Abstract 2219: Measurement of Clopidogrel Inhibition With A Point-of-Care Assay Identifies Patients At Risk for Stent Thrombosis After Percutaneous Coronary Intervention
Background: The clinical utility of measuring clopidogrel (CLOP)-induced platelet inhibition using a point-of-care (POC) assay is not well studied. We sought to identify the clinical predictors of CLOP non-responsiveness and any association with stent thrombosis in patients undergoing PCI with drug-eluting stents.
Methods: Platelet inhibition due to CLOP in patients not receiving glycoprotein inhibitors was measured with the VerifyNow P2Y12 assay (Accumetrics, Inc) at baseline prior to PCI and 12 hours post-procedure. Pts not on prior CLOP received 600-mg at the time of the procedure, and all pts received 75-mg daily for at least 3 months post-procedure. The magnitude of ADP-induced aggregation is reported by the assay using P2Y12 Reaction Units (PRU). In pts receiving a loading dose, % inhibition (PI) due to CLOP was defined as 1-PRU (post-CLOP)/PRU(baseline)*100. In pts on chronic CLOP without a baseline value, PI was determined using the control channel as calculated by the Verify Now device. Pts in the lowest quartile of PI were defined as being CLOP non-responsive (NONRESP). Univariate analysis was performed using contingency tables and Mann-Whitney test; multivariate analysis was performed using logistic regression.
Results: CLOP assays were complete in 264 pts, 169 of whom were CLOP-naïve prior to the procedure. Diabetes (DM) was present in 26%, and 76% were male. The indication for procedure was unstable angina (USA) in 4% and stable angina/ischemia in 94%. The median PI was 28% (range, 0 to 98). A PI < 10% defined the lowest quartile of pts (CLOP NONRESP). CLOP NONRESP pts were heavier (p = 0.02) and tended to be male (p = 0.08), but there was no association with USA, AMI, DM, baseline PRU activity, or prior CLOP use. Weight > 100 kg was independently associated with CLOP NONRESP (p = 0.04). Acute and sub-acute stent thrombosis occurred in 1 pt (0.3%) and 3 pts (1.1%) respectively. CLOP NONRESP was significantly associated with stent thrombosis (3 of the 4 pts, p = 0.04).
Conclusions: Clopidogrel-induced inhibition is < 10% in 25% of pts undergoing PCI. Non-responsiveness to clopidogrel is associated with heavier weight. Increased dosing in patients > 100 kg should be considered. A point-of care assay may identify patients at higher risk for stent thrombosis.