title: Switching to aggressive statin improves vascular endothelial function in patients with stable coronary artery disease.
abstract: OBJECTIVE
  The clinical relevance of the suggested pleiotropic effects of hydroxymethylglutaryl coenzyme A reductase inhibitors (statins) is controversial. Aggressive statins effectively reduce lipid levels, but whether their other effects are more powerful than those of regular statins is unknown.
  
  
  METHODS
  We enrolled 32 patients (mean age, 65 y; male, 23) who had undergone coronary revascularization over 6 months previously and whose serum LDL cholesterol levels persisted at >100 mg/dL, regardless of pravastatin (10 mg/day). Before and 1 and 6 months after switching to atorvastatin (10 mg/day), we evaluated lipid profiles, including RLP-C (remnant-like particle cholesterol), high sensitive CRP (hsCRP), soluble CD40 ligand (sCD40L), TBARS (thiobarbituric acid reactive substances), and endothelial function determined from flow-mediated dilation (FMD) of the brachial artery.
  
  
  RESULTS
  One month on atorvastatin lowered LDL cholesterol by 24% (131 to 100 mg/dL, p<0.001). In addition, RLP-C, sCD40L and hsCRP significantly decreased, whereas FMD did not change. After 6 months of this therapy, FMD significantly improved compared to baseline values (5.1 vs 3.6%, p=0.04). Changes in FMD and in total and RLP cholesterol significantly correlated. Moreover, FMD was remarkably improved in patients who achieved target LDL levels (<100 mg/dL).
  
  
  CONCLUSIONS
  Switching from a regular to an aggressive statin can improve endothelial function at 6 months in patients with previous coronary artery disease. This effect is suggested to be mainly due to the lipid-lowering effect. Achievement and maintenance of the target LDL level by switching statins is beneficial in the clinical setting.
authors.affiliation: First Department of Internal Medicine, Osaka Medical College, 2-7 Daigakumachi, Takatsuki, Osaka, Japan. in1026@poh.osaka-med.ac.jp
authors.forename: Masaaki
authors.initials: M
authors.lastname: Hoshiga
authors.forename: Kumiko
authors.initials: K
authors.lastname: Arishiro
authors.forename: Takahiro
authors.initials: T
authors.lastname: Nakakoji
authors.forename: Norihiko
authors.initials: N
authors.lastname: Miyazaki
authors.forename: Nobuyuki
authors.initials: N
authors.lastname: Negoro
authors.forename: Taichi
authors.initials: T
authors.lastname: Okabe
authors.forename: Eiko
authors.initials: E
authors.lastname: Kohbayashi
authors.forename: Tadashi
authors.initials: T
authors.lastname: Ishihara
authors.forename: Toshiaki
authors.initials: T
authors.lastname: Hanafusa
mesh_terms: D000328:Adult; D000368:Aged; D000924:Anticholesteremic Agents / Q000627:therapeutic use*; D000069059:Atorvastatin; D001794:Blood Pressure / Q000187:drug effects; D002097:C-Reactive Protein / Q000378:metabolism; D002784:Cholesterol / Q000378:metabolism; D008076:Cholesterol, HDL / Q000378:metabolism; D008078:Cholesterol, LDL / Q000378:metabolism; D003327:Coronary Disease / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D004730:Endothelium, Vascular / Q000378:metabolism*; D005260:Female; D006538:Heptanoic Acids / Q000627:therapeutic use*; D006801:Humans; D008055:Lipids / Q000032:analysis; D008074:Lipoproteins / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D017035:Pravastatin / Q000627:therapeutic use*; D011379:Prognosis; D011758:Pyrroles / Q000627:therapeutic use*; D012307:Risk Factors; D014280:Triglycerides / Q000378:metabolism
chemical_list: D000924:Anticholesteremic Agents; D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D006538:Heptanoic Acids; D008055:Lipids; D008074:Lipoproteins; D011758:Pyrroles; D014280:Triglycerides; C112017:remnant-like particle cholesterol; D002097:C-Reactive Protein; D002784:Cholesterol; D000069059:Atorvastatin; D017035:Pravastatin