Individual propensity for arterial thrombosis and variables governing this propensity. The relationship between atherosclerosis and arterial platelet-rich thrombosis is complex and poorly understood. Among individuals with atherosclerosis, the clinical presentation of the disease varies broadly. On one end of the spectrum are young patients who suffer acute luminal thrombosis (eg. myocardial infarction; MI) with minimal arterial wall atherosclerosis. On the other end are elderly patients, seemingly resistant to thrombosis, who have gradually developed advanced atherosclerosis without suffering clinical thrombosis. This poor correlation between atherosclerosis and thrombosis suggests that additional factors other than simply the extent of atherosclerosis are important in determining in situ thrombosis. We hypothesize that the thrombotic complications of atherosclerosis are governed by an intrinsic propensity for arterial thrombosis. Gaining an understanding of variables contributing to this propensity would be helpful in developing tools to prevent this complication. Our long-term goal is to systematically determine the platelet and genetic variables contributing to the propensity to develop the acute thrombotic complications of atherosclerosis.
Methodology employed in these investigations includes animal cardiovascular surgery, protein biochemistry, immunohistochemistry, flow cytometry, in vitro thrombin dependent and independent flow chambers, and molecular biology.
Future experiments will include investigations into platelet, monocyte, and lymphocyte physiology as they relate to arterial thrombosis. We are furthermore interested in defining platelet subpopulations which may contribute to the propensity for thrombosis.