Compensatory Enlargement, Remodeling, and Restenosis

Abstract

Coronary atherosclerosis is associated with vessel remodeling and dilatation. Quantitative analysis of arterial morphometry documents that as the cross sectional area of the plaque increases within a diseased vessel segment, the outer wall of the artery expands in an attempt to compensate for the accumulation of plaque. This focal compensatory enlargement maintains cross sectional area at stenotic sites of arteries, and the angiographic appearance of the vessel may be normal, despite marked accumulation of atherosclerotic plaque. Compensatory enlargement may develop as a response to increased shear stress caused by atherosclerotic plaque in conjunction with endothelial dependent factors, or alternatively, due to medial attenuation with loss of underlying structural support. The mechanism of arterial remodeling plays an important role in the development of arterial restenosis late after balloon dilatation or other interventional modalities. Stents prevent the remodeling process and restenosis with stents is the result of a relatively uniform neointimal tissue proliferation throughout the stent. Endovascular stents induce tissue proliferation both within the endoluminal stent surface and in the tissue layers surrounding the metallic Palmaz-Schatz stent struts. The therapeutic goals to prevent restenosis have to be oriented towards prevention of acute recoil, reduction of intimai, medial and adventitial prolific response and the phenomenon of inadequate arterial remodeling.