Modeling the transport, activation, and adhesion of platelets is crucial in predicting
thrombus formation and growth following a thrombotic event in normal or pathological
conditions. We propose a shear-dependent platelet adhesive model based on the Morse
potential that is calibrated by existing
vitro experimental data and can be used over a wide range of flow shear rates (
Hemostasis (thrombus formation) is the normal physiological response that prevents significant blood loss after vascular injury. The resulting clots can form under different flow conditions in the veins as well as the arteries. The excessive and undesirable formation of clots (i.e., thrombosis) in our circulatory system may lead to significant morbidity and mortality. Some of these pathologies are deep vein thrombosis and pulmonary embolism and atherothrombosis (thrombosis triggered by plaque rupture) in coronary arteries, to name a few. The process of clot formation and growth at a site on a blood vessel wall involves a number of simultaneous processes including: multiple chemical reactions in the coagulation cascade, species transport and platelet adhesion all of which are strongly influenced by the hydrodynamic forces. Numerical models for blood clotting normally focus on one of the processes under a specific flow condition. Here, we propose a general numerical model that encompass a wide range of hemodynamic conditions in the veins and arteries, with individual platelets and their adhesive dynamics included explicitly in the models. Further, we include the biochemistry of coagulation cascade, which is essential to modeling thrombus formation, and couple that to our platelet aggregation model. The simulation results—tested against three different experiments—demonstrate that the proposed model is effective in capturing the in vivo and in vitro experimental observations.