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A team of scientists mixed the new coronavirus with heart cells and discovered that the SARS-CoV-2 virus carved long heart muscle fibers into smaller fragments. While the snipping of heart muscle fibers happened in a lab dish, evidence shows that a similar process could be occurring in COVID-19 patients.

The team used special stem cells to create cardiomyocytes, cardiac fibroblasts, and endothelial cells. When they were exposed to SARS-CoV-2, of the three types of heart cells, the virus only infected and made copies of itself inside cardiomyocytes or heart muscle cells.

Muscle fibers, which are made up of sarcomeres, make up cardiomyocytes, and they are critical to the muscle contractions that produce heartbeats. Upon exposure to the new coronavirus, the scientists discovered that the sarcomere filaments were sliced into small fragments. These sarcomere disruptions would then make it impossible for the heart to beat properly.

According to the co-author of the study, Todd McDevitt, a senior investigator at Gladstone Institutes in San Francisco, no disease had been known to affect heart cells similarly. This may explain how COVID-19 inflicts damage to the heart, as seen in the signs of heart abnormalities found in patients, even in milder cases.

Since the study was done on cells on a lab dish, the team of researchers went to analyze autopsy samples of heart tissue from three actual COVID-19 patients. While the results were not exactly the same, they saw that the sarcomere filaments were disordered and rearranged to follow a pattern similar to what they had seen in the experiment.

More research is needed to see if these sarcomere disruptions are permanent.

Aside from sarcomere effects, the team also observed another finding evident in both their experiment and the heart tissue sample of COVID-19 patients. They found that the DNA inside some heart cells’ nucleus was missing, rendering the cells unable to perform normal functions.

McDevitt said that it is important to identify a protective therapy that safeguards the heart from the damages seen in the team’s study. Even if the drug could not prevent the virus from infecting heart cells, it might be able to prevent the negative consequences of the disease from occurring.

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