title: High-intensity statin therapy alters the natural history of diabetic coronary atherosclerosis: insights from SATURN.
abstract: OBJECTIVE
  Although statins can induce coronary atheroma regression, this benefit has yet to be demonstrated in diabetic individuals. We tested the hypothesis that high-intensity statin therapy may promote coronary atheroma regression in patients with diabetes.
  
  
  METHODS
  The Study of Coronary Atheroma by Intravascular Ultrasound: Effect of Rosuvastatin Versus Atorvastatin (SATURN) used serial intravascular ultrasound measures of coronary atheroma volume in patients treated with rosuvastatin 40 mg or atorvastatin 80 mg for 24 months. This analysis compared changes in biochemistry and coronary percent atheroma volume (PAV) in patients with (n = 159) and without (n = 880) diabetes.
  
  
  RESULTS
  At baseline, patients with diabetes had lower LDL cholesterol (LDL-C) and HDL cholesterol (HDL-C) levels but higher triglyceride and CRP levels compared with patients without diabetes. At follow-up, diabetic patients had lower levels of LDL-C (61.0 ± 20.5 vs. 66.4 ± 22.9 mg/dL, P = 0.01) and HDL-C (46.3 ± 10.6 vs. 49.9 ± 12.0 mg/dL, P < 0.001) but higher levels of triglycerides (127.6 [98.8, 163.0] vs. 113.0 mg/dL [87.6, 151.9], P = 0.001) and CRP (1.4 [0.7, 3.3] vs. 1.0 [0.5, 2.1] mg/L, P = 0.001). Both patients with and without diabetes demonstrated regression of coronary atheroma as measured by change in PAV (-0.83 ± 0.13 vs. -1.15 ± 0.13%, P = 0.08). PAV regression was less in diabetic compared with nondiabetic patients when on-treatment LDL-C levels were >70 mg/dL (-0.31 ± 0.23 vs. -1.01 ± 0.21%, P = 0.03) but similar when LDL-C levels were ≤70 mg/dL (-1.09 ± 0.16 vs. -1.24 ± 0.16%, P = 0.50).
  
  
  CONCLUSIONS
  High-intensity statin therapy alters the progressive nature of diabetic coronary atherosclerosis, yielding regression of disease in diabetic and nondiabetic patients.
authors.affiliation: Department of Cardiovascular Medicine, Cleveland Clinic, Cleveland, OH.
authors.forename: Brian
authors.initials: B
authors.lastname: Stegman
authors.affiliation: Department of Cardiovascular Medicine, Cleveland Clinic, Cleveland, OH C5Research, Department of Cardiovascular Medicine, Cleveland Clinic, Cleveland, OH.
authors.forename: Rishi
authors.initials: R
authors.lastname: Puri
authors.affiliation: Department of Cardiovascular Medicine, Cleveland Clinic, Cleveland, OH.
authors.forename: Leslie
authors.initials: L
authors.lastname: Cho
authors.affiliation: C5Research, Department of Cardiovascular Medicine, Cleveland Clinic, Cleveland, OH.
authors.forename: Mingyuan
authors.initials: M
authors.lastname: Shao
authors.affiliation: Section of Cardiovascular Research, Baylor College of Medicine, and the Methodist DeBakey Heart and Vascular Center, Houston, TX.
authors.forename: Christie M
authors.initials: CM
authors.lastname: Ballantyne
authors.affiliation: Centre for Vascular Research, University of New South Wales, Sydney, Australia.
authors.forename: Phillip J
authors.initials: PJ
authors.lastname: Barter
authors.affiliation: INSERM Dyslipidaemia and Atherosclerosis Research Unit, Pitié-Salpètrière University Hospital, Paris, France.
authors.forename: M John
authors.initials: MJ
authors.lastname: Chapman
authors.affiliation: West German Heart Center, Essen, Germany.
authors.forename: Raimund
authors.initials: R
authors.lastname: Erbel
authors.affiliation: Cardiovascular Division, Brigham and Women's Hospital, Boston, MA.
authors.forename: Peter
authors.initials: P
authors.lastname: Libby
authors.affiliation: AstraZeneca, Wilmington, DE.
authors.forename: Joel S
authors.initials: JS
authors.lastname: Raichlen
authors.affiliation: Department of Cardiovascular Medicine, Cleveland Clinic, Cleveland, OH.
authors.forename: Kiyoko
authors.initials: K
authors.lastname: Uno
authors.affiliation: South Australian Health and Medical Research Institute, University of Adelaide, Adelaide, Australia.
authors.forename: Yu
authors.initials: Y
authors.lastname: Kataoka
authors.affiliation: Department of Cardiovascular Medicine, Cleveland Clinic, Cleveland, OH C5Research, Department of Cardiovascular Medicine, Cleveland Clinic, Cleveland, OH.
authors.forename: Steven E
authors.initials: SE
authors.lastname: Nissen
authors.affiliation: South Australian Health and Medical Research Institute, University of Adelaide, Adelaide, Australia stephen.nicholls@sahmri.com.
authors.forename: Stephen J
authors.initials: SJ
authors.lastname: Nicholls
mesh_terms: D000368:Aged; D000069059:Atorvastatin; D008076:Cholesterol, HDL / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood; D003324:Coronary Artery Disease / Q000188:drug therapy; D003920:Diabetes Mellitus / Q000188:drug therapy; D005260:Female; D005464:Fluorobenzenes / Q000627:therapeutic use*; D006538:Heptanoic Acids / Q000627:therapeutic use*; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use*; D008297:Male; D008875:Middle Aged; D058226:Plaque, Atherosclerotic / Q000188:drug therapy* / Q000209:etiology; D011743:Pyrimidines / Q000627:therapeutic use*; D011758:Pyrroles / Q000627:therapeutic use*; D000068718:Rosuvastatin Calcium; D013449:Sulfonamides / Q000627:therapeutic use*; D018084:Ultrasonography, Interventional
chemical_list: D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D005464:Fluorobenzenes; D006538:Heptanoic Acids; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D011743:Pyrimidines; D011758:Pyrroles; D013449:Sulfonamides; D000068718:Rosuvastatin Calcium; D000069059:Atorvastatin