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Published on: February 26, 2013

Abrupt cessation of one-year clopidogrel treatment is not associated with thrombotic events

Nina Djukanovic1, Zoran Todorovic, Slobodan Obradovic

  • 1Department of Cardiology, Institute for Cardiovascular Diseases, Clinical Centre of Serbia, Serbia.

Journal of Pharmacological Sciences
|August 9, 2011
PubMed

Insights

Discontinuing one year of clopidogrel therapy after coronary stent implantation showed a low rate of thrombotic events. Platelet aggregation increased with adenosine diphosphate and arachidonic acid, but not thrombin receptor activating peptide.

Area of Science:

  • Cardiology
  • Pharmacology
  • Thrombosis

Background:

  • Dual antiplatelet therapy with aspirin and clopidogrel is standard after coronary stent implantation.
  • The optimal duration of clopidogrel therapy and the risks of its discontinuation require further investigation.

Purpose of the Study:

  • To evaluate the incidence of thrombotic events after one year of clopidogrel discontinuation in patients with coronary stents.
  • To assess changes in platelet aggregability following clopidogrel cessation.

Main Methods:

  • Prospective, multicenter study of 200 patients treated with aspirin + clopidogrel for one year post-stent.
  • Platelet aggregation measured using adenosine diphosphate with PGE(1) (ADPHS), arachidonic acid (ASPI), and thrombin receptor activating peptide (TRAP) at baseline and 10, 45, 90 days post-cessation.
  • Six-month follow-up for thrombotic events.

Main Results:

  • A low incidence of thrombotic events (1%) was observed, including one ischemic stroke and one myocardial infarction.
  • Platelet aggregation induced by ADPHS and ASPI significantly increased 10-90 days after clopidogrel cessation (P < 0.001).
  • TRAP-induced platelet aggregation remained unchanged throughout the study period.

Conclusions:

  • The risk of thrombotic events after one year of clopidogrel discontinuation in patients with coronary stents may be lower than anticipated.
  • While platelet reactivity to certain agonists increases post-cessation, this may not translate to a high thrombotic event rate.

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