title: Attenuated plaque at nonculprit lesions in patients enrolled in intravascular ultrasound atherosclerosis progression trials.
abstract: OBJECTIVE
  We investigated attenuated plaque (hypoechoic plaque with deep ultrasonic attenuation despite absence of bright calcium) in nonculprit lesions.
  
  
  BACKGROUND
  Recent intravascular ultrasound (IVUS) studies describe acoustic shadowing behind large, echolucent, acute culprit lesion sites in the absence of bright calcium. Such "attenuated plaque" is considered a characteristic of high-risk lesions, but its prevalence in stable nonculprit lesions is incompletely known.
  
  
  METHODS
  We reviewed IVUS pullback data from nonculprit vessels in 159 patients from the ASTEROID (A Study to Evaluate the Effect of Rosuvastatin on Intravascular Ultrasound-Derived Coronary Atheroma Burden) trial. We identified attenuated plaque and compared volumetric IVUS data in the segments with and without attenuation. In addition, we described plaque morphology in segments with attenuation at baseline and follow-up.
  
  
  RESULTS
  Attenuated plaque was found in 17 of 159 patients (10.7%, 95% confidence interval: 6% to 17%). At baseline, there were no significant differences in clinical presentation and cardiovascular risk factors between patients with and without attenuation. Other than a greater plaque eccentricity index (p = 0.008), there were no significant differences between segments with and without attenuation. In segments with attenuated plaque, expansive remodeling was observed in 53%, and calcified plaque adjacent to the attenuation site in 70% of patients. During follow-up, attenuation remained stable, and no events occurred in the patients with attenuation.
  
  
  CONCLUSIONS
  Attenuated plaque is present in a significant number of nonculprit segments in patients enrolled in IVUS progression trials and remains stable during follow-up. There is a relationship with mixed calcified lesions. These findings challenge the prior assumption that attenuated plaque is a finding limited to culprit lesions associated with acute clinical presentation.
authors.affiliation: Department of Cardiovascular Medicine, Cleveland Clinic, Cleveland, OH 44195, USA.
authors.forename: Ozgur
authors.initials: O
authors.lastname: Bayturan
authors.forename: E Murat
authors.initials: EM
authors.lastname: Tuzcu
authors.forename: Stephen J
authors.initials: SJ
authors.lastname: Nicholls
authors.forename: Craig
authors.initials: C
authors.lastname: Balog
authors.forename: Andrea
authors.initials: A
authors.lastname: Lavoie
authors.forename: Kiyoko
authors.initials: K
authors.lastname: Uno
authors.forename: Timothy D
authors.initials: TD
authors.lastname: Crowe
authors.forename: William A
authors.initials: WA
authors.lastname: Magyar
authors.forename: Kathy
authors.initials: K
authors.lastname: Wolski
authors.forename: Samir
authors.initials: S
authors.lastname: Kapadia
authors.forename: Steven E
authors.initials: SE
authors.lastname: Nissen
authors.forename: Paul
authors.initials: P
authors.lastname: Schoenhagen
mesh_terms: D000368:Aged; D050197:Atherosclerosis / Q000150:complications / Q000000981:diagnostic imaging* / Q000188:drug therapy; D002114:Calcinosis / Q000000981:diagnostic imaging; D018450:Disease Progression; D005260:Female; D005464:Fluorobenzenes / Q000627:therapeutic use; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use; D008297:Male; D008875:Middle Aged; D011237:Predictive Value of Tests; D011743:Pyrimidines / Q000627:therapeutic use; D000068718:Rosuvastatin Calcium; D013449:Sulfonamides / Q000627:therapeutic use; D013997:Time Factors; D016896:Treatment Outcome; D018084:Ultrasonography, Interventional
chemical_list: D005464:Fluorobenzenes; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D011743:Pyrimidines; D013449:Sulfonamides; D000068718:Rosuvastatin Calcium