title: Increased intimal apoptosis in coronary atherosclerotic vessel segments lacking compensatory enlargement.
abstract: OBJECTIVE
  In a histopathologic study, we assessed the balance of cell proliferation and apoptosis by counting the number of apoptotic and proliferating cell nuclear antigen-positive cells in freshly harvested atherectomy specimens from 34 patients.
  
  
  BACKGROUND
  Remodeling of human coronary arteries is an adaptive process that alters vascular lumen size.
  
  
  METHODS
  Intravascular ultrasound was performed prior to atherectomy. Total vessel area (area within the external elastic lamina [EEL]), lumen area and plaque area were measured at the region of interest (ROI), and at a proximal and distal reference segment, utilizing the formula Delta(%)=100x(ROI-reference segment)/reference segment. Positive arterial remodeling (R+) resulting in luminal expansion was defined as DeltaEEL >10%. Absence of remodeling (0 < DeltaEEL <10%) and constrictive arterial remodeling (DeltaEEL <0) were considered as neutral remodeling (R0) and negative remodeling (R-), respectively.
  
  
  RESULTS
  In R- lesions, apoptotic indices (APO) were significantly elevated (17.17 +/- 2.19%) compared with R+ lesions (4.89 +/- 1.7%; p = 0.0007). In a rabbit iliac percutaneous transluminal coronary angioplasty model intimal apoptosis was increased four weeks after balloon angioplasty injury (APO 8.8 +/- 0.03%) compared with contralateral untreated segments (APO 3.0 +/- 0.04%, n = 6). Lesions with an EEL/intimal area <3.0 showed significantly more intimal apoptosis than untreated lesions (p = 0.02).
  
  
  CONCLUSIONS
  The data indicate that constrictive remodeling of atherosclerotic coronary lesions is associated with increased apoptosis of intimal cells. We speculate that increased apoptosis is due to extensive plaque healing after episodes of symptomatic or asymptomatic plaque rupture.
authors.affiliation: Department of Cardiology, University of Vienna, Vienna, Austria.
authors.forename: A H
authors.initials: AH
authors.lastname: Hassan
authors.forename: I M
authors.initials: IM
authors.lastname: Lang
authors.forename: M
authors.initials: M
authors.lastname: Ignatescu
authors.forename: R
authors.initials: R
authors.lastname: Ullrich
authors.forename: D
authors.initials: D
authors.lastname: Bonderman
authors.forename: P
authors.initials: P
authors.lastname: Wexberg
authors.forename: F
authors.initials: F
authors.lastname: Weidinger
authors.forename: H D
authors.initials: HD
authors.lastname: Glogar
mesh_terms: D000222:Adaptation, Physiological; D000368:Aged; D000704:Analysis of Variance; D015906:Angioplasty, Balloon, Coronary / Q000009:adverse effects; D000818:Animals; D017209:Apoptosis; D017225:Atherectomy, Coronary; D002455:Cell Division; D017023:Coronary Angiography; D003324:Coronary Artery Disease / Q000175:diagnosis / Q000473:pathology* / Q000601:surgery; D004195:Disease Models, Animal; D018450:Disease Progression; D006801:Humans; D006965:Hyperplasia; D007150:Immunohistochemistry; D020287:In Situ Nick-End Labeling; D008297:Male; D008875:Middle Aged; D018809:Proliferating Cell Nuclear Antigen / Q000032:analysis; D011817:Rabbits; D012008:Recurrence; D017539:Tunica Intima / Q000293:injuries / Q000648:ultrastructure*; D017540:Tunica Media / Q000293:injuries / Q000648:ultrastructure*; D018084:Ultrasonography, Interventional
chemical_list: D018809:Proliferating Cell Nuclear Antigen