title: Rosuvastatin combined with ramipril significantly reduced atheroma volume by anti-inflammatory mechanism: comparative analysis with rosuvastatin alone by intravascular ultrasound.
abstract: BACKGROUND
  We tested the effects of rosuvastatin combined with ramipril on atheroma volume and its mechanism in de novo, intermediate coronary artery disease.
  
  
  METHODS
  Subjects were randomly assigned to 2 treatment groups (rosuvastatin alone group; 20mg/day, combined group; rosuvastatin 20mg/day and ramipril 10mg/day). Total atheroma volume per 10mm segment (TAV/10mm), percent atheroma volume per 10mm segment (PAV/10mm) in entire indexed segments and TAV(most10), PAV(most10) in a 10mm subsegment with the greatest disease by intravascular ultrasound, and lipids, metabolic parameters (adiponectin, insulin sensitivity), biomarkers (hsCRP, matrix metalloproteinase-9) were analyzed at baseline and at 9-12 months follow-up.
  
  
  RESULTS
  A total of 40 patients (rosuvastatin group; 21, combined group; 19), 46 lesions (rosuvastatin group; 24, combined group; 22) were finally analyzed. Rosuvastatin alone significantly reduced TAV/10mm (-7.8 ± 17.4%, p<0.001) but did not change PAV/10mm, TAV(most10), PAV(most10) after therapy. In combined group, TAV/10mm, TAV(most10), PAV(most10) were significantly reduced after therapy (-10.7 ± 11.5%, -13.4 ± 14.5%, -2.7 ± 5.8%, p<0.001, <0.001 and p=0.04) but PAV/10mm did not change. The magnitude of changes of all IVUS derived parameters did not differ significantly between 2 groups. Of interest, the most important factor for the changes of PAV(most10) was the percent changes of LDL cholesterol (β=0.23, 95% CI [0.07-0.39], p=0.007) in rosuvastatin alone group and the changes in hsCRP (β=1.89, 95% CI [0.63-3.14], p=0.005) and baseline fasting blood glucose (β=0.06, 95% CI [0.01-0.11], p=0.02) in combined group by multivariate analysis.
  
  
  CONCLUSIONS
  Rosuvastatin combined ramipril therapy significantly reduced atheroma volume that was related with anti-inflammatory effects.
authors.affiliation: Division of Cardiovascular Disease, Gachon University Gil Hospital, Incheon, South Korea.
authors.forename: Seung Hwan
authors.initials: SH
authors.lastname: Han
authors.forename: Wook-Jin
authors.initials: WJ
authors.lastname: Chung
authors.forename: Woong Chol
authors.initials: WC
authors.lastname: Kang
authors.forename: Kyounghoon
authors.initials: K
authors.lastname: Lee
authors.forename: Yae Min
authors.initials: YM
authors.lastname: Park
authors.forename: Mi-Seung
authors.initials: MS
authors.lastname: Shin
authors.forename: Tae Hoon
authors.initials: TH
authors.lastname: Ahn
authors.forename: In Suck
authors.initials: IS
authors.lastname: Choi
authors.forename: Eak Kyun
authors.initials: EK
authors.lastname: Shin
mesh_terms: D000368:Aged; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000008:administration & dosage; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000008:administration & dosage*; D004359:Drug Therapy, Combination; D005260:Female; D005464:Fluorobenzenes / Q000008:administration & dosage*; D005500:Follow-Up Studies; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000008:administration & dosage; D008297:Male; D008875:Middle Aged; D058226:Plaque, Atherosclerotic / Q000000981:diagnostic imaging* / Q000188:drug therapy* / Q000473:pathology; D011446:Prospective Studies; D011743:Pyrimidines / Q000008:administration & dosage*; D017257:Ramipril / Q000008:administration & dosage*; D000068718:Rosuvastatin Calcium; D013449:Sulfonamides / Q000008:administration & dosage*; D018084:Ultrasonography, Interventional / Q000379:methods
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D000894:Anti-Inflammatory Agents, Non-Steroidal; D005464:Fluorobenzenes; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D011743:Pyrimidines; D013449:Sulfonamides; D000068718:Rosuvastatin Calcium; D017257:Ramipril