title: A randomized placebo-controlled study on the effect of nifedipine on coronary endothelial function and plaque formation in patients with coronary artery disease: the ENCORE II study.
abstract: OBJECTIVE
  Endothelial dysfunction and plaque formation are features of atherosclerosis. Inhibition of L-type calcium channels or HMG-CoA pathway improves endothelial function and reduces plaque size. Thus, we investigated in stable coronary artery disease (CAD) the effects of a calcium antagonist on coronary endothelial function and plaque size.
  
  
  RESULTS
  In 454 patients undergoing PCI, acetylcholine (10(-6) to 10(-4) M) was infused in a coronary segment without significant CAD. Changes in coronary diameter were measured and an intravascular ultrasound examination (IVUS) was performed. On top of statin therapy, patients were randomized in a double-blind fashion to placebo or nifedipine GITS 30-60 mg/day and followed for 18-24 months. Blood pressure was lower on nifedipine than on placebo by 5.8/2.1 mmHg (P < 0.001) as was total and LDL cholesterol (4.8 mg/dL; P = 0.495), while HDL was higher (3.6 mg/dL; P = 0.026). In the most constricting segment, nifedipine reduced vasoconstriction to acetylcholine (14.0% vs. placebo 7.7%; P < 0.0088). The percentage change in plaque volume with nifedipine and placebo, respectively, was 1.0 and 1.9%, ns.
  
  
  CONCLUSIONS
  The ENCORE II trial demonstrates in a multi-centre setting that calcium channel blockade with nifedipine for up to 2 years improves coronary endothelial function on top of statin treatment, but did not show an effect of nifedipine on plaque volume.
authors.affiliation: Department of Cardiology, Universitätsspital, Ramistrassee 100, CH-8091 Zürich, Switzerland. cardiotfl@gmx.ch
authors.forename: Thomas Felix
authors.initials: TF
authors.lastname: Lüscher
authors.forename: Michael
authors.initials: M
authors.lastname: Pieper
authors.forename: Michael
authors.initials: M
authors.lastname: Tendera
authors.forename: Mathy
authors.initials: M
authors.lastname: Vrolix
authors.forename: Wolfgang
authors.initials: W
authors.lastname: Rutsch
authors.forename: Frank
authors.initials: F
authors.lastname: van den Branden
authors.forename: Robert
authors.initials: R
authors.lastname: Gil
authors.forename: Karl-Otto
authors.initials: KO
authors.lastname: Bischoff
authors.forename: Michael
authors.initials: M
authors.lastname: Haude
authors.forename: Dieter
authors.initials: D
authors.lastname: Fischer
authors.forename: Thomas
authors.initials: T
authors.lastname: Meinertz
authors.forename: Thomas
authors.initials: T
authors.lastname: Münzel
mesh_terms: D000109:Acetylcholine; D000328:Adult; D000368:Aged; D015906:Angioplasty, Balloon, Coronary; D001794:Blood Pressure / Q000187:drug effects; D002121:Calcium Channel Blockers / Q000009:adverse effects / Q000627:therapeutic use*; D003131:Combined Modality Therapy; D003324:Coronary Artery Disease / Q000188:drug therapy* / Q000473:pathology / Q000503:physiopathology / Q000628:therapy; D003331:Coronary Vessels / Q000187:drug effects* / Q000503:physiopathology; D018450:Disease Progression; D004311:Double-Blind Method; D004730:Endothelium, Vascular / Q000187:drug effects* / Q000503:physiopathology; D005260:Female; D006801:Humans; D008055:Lipids / Q000097:blood; D008297:Male; D008875:Middle Aged; D009543:Nifedipine / Q000009:adverse effects / Q000627:therapeutic use*; D014665:Vasodilator Agents; D014666:Vasomotor System / Q000187:drug effects / Q000503:physiopathology
chemical_list: D002121:Calcium Channel Blockers; D008055:Lipids; D014665:Vasodilator Agents; D009543:Nifedipine; D000109:Acetylcholine