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Sustained increase in platelet aggregation after the cessation of clopidogrel

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Clinical and Experimental Pharmacology and Physiology

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We have shown that abrupt cessation of one‐year clopidogrel treatment was not associated with thrombotic events in prospective, multicenter study that enrolled 200 patients subjected to coronary stent implantation and treated with aspirin + clopidogrel one year after the stent placement. The aim of this study was to investigate the causes of sustaining increase of platelet aggregability, considering that the values of platelet aggregation stimulated with ADP+PGE1 (ADPHS values) significantly increased 10‐90 days after the cessation of clopidogrel. Values of platelet aggregation induced by thrombin receptor activating peptide (TRAP values) and arachidonic acid (ASPI values) were divided into quartiles on the basis of ADPHS values 10 days after stopping clopidogrel (ADPHS10). There was a significant difference between TRAP values divided into quartiles according to ADPHS10, 10, 45 and 90 days after stopping clopidogrel (p < 0.001, all), and ASPI values across the same quartiles 10 and 45 days after the cessation of clopidogrel (p = 0.028 and 0.003). Results of our study indicate that patients with early pronounced rebound phenomenon to clopidogrel termination have a long‐term (at least 90 days) increased platelet aggregation to other agonists such as thrombin related activated protein and arachidonic acid, suggesting the complex mutual relationship of various factors ‐ agonists influencing the function of platelets. This article is protected by copyright. All rights reserved.