New evidence shows coronavirus can infect and kill heart muscle cells
A robust new study has demonstrated how SARS-CoV-2, the coronavirus that causes COVID-19, can infect and directly damage heart tissue. The research suggests previously reported cases of heart damage in COVID-19 patients are not due to inflammation in response to an infection but the virus itself interfering with heart muscles.
Although COVID-19 was initially deemed a respiratory illness, consistent reports in 2020 indicated patients suffered from notable cardiovascular complications. The common early consensus was the heart problems associated with COVID-19 were a secondary result of widespread inflammation that accompanies the disease.
“Early on in the pandemic, we had evidence that this coronavirus can cause heart failure or cardiac injury in generally healthy people, which was alarming to the cardiology community,” explains Kory Lavine, senior author on the new study. “Even some college athletes who had been cleared to go back to competitive athletics after COVID-19 infection later showed scarring in the heart. There has been debate over whether this is due to direct infection of the heart or due to a systemic inflammatory response that occurs because of the lung infection.”
To better understand how SARS-CoV-2 interacts with human heart tissue, the new research engineered heart muscle models using stem cells. These in vitro models allowed the researchers to definitively demonstrate how the virus specifically infects heart muscle cells.
The modeling also revealed the virus directly destroys the heart cells responsible for muscle contraction, called cardiomyocytes. This particular heart cell damage can occur in the absence of any inflammation or be amplified by any resultant inflammation.
“Inflammation can be a second hit on top of damage caused by the virus, but the inflammation itself is not the initial cause of the heart injury,” adds Lavine.
Lavine suggests SARS-CoV-2 seems to influence the heart in an unusual way, unlike other viruses. Whereas other viruses such as influenza are known to affect the heart, this one attracts a different kind of immune cell which could help explain why heart damage can linger for months in COVID-19 survivors.
“In general, the immune cells seen responding to other viruses tend to be associated with a relatively short disease that resolves with supportive care,” says Lavine. “But the immune cells we see in COVID-19 heart patients tend to be associated with a chronic condition that can have long-term consequences.”
Enduring heart problems are increasingly being recognized in recovered COVID-19 patients. A recent study tracking hospitalized COVID-19 patients in the months after discharge discovered 50 percent suffered some form of continuing heart damage.
Lavine and colleagues from the Washington University School of Medicine in St. Louis are urgently working on developing new animal models to better study the impact of COVID-19 on the heart. It is unclear exactly how long-lasting this heart damage may be, or what impact it has on one’s future cardiovascular health.
“Even young people who had very mild symptoms can develop heart problems later on that limit their exercise capacity,” adds Lavine. “We want to understand what’s happening so we can prevent it or treat it.”
The new research was published in the journal JACC: Basic to Translational Science.