SUMMARY

Thrombosis can result in acute arterial occlusion thereby causing cerebrovascular accidents and myocardial infarction. However, diagnosing the risk of developing thrombosis is difficult due to the limited understanding of how platelets are transported, adhere, and accumulate in flowing blood. A clinician might be better able to predict a patient’s risk for thrombosis with an understanding of how a thrombus forms and why it occludes an artery. Arterial thrombosis location has been found to occur at the peak of an atheromatic lesion, which is near the region of the highest shear rates. In addition platelet deposition rate has been correlated to increase with an increasing shear rate. Most previous studies have focused on initial platelet adhesion to the atheromatic lesion. This study is focused on a growing thrombus past initial platelet attachment to the point of full occlusion, which is the dominant problem in a thrombotic event. Thrombotic development was divided into three main mechanisms and their relation to shear rate in a model of the coronary artery. The first two are transport related, which are known in the field as shear enhanced diffusivity and platelet margination. The third considers an adhesion function of shear rate. These mechanisms are evaluated through a computational model with verification against an in vitro experiment. I propose that the transport phenomena may be the dominant controlling factor in the location of thrombus formation and the occlusive time.