title: Effects of lipid-lowering therapy on coronary artery remodeling.
abstract: BACKGROUND
  Although lipid-lowering therapy affects the luminal size of atherosclerotic coronary arteries the role of vascular remodeling has not been systematically studied.
  
  
  METHODS
  Serial three-dimensional volumetric intravascular ultrasound (IVUS) was used to study remodeling, which was defined as changes in arterial size independent of or dependent on changes in plaque size. Using an automated contour detection algorithm, a 1 mm segment of a moderate atherosclerotic lesion at the site of the maximal plaque volume at baseline was analysed. After 12 months the relationship between the absolute change in vessel volume and plaque volume was calculated in 99 patients. There was a significant relationship between changes in plaque and vessel volume, independent of plaque progression or plaque regression (decrease in plaque size, r = 0.60, P < 0.0001 and increase in plaque size, r = 0.49, P < 0.0008, respectively; the slopes of the regression equation were 1.03 and 0.80). By means of an analysis of covariance we tested whether the regression slopes were equal between groups of patients as defined by the low-density lipoprotein-cholesterol (LDL-c) level achieved with lipid-lowering therapy.
  
  
  RESULTS
  Only patients with plaque progression and a LDL-c level < 100 mg/dl had a significantly smaller slope than patients with a LDL-c level > 100 mg/dl (-0.14 compared with 1.14, P = 0.003 ), indicating diminished coronary remodeling.
  
  
  CONCLUSIONS
  Serial volumetric IVUS confirms the existence of both positive and negative remodeling in relation to an increase and decrease in plaque volume. It has been shown that the outward remodeling process is diminished in patients with plaque progression and intensive lipid-lowering therapy.
authors.affiliation: Universitaetsklinikum Charité Campus Virchow, Humboldt Universität Berlin, Germany. michael.schartl@charite.de
authors.forename: Michael
authors.initials: M
authors.lastname: Schartl
authors.forename: Wolfgang
authors.initials: W
authors.lastname: Bocksch
authors.forename: Susanne
authors.initials: S
authors.lastname: Fateh-Moghadam
mesh_terms: D000368:Aged; D000069059:Atorvastatin; D015415:Biomarkers / Q000097:blood; D008078:Cholesterol, LDL / Q000187:drug effects / Q000378:metabolism; D003324:Coronary Artery Disease / Q000188:drug therapy*; D005260:Female; D005858:Germany / Q000453:epidemiology; D006538:Heptanoic Acids / Q000627:therapeutic use*; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use*; D006937:Hypercholesterolemia / Q000188:drug therapy; D000960:Hypolipidemic Agents / Q000627:therapeutic use*; D008137:Longitudinal Studies; D008297:Male; D008875:Middle Aged; D011758:Pyrroles / Q000627:therapeutic use*; D013223:Statistics as Topic; D016896:Treatment Outcome; D018084:Ultrasonography, Interventional
chemical_list: D015415:Biomarkers; D008078:Cholesterol, LDL; D006538:Heptanoic Acids; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D000960:Hypolipidemic Agents; D011758:Pyrroles; D000069059:Atorvastatin