Not only do COVID-19 patients have a heightened clotting risk, but they may also have an imbalance in their ability to break down clots, according to a study published in the journal Scientific Reports. This imbalance contributes to a high bleeding risk, which raises concerns about the current practice of giving high dose anticoagulants to COVID-19 patients during the course of their disease.
The study, funded by NHLBI, included 118 COVID-19 patients and 30 healthy controls. Almost half of the study’s patients were supported by a ventilator and a quarter breathed room air. Patients that required supplemental oxygen had significantly higher levels of plasminogen activator-inhibitor-1 (PAI-1 ) — a molecule associated with stabilizing clots — compared to patients breathing room air.
High levels of tissue-type plasminogen activator (tPA) — a molecule responsible for removing blood clots — as well as PAI-1 were associated with worse lung function. But high tPA was linked to death. The researchers then asked whether blood plasma from COVID-19 patients with the highest tPA levels might correlate with an enhanced, spontaneous breaking down of clots. They used blood plasma from 30 people — 10 COVID-19 patients with high tPA, 10 COVID-19 patients with low tPA, and 10 healthy volunteers.
The researchers found that blood plasma samples for COVID-19 patients with high tPA significantly enhanced spontaneous clot breakdown compared to the other two groups. These findings suggest that high tPA could be a biomarker for high bleed risk and poorer outcomes in COVID-19, and warrants further studies of tPA levels during disease progression.