Optimizing of thienopyridine therapy by multiple electrode platelet aggregometry in clopidogrel low responders undergoing PCI.

aimsOne possible cause of stent thrombosis is an insufficient effect of clopidogrel. In a prospective study, we aimed to optimize the platelet inhibition of clopidogrel low responders (CLR) by multiple electrode platelet aggregometry (MEA)-guided therapy modifications and to evaluate specific major adverse cardiac and cerebrovascular events (MACCE). METHODS AND

resultsADP-induced platelet aggregation was measured by MEA in 1,005 consecutive patients after stent implantation and 600 mg clopidogrel loading dose. All patients received at least 100 mg aspirin/day. In 118 patients (11.7%), ADP values remained in the reference range generated in 150 controls and were defined as CLR. Significant independent predictors of CLR were acute coronary syndrome (ACS) (OR = 6.54), diabetes (OR = 2.07), use of diuretics (OR = 1.93) or proton pump inhibitors (OR = 1.64) and male gender (OR = 1.83). Ninety-nine CLR were switched to clopidogrel 150 mg/day, leading to an adequate response in 54/99. Subsequently, 44 patients were changed to ticlopidine 2 × 250 mg/day, resulting in an inhibition in 24/44. The remaining 20 patients received 2 × 100 mg cilostazol/day in addition to 75 mg clopidogrel/day. After its recent availability, 19/118 primary CLR were treated with 5-10 mg prasugrel/day. One patient was a prasugrel low responder. The total thienopyridine low response-rate was 2% in our population. The specific MACCE rate (death, non-fatal target vessel myocardial infarction, non-fatal stroke) of the CLR under optimized treatment (except prasugrel) was 2.0% at 30 days and 3.0% during a mean follow-up of 44 weeks.

conclusionClopidogrel low response is present in 1/10 patients and more frequent in ACS-PCI. MEA-guided optimizing of thienopyridine therapy is feasible and results in a very low specific MACCE rate. Low response to all thienopyridines is rare.