COVID-19 and the Response to Antiplatelet Therapy

The coronavirus SARS-CoV2 disease (COVID-19) is connected with significant morbidity and mortality (3.4%), disorders in hemostasis, including coagulopathy, activation of platelets, vascular injury, and changes in fibrinolysis, which may be responsible for an increased risk of thromboembolism. Many studies demonstrated relatively high rates of venous and arterial thrombosis related to COVID-19. The incidence of arterial thrombosis in severe/critically ill intensive care unit-admitted COVID-19 patients appears to be around 1%. There are several ways for the activation of platelets and coagulation that may lead to the formation of thrombi, so it is challenging to make a decision about optimal antithrombotic strategy in patients with COVID-19. This article reviews the current knowledge about the role of antiplatelet therapy in patients with COVID-19.

Automated summary

The coronavirus disease (COVID-19) caused by SARS-CoV2 is associated with a higher risk of thromboembolism due to clotting disorders, platelet activation, vascular injury, and fibrinolysis changes. Studies have shown a high incidence of venous and arterial thrombosis in COVID-19 patients. The occurrence of arterial thrombosis in severe/critically ill COVID-19 patients admitted to intensive care units is estimated to be around 1%. Determining the optimal antithrombotic strategy in patients with COVID-19 is challenging due to multiple pathways of platelet activation and coagulation leading to thrombus formation. This article reviews the current understanding of antiplatelet therapy in patients with COVID-19.