title: Effect of endothelial shear stress on the progression of coronary artery disease, vascular remodeling, and in-stent restenosis in humans: in vivo 6-month follow-up study.
abstract: BACKGROUND
  Native atherosclerosis and in-stent restenosis are focal and evolve independently. The endothelium controls local arterial responses by transduction of shear stress. Characterization of endothelial shear stress (ESS) may allow for prediction of progression of atherosclerosis and in-stent restenosis.
  
  
  RESULTS
  By using intracoronary ultrasound, biplane coronary angiography, and measurement of coronary blood flow, we represented the artery in accurate 3D space and determined detailed characteristics of ESS and arterial wall/plaque morphology. Patients who underwent stent implantation and who had another artery with luminal obstruction <50% underwent intravascular profiling initially and after 6-month follow-up. Twelve arteries in 8 patients were studied: 6 native and 6 stented arteries. In native arteries, regions of abnormally low baseline ESS exhibited a significant increase in plaque thickness and enlargement of the outer vessel wall, such that lumen radius remained unchanged (outward remodeling). Regions of physiological ESS showed little change. Regions with increased ESS exhibited outward remodeling with normalization of ESS. In stented arteries, there was an increase in intima-medial thickness, a decrease in lumen radius, and an increase in ESS at all levels of baseline ESS.
  
  
  CONCLUSIONS
  The present study represents the first experience in humans relating ESS to subsequent outcomes in native and stented arteries. Regions of low ESS develop progressive atherosclerosis and outward remodeling, areas of physiological ESS remain quiescent, and areas of increased ESS exhibit outward remodeling. ESS may have a limited role in in-stent restenosis. This technology can predict areas of minor plaque likely to exhibit progression of atherosclerosis.
authors.affiliation: Cardiovascular Division, Brigham and Women's Hospital, 75 Francis St, Boston, Mass 02115, USA. pstone@partners.org
authors.forename: Peter H
authors.initials: PH
authors.lastname: Stone
authors.forename: Ahmet U
authors.initials: AU
authors.lastname: Coskun
authors.forename: Scott
authors.initials: S
authors.lastname: Kinlay
authors.forename: Maureen E
authors.initials: ME
authors.lastname: Clark
authors.forename: Milan
authors.initials: M
authors.lastname: Sonka
authors.forename: Andreas
authors.initials: A
authors.lastname: Wahle
authors.forename: Olusegun J
authors.initials: OJ
authors.lastname: Ilegbusi
authors.forename: Yerem
authors.initials: Y
authors.lastname: Yeghiazarians
authors.forename: Jeffrey J
authors.initials: JJ
authors.lastname: Popma
authors.forename: John
authors.initials: J
authors.lastname: Orav
authors.forename: Richard E
authors.initials: RE
authors.lastname: Kuntz
authors.forename: Charles L
authors.initials: CL
authors.lastname: Feldman
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001783:Blood Flow Velocity; D019917:Blood Vessel Prosthesis Implantation / Q000009:adverse effects; D017023:Coronary Angiography; D003324:Coronary Artery Disease / Q000175:diagnosis / Q000503:physiopathology* / Q000601:surgery; D003326:Coronary Circulation; D023903:Coronary Restenosis / Q000175:diagnosis / Q000209:etiology / Q000503:physiopathology*; D003331:Coronary Vessels / Q000000981:diagnostic imaging / Q000601:surgery; D018450:Disease Progression; D004730:Endothelium, Vascular / Q000503:physiopathology*; D005240:Feasibility Studies; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D021621:Imaging, Three-Dimensional; D008297:Male; D008875:Middle Aged; D010865:Pilot Projects; D015607:Stents / Q000009:adverse effects; D013314:Stress, Mechanical; D016896:Treatment Outcome; D018084:Ultrasonography, Interventional; D014654:Vascular Patency