title: Intensity of lipid lowering with statins and brachial artery vascular endothelium reactivity after acute coronary syndromes (from the BRAVER trial).
abstract: The time course and differential effects of statin regimens on endothelial function after acute coronary syndromes (ACSs) are unknown and could contribute to the superiority of a more intense strategy. A subset of subjects who were enrolled in the PROVE IT-TIMI 22 trial (n = 50) underwent evaluation of vascular reactivity by high-resolution brachial ultrasound. Endothelium-dependent flow-mediated dilation (FMD) and endothelium-independent sublingual nitroglycerin-mediated dilation (NMD) were measured at baseline and at 48 hours, 1 month, and 4 months after the initiation of 40 mg of pravastatin (n = 26) or 80 mg of atorvastatin (n = 24). After 4 months, low-density lipoprotein cholesterol was decreased by 32% in the atorvastatin group but was not different from baseline after ACS in the pravastatin group. C-reactive protein decreased similarly in the 2 groups. Brachial artery diameters at rest were similar in the 2 groups and at each time point of the trial. FMD and NMD increased significantly after 4 months by 27% and 24%, respectively (p <0.05), with no difference between groups. There was no correlation between the change in FMD and the change in lipids or C-reactive protein. In subjects who had received previous statin therapy (n = 15), there was no significant variation in FMD (p = 0.140) and NMD (p = 0.129). In conclusion, initiation of statin therapy soon after ACS is associated with improvements in endothelium-dependent and independent vascular reactivities after 4 months.
authors.affiliation: The Research Center of the Montreal Heart Institute and the Department of Medicine of the University of Montreal, Montreal, Quebec, Canada. jocelyn.dupuis@bellnet.ca
authors.forename: Jocelyn
authors.initials: J
authors.lastname: Dupuis
authors.forename: Jean-Claude
authors.initials: JC
authors.lastname: Tardif
authors.forename: Jean-Lucien
authors.initials: JL
authors.lastname: Rouleau
authors.forename: Joseph
authors.initials: J
authors.lastname: Ricci
authors.forename: Malcolm
authors.initials: M
authors.lastname: Arnold
authors.forename: Eva
authors.initials: E
authors.lastname: Lonn
authors.forename: René
authors.initials: R
authors.lastname: Roux
authors.forename: Lawrence M
authors.initials: LM
authors.lastname: Title
authors.forename: Robert
authors.initials: R
authors.lastname: Amyot
authors.forename: Nickie
authors.initials: N
authors.lastname: Bonafede
authors.forename: Anna
authors.initials: A
authors.lastname: Woo
authors.forename: Christopher P
authors.initials: CP
authors.lastname: Cannon
mesh_terms: D000208:Acute Disease; D000924:Anticholesteremic Agents / Q000627:therapeutic use*; D000069059:Atorvastatin; D001783:Blood Flow Velocity / Q000502:physiology; D001916:Brachial Artery / Q000000981:diagnostic imaging / Q000503:physiopathology*; D008078:Cholesterol, LDL / Q000097:blood* / Q000187:drug effects; D003327:Coronary Disease / Q000097:blood / Q000188:drug therapy* / Q000503:physiopathology; D004730:Endothelium, Vascular / Q000187:drug effects / Q000503:physiopathology*; D005260:Female; D006538:Heptanoic Acids / Q000627:therapeutic use*; D006801:Humans; D008297:Male; D008875:Middle Aged; D017035:Pravastatin / Q000627:therapeutic use*; D011379:Prognosis; D011758:Pyrroles / Q000627:therapeutic use*; D013577:Syndrome; D014463:Ultrasonography; D014664:Vasodilation / Q000187:drug effects / Q000502:physiology
chemical_list: D000924:Anticholesteremic Agents; D008078:Cholesterol, LDL; D006538:Heptanoic Acids; D011758:Pyrroles; D000069059:Atorvastatin; D017035:Pravastatin