(Dr. Raymond Vito, advisor)

"Arterial Wall Stress and Vascular Inflammation: A Histology-Based Finite Element Model"

Abstract
 

Hypertension is a major risk factor for coronary artery disease, stroke, and kidney disease.  Preliminary studies suggest that hypertension increases intramural stresses where arteries branch and that these stresses may be correlated with inflammatory changes.  It is hypothesized that intramural stresses peak within branches and can vary significantly with changes in geometry.  Further, it is hypothesized that elevated pressure produces stresses that stimulate the onset of inflammation.  The main objectives of this research are 1) to develop a method to reconstruct small arterial branches from histological data; 2) to use finite element analysis to evaluate intramural stresses where experimental capabilities are limited; 3) to quantify stresses and biological measures of inflammation so they may be visually and statistically compared; and 4) to identify correlations between stress and inflammation.  Hypertension will be induced in mice and the mesentery will be harvested at prescribed time points.  The small size of mesenteric vessels limits what can be determined from mechanical testing and underscores the need for a finite element model to locally characterize the intramural stress distribution where arteries branch.  This approach requires that the mechanical results be closely linked to histological measures of inflammation (macrophage distribution and MCP-1 expression).  In fact, the geometry for finite element analysis will be based on histology and the mechanical and biological data will share a common coordinate system.