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(Circulation. 2002;106:2180.)
© 2002 American Heart Association, Inc.
Brief Rapid Communications |
From the Department of Cardiology (J.H, D.B., C.v.B., M.H., R.E.), the Department of Clinical Chemistry (L.V.), and the Department of Pathophysiology (R.S., G.H.), University Clinic Essen, Essen, Germany, and the Division of Cardiovascular Diseases (J.H., A.L.), Mayo Clinic, Rochester, Minn.
Correspondence to Professor Raimund.Erbel, MD, Department of Cardiology, University of Essen, Hufelandstr. 55, 45122 Essen, Germany. E-mail erbel{at}uni-essen.de
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 nonlipid-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.
Methods and 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.
Key Words: creatine kinase inhibitors myocardial infarction stents
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