title: Factors underlying regression of coronary atheroma with potent statin therapy.
abstract: OBJECTIVE
  Statins can inhibit the progression of coronary atherosclerosis. We aimed to characterize clinical factors that associate with differing measures of coronary atheroma volume following potent statin therapy.
  
  
  RESULTS
  SATURN employed serial intravascular ultrasound (IVUS) to monitor changes in measures of coronary atheroma burden [total atheroma volume (TAV) and per cent atheroma volume (PAV)] in 1039 patients with coronary artery disease, treated with rosuvastatin (40 mg) or atorvastatin (80 mg) daily for 24 months. Rosuvastatin-treated patients demonstrated greater reductions in low-density lipoprotein cholesterol (LDL-C, 47 vs. 40%, P < 0.001) and greater increases in high-density lipoprotein cholesterol (HDL-C, 13 vs. 10%, P = 0.02). These alterations in the lipid profile associated with greater TAV (-6.4 vs. -4.4 mm(3), P = 0.01), but not PAV (-1.22 vs. -0.99%, P = 0.17) regression. Greater TAV reductions with rosuvastatin vs. atorvastatin occurred in patients with diabetes (P = 0.01, treatment by diabetic status interaction P-value 0.05). Greater PAV reductions with rosuvastatin were evident in females (P = 0.01, treatment by sex interaction P-value 0.03) and in those with greater than or equal to median baseline LDL-C (P = 0.02, treatment by LDL-C group interaction P-value 0.03) or HDL-C levels (P = 0.02, treatment by HDL-C group interaction P-value 0.04). On multivariable analysis assessing change in TAV and PAV, both higher baseline TAV and PAV independently associated with TAV and PAV regression, respectively (standardized estimates: TAV -0.25, P < 0.001; PAV -0.23, P < 0.001).
  
  
  CONCLUSIONS
  Higher-risk patients, particularly those with greater baseline coronary atheroma volume, are more likely to experience less disease progression with potent statin therapy.
authors: Department of Cardiovascular Medicine, Cleveland Clinic, Cleveland, OH, USA.
authors: Rishi
authors: R
authors: Puri
authors: Steven E
authors: SE
authors: Nissen
authors: Christie M
authors: CM
authors: Ballantyne
authors: Phillip J
authors: PJ
authors: Barter
authors: M John
authors: MJ
authors: Chapman
authors: Raimund
authors: R
authors: Erbel
authors: Peter
authors: P
authors: Libby
authors: Joel S
authors: JS
authors: Raichlen
authors: Julie
authors: J
authors: St John
authors: Kathy
authors: K
authors: Wolski
authors: Kiyoko
authors: K
authors: Uno
authors: Yu
authors: Y
authors: Kataoka
authors: Stephen J
authors: SJ
authors: Nicholls
mesh_terms: D000704:Analysis of Variance; D000069059:Atorvastatin; D008076:Cholesterol, HDL / Q000187:drug effects; D008078:Cholesterol, LDL / Q000187:drug effects; D003324:Coronary Artery Disease / Q000000981:diagnostic imaging / Q000188:drug therapy* / Q000473:pathology; D019160:Endosonography / Q000379:methods; 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 / Q000000981:diagnostic imaging / Q000188:drug therapy* / Q000473:pathology; D011743:Pyrimidines / Q000627:therapeutic use*; D011758:Pyrroles / Q000627:therapeutic use*; D000068718:Rosuvastatin Calcium; D013449:Sulfonamides / Q000627:therapeutic use*
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
keywords: Atherosclerosis; IVUS; Risk factors; Statins