infections by COVID-19 may cause heart problems threatening life. To assess and understand the mechanism behind post-COVID cardiovascular events, new research from the Columbia University, New Yorkstudied heart tissue from people who died of the coronavirus.
The researchers found that the infection caused changes in the way cells regulate levels of calcium, a mineral essential for heart contractions and pumping blood.
The conclusions of this study were presented on Monday at the 67th annual meeting of the American Biophysical Society in San Diego. The work has not yet been peer-reviewed or published in a peer-reviewed journal.
The researchers noted that previous studies had already indicated that people with COVID-19 had a 55% more likely to have a cardiovascular event major side effects, such as heart attack, stroke and death than people who did not have COVID-19 disease. They are also more likely to have other heart problems, such as arrhythmias (abnormal heart rhythms) or myocarditis (inflammation of the heart muscle).
Andrew Markscardiologist and professor of biophysics at Columbia University, Steven Reykena research scientist in Marks’ lab, and his colleagues studied some of the changes that occur in the heart that could cause these problems.
A person’s immune system mounts a response to infection with the coronavirus in an effort to defend itself against attacks by the pathogen. One such immune response to COVID-19 is inflammation, which new research shows disrupts how calcium is stored in the heart.
The team examined heart tissue from patients who had had COVID-19 and identified increases in oxidative stress (harmful production of unstable molecules) and signs of inflammation, as well as changes in calcium levels. They also detected adverse changes in a protein call RyR2responsible for regulating calcium ion levels in the heart.
Heart muscle, like all muscle cells, needs calcium ions to contract.. The heart’s calcium ion processing system is essential for the coordinated contractions of the atria and ventricles that pump blood throughout the body. When calcium in the heart becomes dysregulated, it can cause arrhythmias or heart failure.
To further study the changes in the heart, they used a mouse model infected with COVID-19. They observed changes in heart tissue, including immune cell infiltration, collagen deposition (indicating injury), heart cell death and blood clots.
They also measured changes in the heart proteome, the proteins that heart cells express, and found patterns consistent with changes seen in human hearts infected with COVID-19as well as markers cardiomyopathymaking it harder for the heart to pump blood to the body and can lead to heart failure.
“The more you raise awareness about particular aspects of a disease, the more likely you are to improve patient care. And doctors need to be aware of and pay attention to heart changes related to COVID-19 infections. Ultimately, we really want to understand what causes heart disease and how to fix it,” Marks said.
Understanding changes at the molecular level may reveal drug targets that could improve COVID-19-related cardiac symptoms and help healthcare professionals diagnose and treat these issues more effectively.
Additionally, understanding the heart complications of COVID-19 can also help public health officials make better decisions about how to respond to the COVID-19 pandemic, especially when advising those at higher risk high in heart problems.
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