The new coronavirus seems to slice heart muscle fibers into small, precisely sized fragments — at least when it infects heart cells in a lab dish, a new study reveals.
This snipping of muscle fibers, which could permanently damage heart cells, is scary enough in a lab dish; but the researchers found evidence that a similar process could be happening in the hearts of COVID-19 patients as well. However, the new finding, which was published to the preprint database bioRXiv on Aug. 25, has not yet been published in a peer-reviewed journal, or proven to happen in people.
The finding is unlike anything researchers have seen before — no other disease is known to affect heart cells in this way. “What we were seeing was completely abnormal,” study co-author Todd McDevitt, a senior investigator at Gladstone Institutes, a nonprofit research organization in San Francisco, said in a statement.
The new finding may explain how COVID-19 inflicts damage to the heart. Previous studies have found signs of heart abnormalities in COVID-19 patients, including inflammation of the heart muscle, even in relatively mild cases.
For the new study, the researchers used special stem cells to create three types of heart cells, known as cardiomyocytes, cardiac fibroblasts and endothelial cells. In lab dishes, these cells were then exposed to SARS-CoV-2, the virus that causes COVID-19. Of the three types of cells, SARS-CoV-2 could infect and make copies of itself only inside cardiomyocytes, or heart muscle cells.
Cardiomyocytes contain muscle fibers that are made up of units called sarcomeres, which are critical to the muscle contractions that produce a heartbeat. These sarcomeres usually line up in the same direction to form long filaments. But the lab dish studies revealed something bizarre — the sarcomere filaments were chopped up into small fragments.
“The sarcomere disruptions we discovered [in lab dishes] would make it impossible for the heart muscle cells to beat properly,” study co-author Dr. Bruce Conklin, also a senior investigator at Gladstone Institutes, said in the statement.
But findings in lab dishes don’t always translate to real life. So the researchers analyzed autopsy samples of heart tissue from three COVID-19 patients. They saw that the sarcomere filaments were disordered and rearranged — a pattern that was similar to, but not exactly the same as, what was seen in the lab dish experiments.
More studies are needed to see if the sarcomere changes seen in heart cells are permanent. The authors note that scientists need to perform a special process to see the sarcomeres, which isn’t usually done, explaining why this finding in autopsies may have been overlooked until now.
“I hope our work motivates doctors to review their patients’ samples to start looking for these features,” McDevitt said.
—20 of the worst epidemics and pandemics in history
—The 12 deadliest viruses on Earth
—11 (sometimes) deadly diseases that hopped across species
The researchers also observed another strange finding in both the lab dish experiments and the heart tissue from COVID-19 patients. They saw that, for some heart cells, the DNA inside the cells’ nucleus seemed to be missing. This would render these cells essentially “brain dead” and unable to perform normal functions, the authors said.
Once scientists understand how SARS-CoV-2 damages heart cells, they could screen for drugs to mitigate these effects. For example, if the virus uses an enzyme to chop up sarcomeres, it may be possible to find a drug that blocks this enzyme. (However, the authors note that it’s still unclear whether the virus directly cuts the sarcomeres, or if the virus triggers cells to cut the fibers through another mechanism.)
“It will be important to identify a protective therapy, one that safeguards the heart from the damage we’re seeing in our models,” McDevitt said. “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.”
Originally published on Live Science.
Source: Read Full Article