title: [Early initiation of statin therapy in patients with acute myocardial infarction after successful percutaneous coronary intervention].
abstract: OBJECTIVE
  To evaluate the effect of statins on the prognosis of acute myocardial infarction after percutaneous coronary intervention (PCI).
  
  
  METHODS
  We reviewed 280 patients with acute myocardial infarction who underwent PCI within 12 hr after the onset of symptoms. Statin therapy was initiated in 72 patients within 8.6 +/- 7.6 days after the onset (statin group) but not in the remaining 208 (no statin group). The time sequential changes of low-density lipoprotein cholesterol (LDL-C) and C-reactive protein (CRP) levels, and the angiographic findings at 6 months after PCI were compared.
  
  
  RESULTS
  At onset, LDL-C levels in the statin group were significantly higher than those in the no statin group (140 +/- 35 vs 118 +/- 28 mg/dl, p < 0.01). However, at restudy, the values were similar between the two groups (113 +/- 19 vs 118 +/- 21 mg/dl, p = 0.19). CRP levels at restudy tended to be lower in the statin group than in the no statin group (0.11 +/- 0.12 vs 0.14 +/- 0.13 mg/dl, p = 0.07). Although the binary restenosis rates of the culprit lesion were almost equivalent (statin group 29% vs no statin group 23%, p = 0.30), new lesions in the non-culprit vessels tended to be found more frequently in the no statin group than in the statin group (13% vs 4%, p = 0.07). CRP levels at restudy were significantly higher in the patients with new lesions (n = 27) than in those without (n = 253; 0.25 +/- 0.17 vs 0.11 +/- 0.19 mg/dl, p < 0.01), whereas LDL-C levels were similar between the two groups (117 +/- 20 vs 113 +/- 27 mg/dl, p = 0.75). LDL-C, CRP at restudy and the rates of new lesions were similar in the patients receiving water-soluble statins (n = 42) and liposoluble statins (n = 30).
  
  
  CONCLUSIONS
  Statin therapy initiated at the early phase of acute myocardial infarction might prevent the development of new lesions in non-culprit vessels without any influence on the restenosis rate of the culprit lesion.
authors.affiliation: Cardiovascular Center, Saiseikai Kumamoto Hospital, Kumamoto.
authors.forename: Naoyuki
authors.initials: N
authors.lastname: Katayama
authors.forename: Koichi
authors.initials: K
authors.lastname: Nakao
authors.forename: Kenji
authors.initials: K
authors.lastname: Horiuchi
authors.forename: Hisao
authors.initials: H
authors.lastname: Ogawa
authors.forename: Takashi
authors.initials: T
authors.lastname: Honda
mesh_terms: D000368:Aged; D015906:Angioplasty, Balloon, Coronary; D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein; D008078:Cholesterol, LDL / Q000097:blood; D017023:Coronary Angiography; D003327:Coronary Disease / Q000517:prevention & control*; D005260:Female; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000008:administration & dosage*; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000175:diagnosis / Q000628:therapy*; D009821:Oils; D012189:Retrospective Studies; D012995:Solubility; D013997:Time Factors; D014867:Water
chemical_list: D015415:Biomarkers; D008078:Cholesterol, LDL; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D009821:Oils; D014867:Water; D002097:C-Reactive Protein