Clopidogrel: the future choice for preventing platelet activation during coronary stenting?

P A Gurbel1, C M O'Connor, C C Cummings

  • 1Center for Thrombosis Research, Sinai Hospital of Baltimore, 2401 West Belvedere Avenue, Schapiro Research Building-R202, Baltimore, MD 21215, USA.

Insights

Clopidogrel, a thienopyridine, offers an alternative to ticlopidine for preventing arterial and venous thrombi. While superior to aspirin in vascular disease, its superiority over ticlopidine in coronary stenting requires further investigation.

Area of Science:

  • Cardiology
  • Pharmacology
  • Thrombosis

Background:

  • Ticlopidine is established for stroke and coronary artery stenting.
  • Clopidogrel, a thienopyridine, inhibits ADP-induced platelet aggregation.
  • Clopidogrel demonstrated superiority over aspirin in the CAPRIE trial for atherosclerotic vascular disease.

Purpose of the Study:

  • To compare the antiplatelet efficacy of clopidogrel versus ticlopidine in coronary stenting.
  • To determine the effects of clopidogrel and ticlopidine on platelet and endothelial function.
  • To evaluate the impact of these effects on outcomes following coronary stent placement.

Main Methods:

  • Review of existing clinical trials and data on thienopyridines.
  • Analysis of platelet aggregation inhibition.
  • Assessment of effects on thrombus formation and endothelial function.

Main Results:

  • Clopidogrel is superior to aspirin in preventing ischemic events in atherosclerotic vascular disease.
  • Clopidogrel enhances reperfusion during stent placement by inhibiting platelet activation.
  • Direct comparison of clopidogrel and ticlopidine in coronary stenting is lacking.

Conclusions:

  • Clopidogrel presents a safe alternative to ticlopidine in interventional cardiology.
  • Further trials are needed to elucidate clopidogrel's benefits in coronary interventions, especially with new reperfusion techniques.
  • Clopidogrel's platelet inhibition may offer benefits in myocardial infarction and as an alternative to glycoprotein IIb/IIIa inhibitors.

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