title: Coronary artery wall shear stress is associated with progression and transformation of atherosclerotic plaque and arterial remodeling in patients with coronary artery disease.
abstract: BACKGROUND
  Experimental studies suggest that low wall shear stress (WSS) promotes plaque development and high WSS is associated with plaque destabilization. We hypothesized that low-WSS segments in patients with coronary artery disease develop plaque progression and high-WSS segments develop necrotic core progression with fibrous tissue regression.
  
  
  RESULTS
  Twenty patients with coronary artery disease underwent baseline and 6-month radiofrequency intravascular ultrasound (virtual histology intravascular ultrasound) and computational fluid dynamics modeling for WSS calculation. For each virtual histology intravascular ultrasound segment (n=2249), changes in plaque area, virtual histology intravascular ultrasound-derived plaque composition, and remodeling were compared in low-, intermediate-, and high-WSS categories. Compared with intermediate-WSS segments, low-WSS segments developed progression of plaque area (P=0.027) and necrotic core (P<0.001), whereas high-WSS segments had progression of necrotic core (P<0.001) and dense calcium (P<0.001) and regression of fibrous (P<0.001) and fibrofatty (P<0.001) tissue. Compared with intermediate-WSS segments, low-WSS segments demonstrated greater reduction in vessel (P<0.001) and lumen area (P<0.001), and high-WSS segments demonstrated an increase in vessel (P<0.001) and lumen (P<0.001) area. These changes resulted in a trend toward more constrictive remodeling in low- compared with high-WSS segments (73% versus 30%; P=0.06) and more excessive expansive remodeling in high- compared with low-WSS segments (42% versus 15%; P=0.16).
  
  
  CONCLUSIONS
  Compared with intermediate-WSS coronary segments, low-WSS segments develop greater plaque and necrotic core progression and constrictive remodeling, and high-WSS segments develop greater necrotic core and calcium progression, regression of fibrous and fibrofatty tissue, and excessive expansive remodeling, suggestive of transformation to a more vulnerable phenotype. Clinical Trial Registration URL: http://www.clinicaltrials.gov. Unique identifier: NCT00576576.
authors.affiliation: Department of Medicine, Emory University School of Medicine, 1365 Clifton Rd, Ste F606, Atlanta, GA 30322, USA. hsamady@emory.edu
authors.forename: Habib
authors.initials: H
authors.lastname: Samady
authors.forename: Parham
authors.initials: P
authors.lastname: Eshtehardi
authors.forename: Michael C
authors.initials: MC
authors.lastname: McDaniel
authors.forename: Jin
authors.initials: J
authors.lastname: Suo
authors.forename: Saurabh S
authors.initials: SS
authors.lastname: Dhawan
authors.forename: Charles
authors.initials: C
authors.lastname: Maynard
authors.forename: Lucas H
authors.initials: LH
authors.lastname: Timmins
authors.forename: Arshed A
authors.initials: AA
authors.lastname: Quyyumi
authors.forename: Don P
authors.initials: DP
authors.lastname: Giddens
mesh_terms: D000368:Aged; D002114:Calcinosis / Q000000981:diagnostic imaging / Q000473:pathology / Q000503:physiopathology; D003324:Coronary Artery Disease / Q000000981:diagnostic imaging / Q000473:pathology / Q000503:physiopathology; D003331:Coronary Vessels / Q000000981:diagnostic imaging / Q000473:pathology / Q000503:physiopathology; D018450:Disease Progression; D005260:Female; D005355:Fibrosis; D006801:Humans; D057446:Hydrodynamics; D008297:Male; D008875:Middle Aged; D009336:Necrosis; D058226:Plaque, Atherosclerotic / Q000000981:diagnostic imaging / Q000473:pathology / Q000503:physiopathology; D011446:Prospective Studies; D013314:Stress, Mechanical; D018084:Ultrasonography, Interventional / Q000379:methods*