Blood clots in COVID-19 patients are formed much more effectively and have a denser and more stable clot network than those of flu patients or healthy individuals. This was found by an international research team involving DZL scientists from Giessen, Berlin and Hannover.
Infection with SARS-CoV-2 can be fatal not only because of severe pneumonia with acute lung failure. The disease is also characterized by increased clot formation (thrombosis) and associated complications, such as the development of pulmonary embolism, stroke or myocardial infarction, and even multiple organ failure.
Early in the pandemic, clinical studies showed that elevated levels of the clotting protein fibrinogen and other specific thrombosis biomarkers were detectable in the blood of COVID-19 patients, indicating increased activation of blood clotting. The team led by Prof. Malgorzata Wygrecka and Prof. em. Klaus T. Preissner (both Justus Liebig University Giessen) now investigated the coagulation parameters, the structure of the fibrin clots formed, and the coagulability in blood plasma in patients with COVID-19 and influenza. The microscopic and functional examinations showed that "coronary thrombi" were formed much more effectively and had a denser and more stable clot network than those from influenza patients or the healthy control group.
Activated clotting factor in corona patients
The scientists took a closer look at clotting factor XII in particular. In the blood plasma of corona patients, they observed that the clotting factor activated there additionally drives blood clotting and can thus contribute to increased clot formation. In addition, the clots from the Corona patient plasmas were difficult to dissolve (fibrinolysis) because the patients had more fibrinolysis inhibitors in their blood. This suggests that "corona clots" are more durable and thus may contribute to thromboembolic complications in patients. In the lung tissue of deceased corona patients, the researchers also found massive clot deposits in vessels and alveoli to which clotting factor XII/XIIa was bound.
Option for anti-thrombotic therapy
The studies of the research team coordinated from Giessen suggest that the already known "hypercoagulation" in the blood of corona-infected individuals can be attributed primarily to the activation of coagulation factor XII and the described subsequent reactions. The team recommends that medical societies include factor XII/XIIa as a causal factor for thrombosis in their guidelines for thrombosis prophylaxis and therapy in corona patients.
"Since it is possible to inhibit factor XIIa by specific inhibitors that have already been researched, this could provide effective antithrombotic therapy in corona patients without compromising their physiological hemostasis and wound healing," Preissner explains. The extent to which these conclusions from the scientific work can also be implemented clinically will be verified by further studies in the near future.
Further information:
Original publication: Altered fibrin clot structure and dysregulated fibrinolysis contribute to thrombosis risk in severe COVID-19.
Source: Press release of the Justus Liebig University Giessen
