Beschreibung:
<jats:title>Summary</jats:title><jats:p>This study shows that the abrupt cessation of one‐year clopidogrel treatment was not associated with thrombotic events in a prospective, multicentre study that enrolled 200 patients subjected to coronary stent implantation and treated with aspirin + clopidogrel 1 year after the stent placement. The aim of the study was to investigate the causes of a sustained increase of platelet aggregability, considering that the values of platelet aggregation stimulated with <jats:styled-content style="fixed-case">ADP</jats:styled-content> + <jats:styled-content style="fixed-case">PGE</jats:styled-content><jats:sub>1</jats:sub> (<jats:styled-content style="fixed-case">ADPHS</jats:styled-content> values) significantly increased 10–90 days after the cessation of clopidogrel. Values of platelet aggregation induced by thrombin receptor activating peptide (<jats:styled-content style="fixed-case">TRAP</jats:styled-content> values) and arachidonic acid (<jats:styled-content style="fixed-case">ASPI</jats:styled-content> values) were divided into quartiles on the basis of <jats:styled-content style="fixed-case">ADPHS</jats:styled-content> values 10 days after stopping clopidogrel (<jats:styled-content style="fixed-case">ADPHS</jats:styled-content><jats:sub>10</jats:sub>). There was a significant difference between <jats:styled-content style="fixed-case">TRAP</jats:styled-content> values divided into quartiles according to <jats:styled-content style="fixed-case">ADPHS</jats:styled-content><jats:sub>10</jats:sub>, 10, 45 and 90 days after stopping clopidogrel (<jats:italic>P </jats:italic><<jats:italic> </jats:italic>0.001, all), and <jats:styled-content style="fixed-case">ASPI</jats:styled-content> values across the same quartiles 10 and 45 days after the cessation of clopidogrel (<jats:italic>P </jats:italic>=<jats:italic> </jats:italic>0.028 and 0.003). The results of the study indicate that patients with early pronounced rebound phenomena 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.</jats:p>