Hyperactive blood coagulation puts COVID-19 patients at risk

Stuttgart/New York – Severe infections with the novel coronavirus SARS-CoV-2 activates the blood coagulation mechanism and increases the risk of life-threatening complications such as heart attack or stroke. In a review article published in Thrombosis and Haemostasis (Thieme, New York, 2020), one expert attributes these complications to the strong inflammatory response triggered by the pneumonia.

SARS-CoV-2 does not only affect the lungs but also damages other organs, for instance the heart and kidneys. The reasons are not yet known. Professor Francesco Violi at Sapienza University of Rome suspects that the disturbances in the blood clotting mechanism play a central role in the disease. Hyperactivity of the blood coagulation process (thrombophilia) could explain why many patients suffer a heart attack or stroke, which are caused by blood clots in the coronary or cerebral arteries.

Prof. Violi has examined nine studies published by Chinese doctors since the start of the epidemic for laboratory results relating to blood clotting. In fact, many COVID-19 patients actually showed changes in the laboratory values. The increase in the D-dimer in 14 to 46 percent of the patients was particularly noticeable, according to Violi. The protein is increasingly produced when clots have already formed in the blood vessels. A significant increase in D-dimer is a warning sign of thrombosis. The reason for the thrombosis could be excessive activation of the coagulation factors and platelets.

The Chinese studies quoted by Prof. Violi also document an increase in prothrombin times in 2 to 11 percent of patients, and an increased activated partial thromboplastin times in 6 to 26 percent of patients. Platelets were reduced in 5 to 18 percent of patients. These findings would suggest the presence of a hypercoagulation state.

The disturbances in the clotting mechanism were more extensive in patients with severe COVID-19 and could therefore increase their risk of succumbing to the disease. Prof. Violi suggests treatment with low-molecular-weight heparins, which decreases clotting. Acetylsalicylic acid (Aspirin) could prevent platelets sticking together. Whether or not these agents are used would have to depend on the severity of the disease and a rise in D-dimer levels.

The internationally renowned expert has an assumption of why COVID-19 can so often lead to coagulation disorders. He says that thrombophilia has also been observed in pneumonias caused by other organisms, where it is a result of a systemic inflammatory response. Apparently, the Nox2 protein is activated in cells and forms “reactive oxygen species”. According to Prof. Violi, these “reactive oxygen species” not only activate blood clotting and platelets but also cause the blood vessels to constrict (vasoconstriction). This then compromises the blood supply to the organs even further. All three of these factors could contribute to a fatal course of COVID-19.

F. Violi et al.:
Hypercoagulation and Antithrombotic Treatment in Coronavirus 2019: A New Challenge.
Thrombosis and Haemostasis 2020; published online 29 April, 2020

In addition to Prof. Violi, several other scientists also point to coagulation disorders in their works published in the Thieme medical journal Thrombosis and Haemostasis and recommend appropriate treatment for these patients.

M. Cattaneo et al.:
Pulmonary Embolismor Pulmonary Thrombosisin COVID-19? Is the Recommendation to Use High Dose Heparin for Thromboprophylaxis Justified?
Thrombosis and Haemostasis 2020; published online as “Letter to the Editor” 29 April, 2020

L. Spiezia et al.:
COVID-19-Related Severe Hypercoagulability in Patients Admitted to Intensive Care Unit for Acute Respiratory Failure
Thrombosis and Haemostasis 2020; published online 21 April, 2020

Z. Zhai et al.:
Prevention and Treatment of Venous Thromboembolism Associated with Coronavirus Disease 2019 Infection: A Consensus Statement before Guidelines
Thrombosis and Haemostasis 2020; published online 21 April, 2020