New treatment may prevent heart damage from COVID-19
An experimental drug has stopped the coronavirus from entering lab-grown heart cells — a sign that it may be able to prevent heart damage from COVID-19.
The challenge: COVID-19 might target the respiratory system first, but it doesn’t stop there — an infection can damage every major organ in the body.
While we have effective vaccines to prevent COVID-19, we’re still short on treatments for the disease, and once an infection takes hold, there’s no way for doctors to guarantee it won’t spread to other organs, including the heart.
People with heart problems are more than four times as likely to die from COVID-19.
Why it matters: Survivors who sustain heart damage from COVID-19 are more likely to experience long COVID — symptoms that linger after an infection clears.
People who had heart problems before contracting COVID-19, meanwhile, are at higher risk of complications from the disease and more than four times as likely to die from it.
Preventing heart damage from COVID-19: In recent years, researchers have begun using stem cells to grow tiny models of organs in the lab. These “organoids” can mimic the structure and function of human organs and can be used to test new disease treatments.
At the University of Cambridge, researchers grew mini hearts so advanced, the cells actually beat as if pumping blood. They then exposed their lab-grown organoids to a synthetic virus they’d equipped with the coronavirus’s spike protein.
In addition to studying how the virus infected the heart cells, the researchers also tested the ability of a variety of drugs to prevent an infection — and discovered that an experimental drug called DX600 appeared to be an effective blocker.
“The spike protein is like a key that fits into the ‘lock’ on the surface of the cells — the ACE2 receptor — allowing it entry,” researcher Anthony Davenport said. “DX600 acts like gum, jamming the lock’s mechanism, making it much more difficult for the key to turn and unlock the cell door.”
The number of heart cells didn’t decrease after treatment with DX600, either, which hints that the drug isn’t likely to be toxic.
The next steps: Being able to stop an infection in a clump of cells isn’t the same as preventing heart damage from COVID-19, so more testing is needed to find out if DX600 works as hoped in patients.
The coronavirus can damage the heart indirectly, too, by lowering blood oxygen levels, causing blood clots, and more, so people could still sustain cardiovascular damage even if direct infection of heart cells is blocked.
Still, if DX600 does prove safe and effective, it could be a powerful weapon in the fight against COVID-19.
“We need to do further research on this drug, but it could provide us with a new treatment to help reduce harm to the heart in patients recently infected with the virus,” Davenport said, “particularly those who already have underlying heart conditions or who have not been vaccinated.”
“We believe it may also help reduce the symptoms of long COVID,” he added.
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