Creating a Low Volume Model of Occlusive Thrombosis

Heart disease is the leading cause of death in industrialized countries. Heart attacks and strokes can cause mortality within an hour following plaque rupture. Unfortunately, as it is impossible to study heart attacks in real time, little is known about the mechanism which contributes to mortality. The mechanism of thrombosis under high shear is currently in dispute. Some investigators have shown that GPIIb/IIIa is important in stabilizing a thrombus under high shear conditions.[1] We have independently shown occlusive thrombosis in a gravity-fed tubular stenosis is predicated on a delayed phase of Rapid Platelet Accumulation (RPA) that occurs only at pathologically high shear rates with fast occlusion times consistent with Acute Coronary Syndrome.[2] However, Ruggeri has recently shown that platelet deposition and aggregation can occur at high shear model independent of GPIIb/IIIa which must be activated for binding.[3] Thus, the role of GPIIb/IIIa on high shear thrombosis to occlusion is not known.