A new study found how the SARS-CoV-2 virus attacks and damages the heart, answering a long-standing question about mysterious heart disease after COVID-19 infection. The results can have major implications for how to treat serious infections effectively and develop new therapies to prevent long-term damage.
During the pandemic, people with severe COVID-19 infection often exhibited symptoms of cardiac distress. Those with underlying heart problems are at an increased risk of serious illness if they contract 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 so far. The researchers are not sure whether the cardiac symptoms are the result of severe inflammation when the body reacts to the infection or whether the virus particles themselves invade and attack the cells of the heart.
In the new study, published in the Journal of the American College of Cardiology, scientists finally unveiled the elusive mechanism behind COVID-19’s heart damage, discovering that the virus enters and replicates directly in the cells of the heart, leading to its destruction . The resulting damage interferes with contraction, leading to serious complications and long-term damage.
“Our study is unique because it definitely shows that in patients with COVID-19 who have developed heart failure, the virus infects the heart, specifically the heart muscle cells,” said Kory Lavine, senior author and associate professor of medicine, in a statement .
“Inflammation can be a second blow in addition to the damage caused by the virus, but inflammation itself is not the initial cause of heart damage.”
The study began with autopsies of COVID-19 patients who had severe myocarditis (inflammation of the cardiac tissue). Samples from four patients were obtained and analyzed for evidence of SARS-CoV-2 in the heart muscle cells, to determine whether the virus enters these cells. The results showed evidence that the virus particles were inside the cells, including evidence for the protein spike and the capsule surrounding the viral genome.
Subsequently, the researchers manipulated human heart tissue using stem cells to model the 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 extremely important for understanding how COVID-19 damages the heart, but the methods can also have other applications. Specifically, the projected heart muscle cells may be useful for future research on COVID-19 and for the creation of a new and effective therapy against it.
Until then, researchers had a powerful message for people who still need to hear it.
“Even young people with very mild symptoms can develop heart problems later, which limits their ability to exercise,” said Lavine.
“We want to understand what is happening so that we can prevent or treat it. In the meantime, we want everyone to take this virus seriously and do their best to take precautions and prevent it from spreading so that we don’t have an even greater epidemic of preventable heart disease in the future. ”