title: Compensatory vascular changes of remote coronary segments in response to lesion progression as observed by sequential angiography from a controlled clinical trial.
abstract: BACKGROUND
  Local coronary artery enlargement to compensate for atherosclerotic plaques preserves the vessel lumen. The extent to which coronary segments remote from progressing lesions enlarge is unknown. This is clinically relevant since compensatory enlargement may be important in determining whether clinical complications result from progression of coronary artery disease (CAD). Additionally, compensatory change has implications for quantitative coronary angiographic (QCA) trials, since the effect of progression on diameter means may be mitigated by compensatory changes in remote coronary segments when QCA change is averaged over all lesions.
  
  
  RESULTS
  Serial QCA data from 78 subjects in the Monitored Atherosclerosis Regression Study were used to demonstrate compensatory changes in coronary segments remote from progressing or regressing lesions. Coronary segments were first classified as progressing (regressing) if percent diameter stenosis (PS) increased or decreased by > 10 with a concurrent decrease or increase in minimum lumen diameter (MLD) of either > 0.32 mm or > 10% of the normal baseline reference diameter (DNORM). Segments not meeting these criteria were labeled stenosis stable. Stenosis-stable segments opposite progressing lesions showed increases in MLD (P = .0006), DNORM (P = .001), and average diameter (P = .001). On-trial apolipoprotein (apo) B, apo C-III, and blood pressure levels inversely correlated with these compensatory changes.
  
  
  CONCLUSIONS
  Lesion progression in one coronary segment is associated with significant increases in segmental diameter of remote parts of the coronary tree. We hypothesize these increases to be vascular compensatory changes in response to progression of CAD. Vascular compensatory change is enhanced by LDL cholesterol and triglyceride-rich lipoprotein reduction and appears to be part of the treatment effect itself.
authors.affiliation: Atherosclerosis Research Unit, University of Southern California School of Medicine, Los Angeles 90033, USA.
authors.forename: A M
authors.initials: AM
authors.lastname: Shircore
authors.forename: W J
authors.initials: WJ
authors.lastname: Mack
authors.forename: R H
authors.initials: RH
authors.lastname: Selzer
authors.forename: P L
authors.initials: PL
authors.lastname: Lee
authors.forename: S P
authors.initials: SP
authors.lastname: Azen
authors.forename: P
authors.initials: P
authors.lastname: Alaupovic
authors.forename: H N
authors.initials: HN
authors.lastname: Hodis
mesh_terms: D000328:Adult; D000368:Aged; D001055:Apolipoproteins B / Q000097:blood; D001056:Apolipoproteins C / Q000097:blood; D017023:Coronary Angiography; D003324:Coronary Artery Disease / Q000097:blood / Q000000981:diagnostic imaging / Q000473:pathology*; D003327:Coronary Disease / Q000097:blood / Q000000981:diagnostic imaging / Q000473:pathology*; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged
chemical_list: D001055:Apolipoproteins B; D001056:Apolipoproteins C