Computational Modeling of the Hypercoagulability in COVID-19

Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has affected near 50 million people worldwide and claimed more than 230,000 lives in United States as of Nov 2020. While the leading cause of mortality in patients with COVID-19 is hypoxic respiratory failure from acute respiratory distress syndrome, emerging evidence suggests that people with COVID-19 are prone to experience thrombotic events, such as acute pulmonary embolism and arterial thrombosis and develop cardiovascular complication. Hence, better quantitative understanding of the pathogenesis of hypercoagulability in COVID-19 is required to improve the disease management to prevent or treat thrombosis for COVID-19 patients. Recent studies indicated that all three components of Virchow’s triad, namely stasis, endothelial injury and hypercoagulable state, are likely to contribute to the increased thrombotic risk of COVID-19 patients, but the detailed mechanism is not well-understood. Herein, we propose to develop a novel computational framework to simulate the excessive thrombosis in microcirculation under hypercoagulability in COVID-19. This new framework will integrate seamlessly four key components in the process of blood clotting, namely hemodynamics, transport of coagulation factors and coagulation kinetics, blood cell mechanics and platelet adhesive dynamics, such that we can dissect the complicated process of pathological thrombus formation and investigate the detailed mechanism of hypercoagulability in COVID-19. Our simulation results can help to improve our understanding of the pathogenesis of hypercoagulability in COVID-19, identify the key coagulation factors in triggering thrombosis and test the efficacy of anti-coagulation and antiplatelet drugs, thereby improving the thrombosis prevention and treatment for COVID-19 patients.