Impact of geometric factors and shear stress on endothelial function: Hemodynamic insights from human cerebral arterial bifurcations.

摘要

Vascular inflammation is not a random biological event but rather a process that is strictly regulated by physical forces. While biochemical mediators are well characterized, the local physical mechanisms that predispose specific cerebral vascular sites to inflammation, specifically the geometry of arterial bifurcations, remain underappreciated. This study aims to determine how distinct arterial bifurcation geometries physically regulate the local inflammatory microenvironment by modulating wall shear stress (WSS), relative residence time (RRT), and endothelial cell activation potential (ECAP). We performed a high-resolution morphometric analysis of 1512 arterial bifurcations. They were categorized based on parent-daughter diameter relationships: open-shaped (87.4%), neutral-shaped (10.4%), and closed-shaped (2.2%). The open-shaped configuration acts as a low-shear trap, exhibiting the highest median RRT (1.68 s) and ECAP (0.092). The closed-shaped configuration concentrates mechanical energy, subjecting the endothelium to significantly elevated high median WSS (7 Pa) and peak pressures (17.16 kPa). Cerebral arterial bifurcations create distinct hemodynamic microenvironments that govern local vascular vulnerability. The prevalent open-shaped geometry minimizes energy loss at the cost of a high residence time, physically priming the endothelium for stagnation-induced inflammation. In contrast, closed-shaped geometries protect downstream microvessels by dissipating energy but sacrifice the local endothelium to high-shear mechanical stress.