Abstract 17312: Excessive Expansive Coronary Remodeling is Associated with an Adverse Hemodynamic Profile Leading to Rapid Progression of Atherosclerosis in Humans
Introduction: Coronary hemodynamic factors, in particular low endothelial shear stress (ESS) determine atherosclerosis progression. Vascular remodeling in response to plaque growth affects local blood flow profile and therefore the natural history of individual lesions. Compensatory expansive remodeling (ER) prevents a plaque from encroaching into the lumen, but an excessive ER response promotes high-risk lesions. Hypothesis: Excessive ER aggravates the local ESS microenvironment in humans, leading to accelerated coronary atherosclerosis.
Methods: We investigated the PREDICTION Study database of 3D coronary reconstruction by angiography & IVUS at the time of an acute coronary event (baseline, BL) and at 6-10 months followup (FU). At BL, we identified discrete plaques (max thickness >0.5 mm, length 9 to 30 mm) with normal adjacent regions and assessed ESS (using computational fluid dynamics) and remodeling in 3mm-long segments of these plaques. At FU, we assessed ESS and plaque growth in the same locations.
Results: In 83 total lesions (65 patients, length 13.7±0.7 mm) remodeling was evident in 64.9% of segments. Of these, 13.7% manifested Excessive ER, 15.3% Compensatory ER, 21% Inadequate ER and 50% Constrictive remodeling. At BL, there was no association between remodeling and ESS (Excessive ER 2.2±0.4; Compensatory ER 2.4±0.4; Inadequate ER 2.6±0.2 Pa; p=ns). At FU however, regions of BL Excessive ER exhibited a decrease in ESS (−0.6±0.4 Pa) unlike other plaque areas (Compensatory ER 0.4±0.2; Inadequate ER 0.6±0.3 Pa; p<0.01) culminating in significantly lower FU ESS (Excessive ER 1.6±0.2; Compensatory ER 2.8±0.4; Inadequate ER 3.2±0.4 Pa; p<0.05). Segments with BL Excessive ER showed an increase in plaque area at FU (1.5±2.9%) while those with Compensatory ER and Inadequate ER exhibited plaque regression (−12.8±4.0% and −13.6±2.7% respectively, p<0.01).
Conclusion: Excessive ER is associated with accelerated progression of atherosclerosis. Consistent with previous animal studies, progressive lowering of ESS in plaques with BL Excessive ER exacerbates the local inflammatory/atherogenic stimulus and promotes plaque progression at FU. ESS and Excessive ER synergistically exacerbate the development of high-risk plaque.
- © 2012 by American Heart Association, Inc.