title: Protective role of chronic statin therapy in reducing myocardial damage during percutaneous coronary intervention.
abstract: OBJECTIVE
  Percutaneous coronary intervention (PCI) is frequently associated with troponin I (TnI) elevation. Experimental studies suggest that statins may reduce ischaemia-reperfusion myocardial injury. The study objective was to verify whether chronic treatment with statins might reduce the occurrence and the extent of periprocedural myocardial damage in patients undergoing PCI.
  
  
  METHODS
  Five hundred and fifty-two consecutive patients undergoing PCI were included: 279 were not on statins before PCI, 273 were on statins. TnI levels >or= 0.3 ng/ml were considered indicative of myocardial injury.
  
  
  RESULTS
  Statin-treated patients had a higher prevalence of hyperlipidaemia, previous myocardial infarction, and revascularization procedures. Coronary angiography also documented a higher prevalence of multivessel disease. No difference between the two groups was observed regarding the PCI-treated vessel, type of lesions, use of stents and of anti-IIb/IIIa inhibitors. Patients on statins showed the lowest incidence of TnI >or= 0.3 ng/ml (29 vs. 48%, P = 0.00001) and of creatine kinase-MB elevation (7 vs. 12%, P = 0.04). The mean peak TnI levels were significantly lower in patients on statins (1.07 +/- 3.8 vs. 2.73 +/- 12.3, P = 0.00006). Multivariate analysis identified preprocedural statin therapy as the only independent negative predictor of postprocedural abnormal TnI levels (odds ratio = 0.52; 95% confidence intervals 0.34-0.79; P = 0.003).
  
  
  CONCLUSIONS
  This study shows that chronic therapy with statins reduces the incidence of periprocedural myocardial damage after PCI. The beneficial effect of statins was independent of either the most important clinical and angiographic characteristics or the use of other cardiovascular drugs including beta-blockers. These data support the specific cardioprotective role of statins.
authors.affiliation: Department of Cardiology, Policlinico of Monza, Monza (MI), Italy. cauguadro@libero.it
authors.forename: Carla
authors.initials: C
authors.lastname: Auguadro
authors.forename: Mariella
authors.initials: M
authors.lastname: Manfredi
authors.forename: Filippo
authors.initials: F
authors.lastname: Scalise
authors.forename: Andrea
authors.initials: A
authors.lastname: Mortara
authors.forename: Giuseppe
authors.initials: G
authors.lastname: Specchia
mesh_terms: D000787:Angina Pectoris / Q000000981:diagnostic imaging / Q000628:therapy*; D015906:Angioplasty, Balloon, Coronary; D015415:Biomarkers / Q000097:blood; D016009:Chi-Square Distribution; D017023:Coronary Angiography; D003402:Creatine Kinase / Q000097:blood; D052279:Creatine Kinase, MB Form / Q000097:blood; D004359:Drug Therapy, Combination; D005260:Female; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000008:administration & dosage*; D016015:Logistic Models; D008297:Male; D017202:Myocardial Ischemia / Q000000981:diagnostic imaging / Q000628:therapy*; D009206:Myocardium / Q000378:metabolism / Q000473:pathology*; D012189:Retrospective Studies; D040242:Risk Reduction Behavior; D018709:Statistics, Nonparametric; D016896:Treatment Outcome; D019210:Troponin I / Q000097:blood
chemical_list: D015415:Biomarkers; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D019210:Troponin I; D003402:Creatine Kinase; D052279:Creatine Kinase, MB Form