The human body strives to keep itself in homeostasis, or balance. When blood clots are created, the body’s innate response is to break the clots down to prevent significant health problems from arising.

Research has found that patients with COVID-19 are prone to serious blood clotting. This is why many patients receive high dose anticoagulants as part of their treatment.

But a new study in Scientific Reports, led by senior author Daniel Lawrence, Ph.D., a Professor of Basic Research in Cardiovascular Medicine at Michigan Medicine, found that aside from this heightened clotting risk, some COVID-19 patients have an unbalanced ability to break down clots as well, which is linked to a potential clinical biomarker seen in later stages of the disease.

This abnormal process of breaking down clots can contribute to a high bleeding risk, raising concerns about the current practice of giving COVID-19 patients high dose anticoagulants throughout the duration of their disease course.

This finding may be consistent with the NIH’s recent decision to pause enrollment of critically ill COVID-19 patients in the Antithrombotic Therapy to Ameliorate Complications of COVID-19 (ATTACC) trial, because “a potential for harm in this sub-group could not be excluded.”

“Pathological blood clotting in COVID-19 patients has been studied extensively, but recognizing and addressing the high bleeding risk in a subgroup of patients is equally important,” says first author Yu (Ray) Zuo, M.D., M.S.C.S., a rheumatologist at Michigan Medicine.

Zuo, Lawrence and their colleagues sought to understand the balance between COVID-19 coagulation and the breakdown of clots to help inform approaches to treatment.

The study included 118 COVID-19 patients and 30 healthy controls. In the COVID-19 patients, the team expected to see high levels of plasminogen activator-inhibitor-1, a molecule associated with stabilizing blood clots. However, they didn’t expect high levels of tissue-type plasminogen activator, the molecule responsible for removing the clots.

According to the researchers, almost half of the study’s patients were supported by a ventilator and a quarter breathed just room air. Compared with the patients breathing room air, patients that required supplemental oxygen had significantly higher levels of plasminogen activator-inhibitor-1, but not of tissue-type plasminogen activator.

High levels of both tissue-type plasminogen activator (tPA) and plasminogen activator-inhibitor-1 (PAI-1) were associated with worse lung function, but high tPA independently correlated with mortality. The levels of either molecule can increase independently of the other, but the research also found a change in one can have consequences on the other.

The team asked whether COVID-19 plasma with the highest tPA levels might correlate with an enhanced, spontaneous breaking down of clots, as compared with low tPA COVID-19 plasma or control plasma.

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