Fig. 7: Differential angular branching points of a human coronary artery cause varying degrees of fluid flow turbulence consequently switching EC towards pro-atherogenic phenotypes.

Vessel branch points are known to affect the WSS levels, cause endothelial dysfunction and thus are the prime spots of atherosclerotic plaque formation. Increasing angles of the branching points differentially impact the balance of genes responsible for EC homeostasis. A bifurcation angle of 30° exhibits no significant alterations in the WSS levels, velocity distribution and protein level expressions of eNOS and ICAM1. On the contrary, vessel branching at an angle of 60° displayed the lowest WSS levels at the outer walls of the bifurcation. EC in the D-Flow regions of such a vessel were found to have a round and flat morphology with high levels of ICAM1 and a concurrent reduction in eNOS expression, in comparison to S-Flow. The larger angular disturbance caused by the 80° branching, affected WSS to similar levels; however, a huge alteration was observed in the velocity dispensation across the bifurcation. These differential velocity gradients are responsible for generating special zones with varying WSS levels and a corresponding change in eNOS and ICAM1 expression.