We Finally Know Why COVID-19 Damages The Heart

Infected engineered heart tissue (red) with SARS-CoV-2 (green). Image credit: Bailey et al. 2021

A new study has discovered how the SARS-CoV-2 virus attacks and damages the heart, answering a long-standing question about mysterious heart conditions following COVID-19 infection. The results could have large implications on how to effectively treat severe infections and develop new therapies for preventing long-term damage. 

Throughout the pandemic, people with severe COVID-19 infection have often displayed symptoms of heart distress. Those with underlying heart conditions are at a greater risk of severe illness if they catch it, and reports of abnormal heart rhythms (arrhythmia) in previously healthy patients with acute COVID-19 have been common. 

However, exactly why this happens has eluded scientists until now. Researchers have been unsure whether the heart symptoms are a result of severe inflammation as the body reacts to the infection, or whether the virus particles themselves invade and attack heart cells. 

In the new study, published in the Journal of the American College of Cardiology, scientists have finally unveiled the elusive mechanism behind COVID-19's heart damage, discovering that the virus directly enters and replicates within heart cells, leading to their destruction. The resulting damage interferes with contraction, leading to severe complications and long-term damage. 

“Our study is unique because it definitively shows that, in patients with COVID-19 who developed heart failure, the virus infects the heart, specifically heart muscle cells,” said Kory Lavine, senior author and associate professor of medicine, in a statement

“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.” 

The study began with autopsies of COVID-19 patients that showed severe myocarditis (inflammation of heart tissue). Samples from four patients were obtained and analyzed for evidence of SARS-CoV-2 within the heart muscle cells, to determine whether the virus enters these cells. The results showed evidence that virus particles were within the cells, including evidence of spike protein and the capsule that surrounds the viral genome. 

Subsequently, the researchers engineering human heart tissue using stem cells to model infection, discovering that the virus could enter and replicate within cardiomyocytes. Even when there was no inflammation present, cell death still occurred. 

The results are incredibly important for understanding how COVID-19 damages the heart, but the methods may also have other applications. Specifically, engineered heart muscle cells could be useful for future COVID-19 research and creating a new, effective therapy against it.  

Until then, the researchers had a powerful message for the people that still need to hear it.  

“Even young people who had very mild symptoms can develop heart problems later on that limit their exercise capacity,” Lavine said.  

“We want to understand what’s happening so we can prevent it or treat it. In the meantime, we want everyone to take this virus seriously and do their best to take precautions and stop the spread, so we don’t have an even larger epidemic of preventable heart disease in the future.” 

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