title: Effect of atherosclerotic regression on total luminal size of coronary arteries as determined by intravascular ultrasound.
abstract: We assessed vascular changes during atherosclerosis regression. Compensatory enlargement of coronary arteries accommodates plaque burden during atherosclerosis development. Lipid-lowering therapy has altered the natural history of coronary atherosclerosis, but the arterial changes that occur during disease regression need to be clarified. Intravascular ultrasound was performed at baseline and after approximately 18 months in 432 patients with coronary disease. Mean plaque, lumen, and total vessel area were computed in a 30-mm coronary segment of interest. Mean low-density lipoprotein cholesterol level was 2.4 mmol/L, and 88% of patients received statins. Overall, changes in plaque and total vessel areas were highly correlated (r = 0.82, p <0.0001). Among the 227 patients with plaque regression, the plaque area decrease was -0.58 +/- 0.54 mm(2), and changes in total vessel and lumen areas were -1.02 +/- 1.10 and -0.44 +/- 0.86 mm(2), respectively. The decrease in plaque area correlated better with the change in total vessel area (r = 0.64, p <0.0001) than with the change in lumen area (r = 0.20, p = 0.003). The relation between plaque regression and decrease in total vessel area was significantly better (p = 0.019) for patients with a >40% atheroma area (r = 0.72; p <0.0001) than for those with <or=40% (r = 0.48; p = 0.0004). In conclusion, regression of atherosclerotic plaque is generally accompanied by a decrease in total vessel size, without an increase in luminal dimensions. This reverse vascular remodeling may be responsible for the "regression paradox," whereby secondary prevention is associated with clinical benefits despite minimal improvement in coronary lumen dimensions.
authors.affiliation: Department of Medicine and Research Center of the Montreal Heart Institute, Université de Montreal, Montreal, Quebec, Canada. jean-claude.tardif@icm-mhi.org
authors.forename: Jean-Claude
authors.initials: JC
authors.lastname: Tardif
authors.forename: Jean
authors.initials: J
authors.lastname: Grégoire
authors.forename: Philippe L
authors.initials: PL
authors.lastname: L'Allier
authors.forename: Reda
authors.initials: R
authors.lastname: Ibrahim
authors.forename: Marc-André
authors.initials: MA
authors.lastname: Lavoie
authors.forename: Michel
authors.initials: M
authors.lastname: LeMay
authors.forename: Eric
authors.initials: E
authors.lastname: Cohen
authors.forename: Sylvie
authors.initials: S
authors.lastname: Levesque
authors.forename: Pierre-Frédéric
authors.initials: PF
authors.lastname: Keller
authors.forename: Therese
authors.initials: T
authors.lastname: Heinonen
authors.forename: Marie-Claude
authors.initials: MC
authors.lastname: Guertin
mesh_terms: D000081:Acetamides; D000085:Acetates / Q000627:therapeutic use; D008078:Cholesterol, LDL / Q000097:blood; D003324:Coronary Artery Disease / Q000000981:diagnostic imaging* / Q000188:drug therapy / Q000473:pathology; D003331:Coronary Vessels / Q000000981:diagnostic imaging* / Q000473:pathology; D018450:Disease Progression; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use; D007091:Image Processing, Computer-Assisted; D008297:Male; D008875:Middle Aged; D012044:Regression Analysis; D013449:Sulfonamides; D013451:Sulfonic Acids / Q000627:therapeutic use; D014109:Total Lung Capacity / Q000502:physiology; D018084:Ultrasonography, Interventional / Q000379:methods*
chemical_list: D000081:Acetamides; D000085:Acetates; D008078:Cholesterol, LDL; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D013449:Sulfonamides; D013451:Sulfonic Acids; C423185:avasimibe