American Heart Journal
Volume 160, Issue 2 , Pages 355-361, August 2010

Platelet response to clopidogrel and restenosis in patients treated predominantly with drug-eluting stents

  • Stefanie Schulz, MD

      Affiliations

    • Deutsches Herzzentrum, Technische Universität, Munich, Germany
    • Corresponding Author InformationReprint requests: Stefanie Schulz, MD, Deutsches Herzzentrum, Lazarettstr. 36, 80636 Munich, Germany.
  • ,
  • Dirk Sibbing, MD

      Affiliations

    • Deutsches Herzzentrum, Technische Universität, Munich, Germany
  • ,
  • Sigmund Braun, MD

      Affiliations

    • Deutsches Herzzentrum, Technische Universität, Munich, Germany
  • ,
  • Tanja Morath, MD

      Affiliations

    • Deutsches Herzzentrum, Technische Universität, Munich, Germany
  • ,
  • Julinda Mehilli, MD

      Affiliations

    • Deutsches Herzzentrum, Technische Universität, Munich, Germany
  • ,
  • Steffen Massberg, MD

      Affiliations

    • Deutsches Herzzentrum, Technische Universität, Munich, Germany
  • ,
  • Robert A. Byrne, MB BCh

      Affiliations

    • Deutsches Herzzentrum, Technische Universität, Munich, Germany
  • ,
  • Albert Schömig, MD

      Affiliations

    • Deutsches Herzzentrum, Technische Universität, Munich, Germany
    • First Medizinische Klinik, Klinikum rechts der Isar, Technische Universität, Munich, Germany
  • ,
  • Adnan Kastrati, MD

      Affiliations

    • Deutsches Herzzentrum, Technische Universität, Munich, Germany

Received 12 March 2010; accepted 6 May 2010.

Background

Preclinical studies suggest a relationship between early thrombotic response after vascular injury and later development of restenosis. The aim of this study was to assess the impact of platelet response to clopidogrel on the risk of restenosis after drug-eluting stenting (DES).

Methods

A total of 1,608 consecutive patients were previously enrolled in a study on the relation between platelet reactivity and outcomes after DES. All patients received a loading dose of 600 mg clopidogrel. Blood samples for the assessment of adenosine diphosphate–induced platelet aggregation with multiple electrode platelet aggregometry were drawn directly before percutaneous coronary intervention. Clopidogrel low response was defined as upper quintile of multiple electrode platelet aggregometry measurements. Accordingly, 323 patients (20%) were considered as low and 1,285 (80%) as normal responders. Primary end point of the present study was target lesion revascularization at 1 year. Secondary end points included binary angiographic restenosis and late lumen loss at 6- to 8-month angiography.

Results

Target lesion revascularization rates were comparable in both groups (10.9% vs 9.5%, hazard rate [HR] 1.2, 95% CI 0.8-1.7, P = .441). Follow-up angiography revealed no difference in binary angiographic restenosis (13.9% vs 15.9%, P = .445) and late lumen loss (0.32 ± 0.64 vs 0.35 ± 0.63 mm, P = .477). Low responders had significantly more stent thromboses (2.5% vs 0.5%, HR 5.4, 95% CI 1.9-15.6, P = .002), Q wave myocardial infarctions (2.5% vs 0.6%, HR 4.0, 95% CI 1.5-10.7, P = .005), and ischemic strokes (1.3% vs 0.2%, HR 5.4, 95% CI 1.2-24.0, P = .028) at 1 year.

Conclusion

Low platelet responsiveness to clopidogrel, a known predictor of thrombotic complications, does not have a significant impact on restenosis after DES.

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PII: S0002-8703(10)00354-6

doi:10.1016/j.ahj.2010.05.003

American Heart Journal
Volume 160, Issue 2 , Pages 355-361, August 2010