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In test tube studies, the researchers found that pre-treating platelets from SARS-CoV-2 infected patients with aspirin did prevent this hyperactivity.
The COVID-19 pandemic causes severe complications in some patients including blood clotting and multi-organ failure. Patients with underlying conditions like diabetes, obesity or high blood pressure are at a higher risk of these complications. Now, according to researchers at the University of Utah, changes in blood platelets triggered by COVID-19 may contribute to the onset of heart attacks, strokes, and other serious complications in some patients who have the disease. The researchers found that inflammatory proteins produced during infection significantly alter the function of platelets. This makes them "hyperactive" and more prone to form dangerous and potentially deadly blood clots.
Researchers say better understanding of the underlying causes of these changes may possibly lead to treatments that prevent them from happening in COVID-19 patients. This study titled, "Platelet Gene Expression and Function in COVID-19 Patients," was funded by the National Institutes of Health, the University of Utah Health 3i Initiative, and the American Heart Foundation and it appears in Blood, an American Society of Hematology journal. According to researchers, this is an important piece of the jigsaw puzzle that is COVID-19. They found that inflammation and systemic changes, due to the infection, are influencing how platelets function, leading them to aggregate faster, which could explain why there is an increase in the number of blood clots in COVID patients.
To find out what might be going on, the researchers studied 41 COVID-19 patients hospitalized at University of Utah Hospital in Salt Lake City. Seventeen of these patients were in the ICU, including nine who were on ventilators. They compared blood from these patients with samples taken from healthy individuals who were matched for age and sex. Using differential gene analysis, the researchers saw that SARS-CoV-2, the virus that causes COVID-19, appears to trigger genetic changes in platelets. In laboratory studies, they studied platelet aggregation, an important component of blood clot formation, and saw that COVID-19 platelets aggregated more readily. They also noted that these changes significantly altered how platelets interacted with the immune system. This led them to conclude that this is what is most likely contributing to inflammation of the respiratory tract that may, in turn, result in more severe lung injury.
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Surprisingly, Campbell and his colleagues didn't detect evidence of the virus in the vast majority of platelets, suggesting that it could be promoting the genetic changes within these cells indirectly. One possible mechanism is inflammation. In theory, inflammation caused by COVID-19 could affect megakaryocytes, the cells that produce platelets. As a result, critical genetic alterations are passed down from megakaryocytes to the platelets, which, in turn, make them hyperactive. Researchers say that there are genetic processes that they can target to prevent platelets from changing. If they can figure out how COVID-19 interacts with megakaryocytes or platelets, then they may be able to block that interaction and reduce someone's risk of developing a blood clot.
In test tube studies, the researchers found that pre-treating platelets from SARS-CoV-2 infected patients with aspirin did prevent this hyperactivity. These findings suggest aspirin may improve outcomes. However, researchers agree that further studies and clinical trials are needed to verify this. They also warn that patients must not use aspirin to treat themselves if they acquire this virus and instead said that they must consult their doctor. For now, Campbell warns against using aspirin to treat COVID-19 unless recommended by your physician.
(With inputs from Agencies)