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European Heart Journal 2001 22(7):587-595; doi:10.1053/euhj.2000.2313
Copyright © 2001 by the European Society of Cardiology.
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Statin therapy is associated with reduced restenosis rates after coronary stent implantation in carriers of the PlA2allele of the platelet glycoprotein IIIa gene

D.H Walter, V Schächinger, M Elsner, S Mach, S Dimmeler, W Auch-Schwelk and A.M Zeiherf1

Department of Internal Medicine IV, Division of Cardiology, University of Frankfurt, Germany

revised June 10, 2000; accepted June 21, 2000

Abstract

Aims Platelets play a central role in the restenosis process by inducing neointimal proliferation after coronary interventions. Glycoprotein IIb/IIIa PlA2polymorphism has been associated with the occurrence of acute coronary syndromes and increased restenosis rates. Statins have been shown to exert potent antiproliferative, antiinflammatory and antithrombotic properties, thereby potentially interfering with the major processes of in-stent restenosis. Therefore, we sought to find out whether statin therapy interferes with restenosis and clinical outcome at 6 months following successful coronary stent implantation in the presence or absence of the PlA2allele.

Methods and Results Six hundred and fifty consecutive patients were followed for 6 months after coronary stent insertion. Carriers of the PlA2allele demonstrated a significantly increased restenosis rate, which was abrogated by statin therapy (50·9% vs 28·6%, P=0·01). Moreover, statin therapy was associated with a significant reduction (28·2% vs 49·3%,P <0·01) in the occurrence of major adverse coronary events (myocardial infarction, cardiac death, target vessel revascularization) in the 6 months after the intervention in patients with the PlA2allele.

Conclusion Statin therapy reduces increased stent restenosis rates and improves clinical outcome following coronary stent implantation in patients bearing the PlA2allele, suggesting that statins interfere with the functional consequence of a genetically determined platelet-mediated risk factor associated with PlA2polymorphism.

Key Words: Stents, restenosis, platelets, glycoproteins, statin

f1 Correspondence: Andreas M. Zeiher, MD, Department of Internal Medicine IV, Division of Cardiology, University of Frankfurt, Theodor-Stern-Kai 7, 60590 Frankfurt, Germany.


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