Date: Thursday, April 7, 2011
Place: EA 409
Coronary heart disease is the leading cause of death in the developed nations. It is the end result of atherosclerotic plaque formation in the coronary arteries. Subendothelial accumulation of low-density lipoprotein (LDL) in arterial walls is believed to be an initiator of atherosclerotic plaque formation. The aim of this work was to understand the mechanisms governing the LDL transport from the artery lumen into the arterial wall. For this purpose, a coupled blood-wall mass transport model of LDL that realistically takes into account the role of endothelium and the effects of flow conditions on the endothelial cells was developed. This model included blood plasma and LDL transport through normal and leaky junctions and via vesicles, and proved to better represent the dependence of blood plasma and LDL fluxes on the local flow dynamics compared to previous single pathway approaches. With the application of this model to real patients, potential correlations between LDL concentration and plaque formation was investigated and quantified. Subendothelial LDL concentration profiles of 60 patients’ coronary arteries in their healthy states were calculated and correlated to subsequent plaque locations in their diseased states. It is shown that subendothelial LDL concentration is high at plaque locations compared to the average subendothelial LDL concentration.