Abstract 20886: Impact of Pre-Dialysis Chronic Kidney Disease on Response to Clopidogrel in Patients Undergoing Coronary Angiography
Background: Response to clopidogrel is highly variable and patients with increased post-treatment residual platelet reactivity (RPR) are at increased risk for adverse events. Patients with chronic kidney disease (CKD) are also at increased risk for atherothrombotic events but the effect of clopidogrel on platelet function in these patients remains unknown. Although several studies have evaluated platelet reactivity in patients with dialysis-dependent CKD, similar data are lacking in patients with less severe CKD. Accordingly, we sought to determine the association between CKD and response to clopidogrel in patients undergoing coronary angiography.
Methods: We studied 185 patients on chronic clopidogrel (75 mg/day) who underwent platelet function testing at the time of coronary angiography between January 1, 2009 and April 30, 2010. Response to clopidogrel was defined as RPR to adenosine diphosphate using the VerifyNow P2Y12 Analyzer and expressed as P2Y12 Reaction Units (PRU). High residual platelet reactivity (HRPR) was defined as PRU values ≥ 240. CKD was defined as an estimated glomerular filtration rate (eGFR) < 60 ml/min/1.73m2.
Results: The mean age of patients with CKD (n = 57) was 67 ± 10 years compared to 61 ± 11 years in patients without CKD (n = 128). Other baseline characteristics, including diabetes mellitus, were similar between groups. The mean PRU value among patients with CKD was 252 ± 107 versus 204 ± 99 in patients without CKD (Figure; p=0.003). The frequency of HRPR among patients with and without CKD was 58% and 37%, respectively (p = 0.007). Compared to non-CKD patients, the multivariable adjusted odds ratio (OR) for HRPR associated with CKD was 2.3 (95% CI: 1.06 - 5.2). Results were similar after excluding patients with diabetes.
Conclusion: Response to clopidogrel is attenuated in patients with CKD undergoing coronary angiography. This association requires further investigation to identify causal mechanisms.
- © 2010 by American Heart Association, Inc.