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Arteries may demonstrate compensatory enlargement in response to plaque accumulation. It has been proposed that enlargement is achieved by the expansion of the nondiseased (plaque-free) vessel wall. In this study, we assessed this hypothesis. Post mortem, 32 atherosclerotic coronary arteries (left anterior descending, n = 10; left circumflex, n = 11; and right coronary, n = 11) and 54 atherosclerotic femoral arteries were pressure fixed. Cross sections (coronary arteries, n = 537; femoral arteries, n = 1602) were obtained for analysis every 2.5 mm for the coronary arteries and every 5.0 mm for the femoral arteries. From these cross sections, we determined the degree of remodeling and an eccentricity index. Finally, we measured the extent of plaque-free vessel wall. The plaque-free vessel wall was defined as (1) no plaque present or (2) plaque thickness &lt; 0.5 mm. A very weak, negative correlation was observed between the degree of remodeling and the extent of the plaque-free vessel wall (coronary arteries: no plaque r2 = .13, P &lt; .01; &lt; 0.5 mm plaque r2 = .15, P &lt; .05; femoral arteries: no plaque r2 = .02, P &lt; .01; &lt; 0.5 mm plaque r2 = 0.04, P &lt; .01). The degree of remodeling did not correlate with the eccentricity index (coronary arteries r2 = .002, P &gt; .05 and femoral arteries r2 = .001, P &gt; .05). Thus, compensatory enlarged segments did not reveal a larger circumference of plaque-free vessel wall compared with segments that failed to enlarge. This study provides no support for the hypothesis that nondiseased vessel-wall expansion is responsible for compensatory enlargement in atherosclerotic arteries.

Compensatory Enlargement in Coronary and Femoral Arteries Is Related to Neither the Extent of Plaque-Free Vessel Wall Nor Lesion Eccentricity