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.
In a new study, researchers 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 high bleeding risk.
The finding raises concerns about the current practice of giving COVID-19 patients high dose anticoagulants throughout the duration of their disease course.
The research was conducted by a team at Michigan Medicine.
In the study, the team tested 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 linked to stabilizing blood clots.
However, they didn’t expect high levels of tissue-type plasminogen activator, the molecule responsible for removing the clots.
They found that almost half of the 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 much 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 linked to worse lung function, but high tPA independently correlated with mortality.
The team then found that patients with high-tPA had much higher clot breakdown compared to the other patients
This means that high tPA may be a biomarker for high bleeding risk and poorer outcomes in COVID-19, and supports further studies of tPA levels during the course of disease progression.
The team suspects the source of these high levels of tPA in COVID-19 patients, and the subsequent clotting issues, is because of damage to endothelial cells, which are cells that line blood vessels.
If badly damaged, the blood vessels can actually break and cause bleeding.
The theory is that a hallmark symptom of COVID-19 ARDS, when fluid builds up in the lungs and causes trouble breathing and low oxygen levels in the blood, may trigger endothelial cell activation, which consequently promotes the release of tPA.
The team says high dose anticoagulants have become standard COVID-19 treatment, but these study findings complicate the clinical picture.
They urge caution regarding this recommendation, pending randomized studies, as COVID-19 clotting seems to be complex and potentially dynamic.
One author of the study is Daniel Lawrence, Ph.D., a Professor of Basic Research in Cardiovascular Medicine.
The study is published in Scientific Reports.
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