Wahle A, Lopez JJ, Olszewski ME, Vigmostad SC, Braddy KC, Brennan TMH, Bokhari SW, Bennett JG, Holper EM, Rossen JD, Chandran KB, Sonka M:


Relationship between Plaque Development and Local Hemodynamics in Coronary Arteries.

In:

Amini AA, Manduca A (eds):

Medical Imaging 2005: Physiology, Function, and Structure from Medical Images.

SPIE Proceedings

Volume 5746, Page 223-232, 2005

Conference paper based on the data of the abstract with details on methodology, also updating previous results on the plaque/curvature study (Paper) (Links)

Abstract: The mechanisms of plaque development in coronary arteries are not yet completely understood. Vessel geometry influences the local hemodynamics within a vessel, and the resulting wall shear stress in turn influences plaque development. Previously, we showed in-vivo that plaque tends to accumulate more on the inner curvature of a vessel than on its outer curvature. While vessel curvature is preserved during plaque progression, the local wall shear stresses change with lumen narrowing. The aim of this study was to test how the hypothesis that locations of low wall shear stress coincide with circumferentially larger plaque accumulation depends on vascular remodeling with or without lumen narrowing. We have analyzed 39 in-vivo intravascular-ultrasound pullbacks, for which geometrically accurate 3-D models were obtained by fusion with x-ray angiography. Distorting subsegments (branches, calcifications, stents) were discarded, and the relative number of vessel locations was determined within a 10-40% area-stenosis range. This range corresponds to compensatory enlargement (outward or positive vessel remodeling), but not yet lumen narrowing, and these vessel segments were a focus of our study. For each segment, we determined the relative number of vessel locations for which circumferentially low wall shear stress coincided with larger plaque thickness and vice versa. The inverse association between wall shear stress and plaque thickness was significantly more pronounced (p<0.005) in vessel cross sections exhibiting compensatory enlargement without luminal narrowing than when the full spectrum of vessel stenosis severity was considered. Thus, the hypothesis is supported more in subsegments with less developed disease.