Research reveals how COVID-19 kills cardiomyocytes and interferes with myocardial contraction

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Research reveals how COVID-19 kills cardiomyocytes and interferes with myocardial contraction

Since the early days of the pandemic, COVID-19 has been thought to be related to heart problems, including reduced pumping ability and abnormal heart rhythms. But whether these problems are caused by a virus that infects the heart or an inflammatory response caused by a viral infection elsewhere in the body, this has always been an open question. Such details are meaningful for understanding how to best treat the new coronavirus infection that affects the heart.

A new study from Washington University (St. Louis) School of Medicine provides evidence that heart damage in patients with COVID-19 is caused by virus invasion and replication in cardiomyocytes, causing cell death and interference Myocardial contraction. Researchers use stem cells to design heart tissue, which is a model of human infection and can help study the disease and develop possible treatments.

The study was published in the Journal of the American College of Cardiology: Fundamentals of Translational Science on February 26, 2021.

“In the early days of the pandemic, we have evidence that this coronavirus can cause heart failure or heart damage in generally healthy people, which is shocking for the cardiology community,” senior researcher Said Dr. Kory J. Lavine, the author and associate professor of medicine. “Even some college athletes were approved to return to competitive sports after being infected with COVID-19, and later scars appeared in the heart. People have been arguing whether this is due to a direct heart infection or a lung infection. Systemic inflammation.”

“Our study is unique because it clearly shows that in COVID-19 patients with heart failure, the virus infects the heart, especially the cardiomyocytes.”< /p>

Research reveals how COVID-19 kills cardiomyocytes and interferes with myocardial contraction(1)

Lavine and his colleagues– Including collaborators Michael S. Diamond, MD, Herbert S. Gasser, Professor of Medicine, and Michael J. Greenberg, Ph.D., assistant professor of biochemistry and molecular biophysics–also use stem cells to design tissues that mimic how human heart tissue shrinks. By studying these heart tissue models, they determined that viral infection not only kills the heart muscle cells, but also destroys the muscle fiber units responsible for the contraction of the heart muscle.

Their research also shows that even in the absence of inflammation, this cell death and loss of myocardial fibers can occur. “Inflammation may be the second blow to the damage caused by the virus, but inflammation itself is not the original cause of heart damage,” Lavine said.

Other viral infections have long been associated with heart damage, but Lavine said that SARS-CoV-2, the virus that causes COVID-19, has unique effects on the heart, especially in response to infection of immune cells. . In COVID-19, immune cells called macrophages, monocytes, and dendritic cells dominate the immune response. For most other viruses that affect the heart, the T cells and B cells of the immune system are on the scene.

“Compared with other viruses, COVID-19 caused a different immune response in the heart, and we don’t yet know what this means,” Lavine said. “In general, the immune cells seen in response to other viruses are often related to relatively short illnesses, which are resolved through supportive care. However, the immune cells we see in COVID-19 heart disease patients are often related to a possibility Chronic diseases with long-term consequences are related. These are all related, so we need more research to understand what happened.”

These causal questions in heart damage have been difficult to answer, partly because of research The heart tissue of COVID-19 patients has difficulties. The researchers verified their findings by studying the tissues of four COVID-19 patients. The heart damage of these patients is related to infection, but more research is needed.

For this, Lavine and Diamond are working to develop a mouse model of heart injury. To emphasize the urgency of this work, Lavine pointed out that the possible heart damage caused by COVID-19 is concealed.

“Even young people with very mild symptoms will have heart problems in the future, limiting their ability to exercise,” Lavine said. “We want to understand what happened so that we can prevent or treat it. At the same time, we want everyone to take this virus seriously and do our best to take preventive measures to stop the spread of the virus so that we will not be in the future There is a larger pandemic that can prevent heart disease.”