A new study, funded by the National Institutes of Health and the National Science Foundation, may help explain why patients who experience only mild COVID-19 symptoms show signs of cardiac dysfunction several months after recovery.
Scientists from Gladstone Institutes in San Francisco found that when cardiomyocytes (heart muscle cells) were exposed to SARS-CoV-2 in the lab, the muscle fibers in some cells appeared to be diced into small fragments.
“The sarcomere disruptions we discovered would make it impossible for the heart muscle cells to beat properly,” said study author Bruce R. Conklin, who is also a professor of medicine, cellular and molecular pharmacology, and ophthalmology at the University of California San Francisco (UCSF).
The study, which was shared on preprint site bioRxiv on August 25, also noted that the nuclear DNA seemed to be missing from many of the heart cells.
“It’s the cell equivalent of being brain dead,” Conklin said. “Even after scouring scientific literature and conferring with colleagues, we cannot find these abnormal cell features in any other cardiac disease model. We believe they are unique to SARS-CoV-2 and could explain the prolonged heart damage seen in many COVID-19 patients.”
In patient samples, what the researchers saw corroborated the structural changes they saw in the lab. Remarkably, even in patients who had not been diagnosed with COVID-19 related heart disease, there was evidence of structural abnormalities in the heart muscle cells. Additional testing needs to be done to validate these findings further, but the immediate similarities are striking.
“These abnormalities haven’t been identified in patients before, so they may have been overlooked,” said study author Todd C. McDevitt, who is also a professor of bioengineering and therapeutic sciences at UCSF. “I hope our work motivates doctors to review their patients’ samples to start looking for these features at a higher magnification, which will be the true test of our hypotheses.”
In addition to providing more insight into the impact of COVID-19 on the heart, the team’s model could be used as a novel way to test and screen drugs that could help mitigate the effects of COVID-19 in the heart, as well as other tissues susceptive to SARS-CoV-2 infection.
“Heart muscle cells are highly infectible, and we have very visually distinct signs of infection,” Conklin said. “Since we can easily see the effects of infection, we can use these cells as a first screen to find drugs that could shut down the virus or prevent it from taking over the cells.”
Moreover, these findings shed light on the long-term ramifications of COVID-19. Unlike some other tissues in the body, the heart does not regenerate. So, it’s possible that someone who becomes infected with COVID-19, even a mild case, could recover and then develop heart disease years later.
“It will be important to identify a protective therapy, one that safeguards the heart from the damage we’re seeing in our models,” says McDevitt. “Even if you can’t prevent the virus from infecting cells, you could put a patient on a drug to prevent these negative consequences from occurring while the disease is present.”
Read more from Gladstone Institutes: https://gladstone.org/index.php/news/new-insights-how-covid-19-causes-he...
Read the study: https://www.biorxiv.org/content/10.1101/2020.08.25.265561v1.full