title: Preprocedural statin medication reduces the extent of periprocedural non-Q-wave myocardial infarction.
abstract: BACKGROUND
  Stenting-related myocardial injury has been recognized as a frequent and prognostically important event, the extent of which depends on microcirculatory impairment in association with platelet aggregation, inflammation, and increased oxidative stress. Recent studies underscored the non-lipid-lowering effects of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (statins) with antithrombotic, antiinflammatory, and antioxidative aspects. Thus, we tested the hypothesis that preprocedural statin therapy is associated with a reduction in the extent of stenting-related myocardial injury.
  
  
  RESULTS
  We stratified 296 consecutive patients who were undergoing stenting of a de novo stenosis according to the preprocedural status of statin therapy (229 statin-treated and 67 control patients). Incidence of periprocedural myocardial injury was assessed by analysis of creatine kinase (CK; upper limit of normal [ULN] 70 IU/L for women, 80 IU/L for men) and cardiac troponin T (cTnT; bedside test; threshold 0.1 ng/mL) before and 6, 12, and 24 hours after the intervention. Relative to control patients, the incidence of CK elevation >3x ULN was more than 90% lower in statin-treated patients (0.4% versus 6.0%, P=0.01). Statin therapy was the only factor independently associated with a lower risk of CK elevation >3x ULN (OR: 0.08, 95% CI: 0.01 to 0.75; P=0.03). The overall incidences of CK and cardiac troponin T elevation were slightly lower in statin-treated than in control patients (14.4% versus 20.9%, P=0.3, and 17.9% versus 22.4%, P=0.5, respectively).
  
  
  CONCLUSIONS
  Preprocedural statin therapy is associated with a reduction in the incidence of larger-sized, stenting-related myocardial infarctions. Prospective, randomized trials are warranted to further assess this cardioprotective effect of statins in coronary intervention.
authors.affiliation: Department of Cardiology, University Clinic Essen, Essen, Germany.
authors.forename: Joerg
authors.initials: J
authors.lastname: Herrmann
authors.forename: Amir
authors.initials: A
authors.lastname: Lerman
authors.forename: Dietrich
authors.initials: D
authors.lastname: Baumgart
authors.forename: Lothar
authors.initials: L
authors.lastname: Volbracht
authors.forename: Rainer
authors.initials: R
authors.lastname: Schulz
authors.forename: Clemens
authors.initials: C
authors.lastname: von Birgelen
authors.forename: Michael
authors.initials: M
authors.lastname: Haude
authors.forename: Gerd
authors.initials: G
authors.lastname: Heusch
authors.forename: Raimund
authors.initials: R
authors.lastname: Erbel
mesh_terms: D015415:Biomarkers / Q000032:analysis; D002316:Cardiotonic Agents / Q000627:therapeutic use; D023921:Coronary Stenosis / Q000601:surgery; D003402:Creatine Kinase / Q000032:analysis; D018572:Disease-Free Survival; D004562:Electrocardiography; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use*; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000175:diagnosis / Q000517:prevention & control*; D009206:Myocardium / Q000737:chemistry / Q000201:enzymology; D015607:Stents / Q000009:adverse effects; D016896:Treatment Outcome; D020107:Troponin T / Q000032:analysis
chemical_list: D015415:Biomarkers; D002316:Cardiotonic Agents; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D020107:Troponin T; D003402:Creatine Kinase