persistent symptoms such as heart palpitations, chest pain, and fatigue.

In summary, this groundbreaking research illuminates the intricate interplay between Covid-19 and cardiovascular health, offering crucial insights into the underlying mechanisms driving increased risks of heart-related complications among infected individuals.