Low density lipoprotein transport through patient-specific thoracic arterial wall

The distribution of Low density lipoprotein (LDL) within the arterial wall is helpful in understanding the onset and development of atherosclerosis. The objective of the study is to study the transport and LDL distribution within patient-specific arterial wall using computational analysis under normal and hypertensive conditions.

Patient specific model of the thoracic aorta is computationally examined. The arterial wall is treated macroscopically as homogeneous (one layered) porous media of variable thickness. The interfacial lumen-arterial wall (endothelium) coupling is achieved by the Kedem-Katchalsky equation.

High values of LDL are located at areas where WSS values range from 0.4 N/m² to 1.5 N/m² for normal conditions. In this case the Pearson correlation coefficient r between LDL values and WSS is equal to -0.655 denoting a strong negative linear correlation. In the case that hypertension takes place, high LDL values are located at areas where WSS values range from 0.59 N/m² to 1.7 N/m² and the corresponding Pearson correlation coefficient r is equal to -0.808 denoting a very strong negative linear correlation. For the same parabolic intake flow velocity profile, the luminal surface concentration of LDL is 0.2-2.1% higher than that of the bulk flow for the normal pressure and 0.4-3.4% higher than that of the bulk flow for the hypertensive pressure. For normal conditions, the concentration of LDL at the endothelium/media interface is considerably lower (almost 20 times) than the LDL concentration value at lumen/endothelium interface. For hypertensive conditions, the LDL concentration at the endothelium/media interface is only 4.5 times lower than the corresponding luminal (endothelium side) concentration. The lumen/endothelium side locations (mainly the concave parts) of low WSS - high LDL concentration values coincide with those of high wall-side LDL concentration.

The transport and LDL distribution is affected by elevated transmural pressure which causes higher LDL concentration. Thus, hypertensive conditions theoretically enhance atherosclerosis.