A common anticoagulant not only improves survival of COVID-19 patients but also appears to lessen the duration of active infection.

A report in the journal Cardiovascular Research points out that infection with SARS-CoV-2 initially was believed to be primarily a respiratory disease. Now, however, it is understood that several system functions are affected, including blood clotting. Researchers from the Medical University of Vienna Department of General Surgery and their colleagues note that clotting problems and resulting complications are common in COVID-19 patients.

COVID-19 patients have an increased risk of thromboses, deep vein thromboses, embolisms (such as strokes), and pulmonary or myocardial infarctions. Anticoagulants became part of the treatment guidelines for COVID-19 in July 2020.

"These complications during hospitalization have a direct impact on the well-being of patients and increased the risk of dying from COVID-19," explains author David Pereyra.

Researchers point out that while anticoagulation was associated with improved survival of hospitalized COVID-19 patients in large-scale studies, exactly how and why that occurred was not fully understood. They sought to explore the effects of anticoagulation and LMWH on patient outcomes, COVID-19-associated coagulopathy (CAC) development, thromboinflammation, cell death, and viral persistence.

To do that, the study team retrospectively evaluated data on 586 hospitalized COVID-19 patients from three different regions of Austria. Of those, 419 (71.5%) patients received LMWH and 62 (10.5%) received non–vitamin K oral anticoagulants (NOACs) during hospitalization. Plasma was collected at different times in a subset of 106 patients to evaluate markers of thromboinflammation and the cell-death marker cell-free DNA (cfDNA).

Results indicate that use of LMWH was associated with improved survival upon multivariable Cox regression (hazard ratio = 0.561, 95% confidence interval: 0.348-0.906). "Interestingly, neither LMWH nor NOAC was associated with attenuation of D-dimer increase over time, or thromboinflammation," the authors write. "In contrast, anticoagulation was associated with a decrease in cfDNA during hospitalization, and curtailed viral persistence was observed in patients using LMWH leading to a 4-day reduction of virus positivity upon quantitative polymerase chain reaction [13 (interquartile range: 6–24) vs. 9 (interquartile range: 5–6) days, P = 0.009]."

The authors conclude that "time courses of hemostatic and thromboinflammatory biomarkers were similar in patients with and without LMWH, indicating either no effects of LMWH on hemostasis or that LMWH reduced hypercoagulability to levels of patients without LMWH. Nonetheless, anticoagulation with LMWH was associated with reduced mortality, improved markers of cell death, and curtailed viral persistence, indicating potential beneficial effects of LMWH beyond hemostasis, which encourages use of LMWH in COVID-19 patients without contraindications."

"The coagulopathy observed in COVID-19 patients is novel and differs in many respects from previously known coagulation problems," added senior author Alice Assinger, PhD, group leader at the Institute of Vascular Biology and Thrombosis Research at the Medical University of Vienna."COVID-19-associated coagulopathy displays characteristics that, although partially comparable with other coagulation diseases, cannot be fully explained by them."

The researchers report that COVID-19-associated coagulopathy occurs primarily in patients requiring intensive care or in those who die as a result of COVID-19. Anticoagulant drugs improve the survival of COVID-19 patients, but they show no effect on immunological processes related to blood coagulation, they add.

At the same time, active SARS-CoV-2 infection is curtailed in patients treated with LMWH, Dr. Pereya noted, adding, "In patients who receive this drug, infection time is an average of four days shorter than in patients who are not treated with low-molecular-weight heparin. We were surprised to see that low-molecular-weight heparin may have a direct effect on coronavirus and its infectivity."

Experimental data suggest that heparin can inhibit the ability of SARS-CoV-2 to bind to cells, thereby preventing them from being infected.

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