Regions of low endothelial shear stress are the sites where coronary plaque progresses and vascular remodelling occurs in humans: an in vivo serial study

Aim We performed serial intracoronary studies of patients withstable coronary artery disease (CAD) to investigate the relationshipsamong baseline endothelial shear stress (ESS), CAD progression,and vascular remodelling. Local haemodynamic factors are criticaldeterminants of plaque progression, vascular remodelling, andclinical CAD manifestations. Methods and results The 3-D anatomy of coronary arteries withlumen obstruction <50% was determined by fusing intracoronaryultrasound and angiographic images in 13 patients at baselineand 8 ± 2 months later. Cross-sectional area of plaque,lumen, and external elastic membrane (EEM), and coronary flowwere measured. Local ESS was calculated. Subsegments with similarESS were categorized based on low (<12 dynes/cm²) and moderate/higherESS (12 dynes/cm²). There were 47 subsegments of similar baselineESS: nine with low ESS and 38 with moderate/higher ESS. Mediansubsegment length was 6.9 mm (25th–75th percentiles =4.2–12.0), and median area of similar ESS of 52.6 mm²(25th–75th percentiles = 26.9–88.0). Subsegmentswith low ESS exhibited plaque progression when compared withsubsegments with moderate/higher ESS (33.3% vs. 7.9%, respectively,P = 0.009 adjusted for clustering of lesions within patients)and constrictive remodelling (44.0% vs. 5.3%, respectively,P = 0.16 adjusted for clustering of lesions within patients).Expansive remodelling occurred with similar frequency in subsegmentswith low vs. moderate/higher baseline ESS. Conclusion Plaque progresses in subsegments with low ESS, associatedwith either constrictive or expansive remodelling. Differentmechanisms are likely responsible for expansive remodellingin different local vascular environments. Early in vivo identificationof arterial subsegments likely to develop high-risk plaque characteristicsmay allow for selective interventions to avoid adverse cardiacoutcomes.