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Glagov et al. observed that positive, compensatory vascular remodeling during plaque build up prevents lumen narrowing until plaque burden, this is the relative plaque area to media bounded area, exceeds a threshold of 40% [1]. Until now it is not clear what mechanism controls the compensatory vascular remodeling during the atherosclerotic plaque build up and what determines absence or limits compensatory vascular remodeling. Plaque burden does not seem to reflect a parameter, which could serve as a limiting step in the known control process in the vascular system. For instance, healthy arteries control vascular remodeling by fluid flow induced shear stress via a number of endothelium dependent pathways [2]. The endothelium at the atherosclerotic plaque side is considered to be dysfunctional [2] and might thereby limit the remodeling process. Since plaques are mostly eccentric, we hypothesize that the healthy part of the artery (or plaque free wall) will respond to changes in shear stress and will determine the capacity of the arteries to remodel up till the moment of complete circumferential involvement of the disease. We investigated whether the size of the plaque free wall contributes to vascular remodeling over a 3 year period using serial intravascular ultrasound measurements by determining 1) the frequency of positive remodeling in segments with varying size of plaque free vessel wall 2) the degree of vascular remodeling for segments with varying size of plaque free vessel wall.Copyright © 2008 by ASME

Aims: Early atherosclerosis is located in low wall shear-stress (WSS) regions, however plaques are also found in the high WSS sensing flowdivider walls of coronary bifurcations. We assessed the plaque distribution and morphology near bifurcations non-invasively with 64 slice computed tomography (MSCT) in relation to the WSS distribution. Methods and results: We inspected 65 cross-sections near coronary bifurcations for the presence of plaque. Cross-sections were divided into four equal parts, which we numbered according to expected levels of WSS, with part I the lowest WSS (outer wall) and increasing WSS’s in part II (inner bend), III (outer bend) and IV (flowdivider). Of the cross-sections 88% had plaque. Of all parts I, 72% contained plaque. This was 62%, 38% and 31% in parts II, III and IV. In cross-sections with only 1 or 2 parts inflicted, plaque was found in part I and/or II in 94%. In 93% of the cross-sections with the flowdivider inflicted, parts I and/or II were also inflicted. Plaque was never found exclusively in the flowdivider part IV. Conclusions: We demonstrated that plaque is mostly present in low WSS regions, whereas plaque in high WSS regions is accompanied by plaque in adjacent low WSS regions. It is therefore plausible that plaque grows from the outer wall (low WSS) of the bifurcation towards the flowdivider (high WSS).