title: Determinants of coronary remodeling in transplant coronary disease: a simultaneous intravascular ultrasound and Doppler flow study.
abstract: BACKGROUND
  Coronary remodeling plays a significant role in lumen loss in transplant allograft vasculopathy (TxCAD), but the determinants of remodeling are unknown. We assessed the relationship between remodeling and plaque topography, coronary compliance, and blood flow in TxCAD.
  
  
  RESULTS
  One artery in each of 27 transplant patients was investigated with simultaneous intravascular ultrasound and coronary flow measurements (basal and hyperemic by Doppler flow wire). At 4 to 8 different cross sections (mean 5.1+/-1. 2), plaque topography (concentric or eccentric) was determined, and total vessel area, lumen area, and intimal/medial area (IMA) were measured. Mean remodeling ratio (vessel area/IMA) in eccentric lesions (E, n=28) was significantly larger than that in concentric lesions (C, n=70) (E 5.87+/-0.93 versus C 3.58+/-0.62; P<0.001), despite similar IMA (E 3.89+/-0.68 versus C 3.90+/-0.41; P=NS) and distribution of imaged segments. Remodeling ratio was consistently larger in eccentric lesions in all 3 vessel segments when analyzed separately, and mean remodeling ratio for each artery was larger in vessels with predominantly eccentric lesions. Coronary compliance ([Delta lumen area/diastolic lumen area]/Delta mean arterial pressure x 10(3)) was also significantly greater in eccentric lesions versus concentric lesions (proximal 1.00+/-0.39 versus 0.22+/-0.04; mid 0.71+/-0.17 versus 0.21+/-0.10; distal 0.43+/-0.13 versus 0. 01+/-0.08; all P<0.01). Coronary flow reserve was also significantly higher in coronary arteries with primarily eccentric lesions (E 2. 49+/-0.64 versus C 1.87+/-0.28; P<0.01).
  
  
  CONCLUSIONS
  Vessel remodeling in transplant vasculopathy is significantly greater in eccentric lesions than in concentric lesions, possibly due to greater coronary compliance and resistive vessel function.
authors.affiliation: Division of Cardiology, Stanford University Medical Center, CA 94305, USA.
authors.forename: S P
authors.initials: SP
authors.lastname: Schwarzacher
authors.forename: N G
authors.initials: NG
authors.lastname: Uren
authors.forename: M R
authors.initials: MR
authors.lastname: Ward
authors.forename: A
authors.initials: A
authors.lastname: Schwarzkopf
authors.forename: N
authors.initials: N
authors.lastname: Giannetti
authors.forename: S
authors.initials: S
authors.lastname: Hunt
authors.forename: P J
authors.initials: PJ
authors.lastname: Fitzgerald
authors.forename: S N
authors.initials: SN
authors.lastname: Oesterle
authors.forename: A C
authors.initials: AC
authors.lastname: Yeung
mesh_terms: D003187:Compliance; D003326:Coronary Circulation / Q000502:physiology; D003327:Coronary Disease / Q000000981:diagnostic imaging* / Q000209:etiology / Q000503:physiopathology; D003331:Coronary Vessels / Q000000981:diagnostic imaging* / Q000502:physiology*; D005260:Female; D016027:Heart Transplantation; D006801:Humans; D008297:Male; D008875:Middle Aged; D011183:Postoperative Complications; D012212:Rheology / Q000379:methods*; D018084:Ultrasonography, Interventional