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COVID-19 patients experience changes in heart tissue

Although COVID-19 is primarily a respiratory illness that affects the lungs, it can also affect other organs in the body, including the heart. Temporary or lasting damage to the heart may arise from a lack of sufficient oxygen as the lung’s air sacs fill up with fluid, from inflammation due to the effects of the SARS-CoV-2 virus, or from inflammation due to a person’s own immune system’s response to infection by the virus. Although these symptoms may resolve themselves with treatment, they can also lead to life-threatening heart issues such as arrhythmias, heart attacks and strokes.

A research study, due to be presented at the 67th Annual Biophysical Society Meeting in San Diego, California, has found that the heart tissue of people who have had COVID-19 can show significant changes that could be related to these heart issues.  Professor Andrew Marks of Columbia University and colleagues have studied changes in the heart and heart muscle of COVID-19 sufferers, and in laboratory mice that have been infected with the virus.

In heart tissue from patients who had COVID-19, the team observed increases in oxidative stress (harmful production of unstable molecules) and signals of inflammation, as well as changes in calcium. They also detected adverse changes to a protein called RyR2, which is responsible for regulating the heart’s calcium ion levels. 

The heart muscle, like all muscle cells, needs calcium ions in order to contract. The heart’s system for managing calcium ions 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 test whether these changes were caused by SARS-CoV-2 infection, the researchers used a mouse model that was also susceptible to infection by the virus. The mice that suffered COVID-19 disease also showed changes to the heart tissue, including immune cell infiltration, collagen deposition (indicative of injury), death of heart cells, and blood clots. 

The researchers also measured changes to the proteins that are expressed by the heart cells and found patterns consistent with changes observed in the hearts of humans that suffered COVID-19 disease. Microscopic examination of mouse hearts showed an increased percentage of fibrosis and dilation of the muscle fibers, which is a common indicator of early cardiomyopathy in mice, and can make it harder for the heart to pump blood to the body, leading potentially to heart failure.

“The more awareness you build around particular aspects of a disease, the more likely you are to improve the care of patients. And doctors should be aware of heart changes related to COVID-19 infections and should be looking for them,” said Professor Marks. Ultimately, “we want to really figure out what’s causing the heart disease and how to fix it.”

If future research is able to uncover the biochemical mechanisms that underlie these changes, then specific medications can be used to target these molecular pathways and could help healthcare professionals to diagnose and treat the cardiac issues more effectively. Additionally, understanding the cardiac complications of COVID-19 can also help public health officials make more informed decisions about how to respond to the COVID-19 pandemic, especially in advising those at higher risk for heart problems.

By Alison Bosman, Staff Writer

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