BACKGROUND: The optimal timing for 600 mg clopidogrel pre-treatment before planned PCI in patients with stable coronary artery disease has never been tested in a randomized trial. METHODS: The time course of platelet inhibition was investigated in 105 patients pre-treated with clopidogrel ≥ 6 h before the planned procedure. Flow cytometric analysis of the vasodilator stimulated phosphoprotein (VASP) phosphorylation state was done and a Platelet Reactivity Index (PRI) was calculated prior to treatment (baseline) and at 12, 28, 36, 60, 84 and 108 h after the clopidogrel loading dose administration. RESULTS: The maximal inhibition of platelet activation was seen at 28 h post administration (PRI mean 36 ± 23%), and 2/3 of patients had PRI value <50%. At 12 h 47% of patients had PRI value ≥ 50% (mean 45±21%). 600 mg of clopidogrel significantly suppressed platelet activation for 4 days. A correlation was between baseline PRI and its values by 28 h (r(S)=0.48, p<0.001), between 12 h-28 h the correlation was strong (r(S)=0.77, p<0.001). CONCLUSION: The time curve of clopidogrel efficacy was dependent on baseline platelet reactivity. Among stable CAD patients, pre-treatment with 600 mg of clopidogrel resulted in maximal antiplatelet efficacy 1 day after drug administration.
RCT Entities:
BACKGROUND: The optimal timing for 600 mg clopidogrel pre-treatment before planned PCI in patients with stable coronary artery disease has never been tested in a randomized trial. METHODS: The time course of platelet inhibition was investigated in 105 patients pre-treated with clopidogrel ≥ 6 h before the planned procedure. Flow cytometric analysis of the vasodilator stimulated phosphoprotein (VASP) phosphorylation state was done and a Platelet Reactivity Index (PRI) was calculated prior to treatment (baseline) and at 12, 28, 36, 60, 84 and 108 h after the clopidogrel loading dose administration. RESULTS: The maximal inhibition of platelet activation was seen at 28 h post administration (PRI mean 36 ± 23%), and 2/3 of patients had PRI value <50%. At 12 h 47% of patients had PRI value ≥ 50% (mean 45±21%). 600 mg of clopidogrel significantly suppressed platelet activation for 4 days. A correlation was between baseline PRI and its values by 28 h (r(S)=0.48, p<0.001), between 12 h-28 h the correlation was strong (r(S)=0.77, p<0.001). CONCLUSION: The time curve of clopidogrel efficacy was dependent on baseline platelet reactivity. Among stable CAD patients, pre-treatment with 600 mg of clopidogrel resulted in maximal antiplatelet efficacy 1 day after drug administration.