COVID-19 Coagulopathy: Advances on Pathophysiology and Therapies

Dear Colleagues,

COVID-19 is a viral infection with a severe multisystemic clinical pathology. COVID-19 infection is associated with high hospitalization and intensive care unit (ICU) admission rates, and high mortality. Patients with severe Covid-19 infections display substantial immunological dysregulation including abnormal cytokine release, endothelial dysfunction, and coagulopathy. Changes in the coagulation status have been reported since the beginning of the epidemic. In the early stages of infection, D-dimer and fibrinogen levels are elevated, but activated partial prothrombin time, prothrombin time and platelet counts are frequently normal. Despite intensive worldwide efforts, the mechanisms behind COVID-19-induced coagulopathy are largely unknown and more reasearch is required to understand and treat these potentially deadly complications.

Thrombosis occurs when the primary components of the Virchow's triad exist, including stagnation of the blood circulation, damage to the endothelial and a hypercoagulable status. Among the proposed mechanisms of COVID-19-related thrombosis, COVID-19 binding to the endothelial cells through the angiotensin-converting enzyme 2 (ACE2) receptor has been shown to cause an inflammatory response that leads to endothelial damage. Angiotensin 2 can stimulate the synthesis of plasminogen activator inhibitor-1 (PAI-1), intercellular adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule-1 (VCAM-1) on cell surface, while P-selectin induces the synthesis of tissue factor (TF) in monocytes. In addition, patient immobilization and the increase in positive end-expiratory force due to the lung pathology and mechanical ventilation impair blood circulation and cause venous stasis.

Several COVID-19-related thrombotic consequences in both the arterial (acute limb ischemia, acute coronary syndrome, stroke, thrombosis of the thoracic and abdominal aorta, mesenteric ischemia) and the venous system (deep venous thrombosis, cerebral venous sinus thrombosis, and pulmonary embolism) have been reported, but it is unclear whether these occur through the same mechanisms.

The purpose of this Special Issue is to publish a series of relevant papers presenting some of the most important current advances in understanding the molecular pathways and the clinical manifestations of the thrombo-embolic events in COVID-19 patients. We hereby welcome researchers to contribute manuscripts focusing on the molecular pathology, diagnostics and therapeutics of COVID-19 coagulopathy.

Dr. Alexandru Schiopu
Dr. Emil Marian Arbănași
Dr. Eliza Russu
Guest Editors

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