Clinical Trial2017 Aug;10(8). pii: e005455.
JOURNAL：Circ Cardiovasc Interv. Article Link
Low Endothelial Shear Stress Predicts Evolution to High-Risk Coronary Plaque Phenotype in the Future: A Serial Optical Coherence Tomography and Computational Fluid Dynamics Study
Yamamoto E, Siasos G, Jang IK et al.
atherosclerosis; coronary vessels; shear stress; tomography, optical coherence
BACKGROUND - Low endothelial shear stress (ESS) is associated with plaque progression and vulnerability. To date, changes in plaque phenotype over time in relation to ESS have not been studied in humans. The aim of this study was to investigate whether local ESS can predict subsequent changes to plaque phenotype using optical coherence tomography.
METHODS AND RESULTS - A total of 25 coronary arteries from 20 patients who underwent baseline and 6-month follow-up optical coherence tomography were included. Arteries were divided into serial 3-mm segments, and plaque characteristics were evaluated in each segment. A total of 145 segments were divided into low-ESS group (ESS <1 Pa) and higher-ESS group (ESS ≥1 Pa) based on baseline computational flow dynamics analyses. At baseline, low-ESS segments had significantly thinner fibrous cap thickness compared with higher-ESS segments (128.2±12.3 versus 165.0±12.0 μm; P=0.03), although lipid arc was similar. At follow-up, fibrous cap thickness remained thin in low-ESS segments, whereas it significantly increased in higher-ESS segments (165.0±12.0 to 182.2±14.1 μm; P=0.04). Lipid arc widened only in plaques with low ESS (126.4±15.2° to 141.1±14.0°; P=0.01). After adjustment, baseline ESS was associated with fibrous cap thickness (β, 9.089; 95% confidence interval, 2.539-15.640; P=0.007) and lipid arc (β, -4.381; 95% confidence interval, -6.946 to -1.815; P=0.001) at follow-up.
CONCLUSIONS - Low ESS is significantly associated with baseline high-risk plaque phenotype and progression to higher-risk phenotype at 6 months.
CLINICAL TRIAL REGISTRATION - URL: http://www.clinicaltrials.gov. Unique identifier: NCT01110538.
© 2017 American Heart Association, Inc.