Renal Function, Assessed Using Cystatin C, and Antiplatelet Efficacy of Clopidogrel Assessed Using the Vasodilator-Stimulated Phosphoprotein Index in Patients Having Percutaneous Coronary Intervention
Abstract
Renal dysfunction is a strong independent predictor of stent thrombosis. The aim of the present study was to evaluate the strength and direction of the association between kidney function and clopidogrel efficacy.
The study group consisted of consecutive patients (N=275) who underwent stent implantation. Drug efficacy was measured using the vasodilator-stimulated phosphoprotein (VASP) index 20 - 4h after 600mg clopidogrel.
Non-response was defined as VASP index GREATER-THAN OR EQUAL TO50%. Renal function was determined using serum cystatin C.
The upper reference levels are: 1.12mg/L for LESS-THAN OR EQUAL TO65 years and 1.21mg/L for >65 years. Estimated glomerular filtration (eGFR) was calculated using cystatin C.
The median value of cystatin C was 1.16 mg/L (25th and 75th percentile, 0.96 and 1.43 mg/L). 47.63% of study population had cystatin C above reference levels. 33.1% of patients were non-responders to clopidogrel. No correlation was found between clopidogrel efficacy assessed using the VASP index and kidney function assessed with cystatin C (rs= MINUS SIGN 0.070, p = 0.248).
Based on cystatin C, the proportion of non-responders to clopidogrel was 34.4% vs. 31.9% (p = 0.702) in patients with impaired renal function compared to normal renal function, respectively. The proportion of clopidogrel-non responders did not differ (p = 0.902) between groups with normal (28.8%), mildly (34.8%), moderately (32.9%) and severely (34.8%) impaired renal function.
In conclusion, renal function, assessed by cystatin C, does not predict clopidogrel efficacy. Renal dysfunction is a complex entity and its significant relation to stent thrombosis cannot be explained simply by a reduction in clopidogrel efficacy.