San Francisco – Patients who recover from even mild infections from COVID-19 demonstrate some heart dysfunction months later.
While Sars-CoV-2 was initially identified as a respiratory virus tests show it can affect several organs including the heart.
“Heart damage is a major determinant of COVID-19 related deaths, and even patients who experience only mild COVID-19 symptoms exhibit signs of cardiac dysfunction several months after recovery,” says a study published online by scientists at the non-profit Gladstone Institutes based in San Francisco.
The team’s findings, shared publicly on bioRxiv, show the virus’s unexpected effects on the structure of heart cells in the lab, as well as in heart tissue from COVID-19 patients.
“The virus only productively infected the cardiomyocytes, or heart muscle cells, meaning that the virus could enter those cells and make new copies of itself.
“Early on in our experiments, we noticed that many of the cardiomyocytes were exhibiting some very strange features,” said Todd McDevitt, who is also a professor of bioengineering and therapeutic sciences at UC San Francisco (UCSF).
“What we were seeing was completely abnormal; in my years of looking at cardiomyocytes, I had never seen anything like it before.”
“The team observed that when they exposed cardiomyocytes to SARS-CoV-2, the sarcomeres in some of the cells appeared to be diced into small, regularly sized fragments. Typically, sarcomeres—units of the muscle fibers in heart cells—are organized into long filaments aligned in the same direction.”
“These sarcomeres control the coordinated contraction of heart cells to produce the normal heartbeat.
“The sarcomere disruptions we discovered would make it impossible for the heart muscle cells to beat properly,” explained another professor who was part of the research team.
“The scientists also noted that the nuclear DNA seemed to be missing from many of the heart cells. Without DNA, cells can no longer perform any normal functions.”
To understand whether these changes to cells in culture were relevant to COVID-19 in humans, the team sought out heart tissue from postmortems.
“When the team was able to receive patient samples, what they 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 McDevitt.
Long-term Consequences for COVID-19 Patients
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.”
