Key result
Poor responders to clopidogrel identified by multiple electrode aggregometry had a significantly higher risk of stent thrombosis compared to responders (12.5% vs. 0.3%, P<0.001).
Why the study?
Does phenotyping or genotyping better predict stent thrombosis and MACE in patients undergoing PCI on clopidogrel?
Cohort (n=416)
Does phenotyping or genotyping better predict stent thrombosis and MACE in patients undergoing PCI on clopidogrel?
Phenotypic assessment of platelet response to clopidogrel using multiple electrode aggregometry is a better predictor of stent thrombosis than CYP2C19 genotyping in patients undergoing PCI.
Answers are grounded in this paper and cite their sources.
MEA phenotyping may better stratify stent thrombosis risk than genotyping post-PCI; leaves open prospective validation and outcome impact.
BACKGROUND: Prognostic values of genotyping and phenotyping for assessment of clopidogrel responsiveness have been shown in independent studies. OBJECTIVES: To compare different assays for prediction of events during long-term follow-up. METHODS: In this prospective cohort study polymorphisms of CYP2C19*2 and CYP2C19*17 alleles, vasodilator-stimulated phosphoprotein phosphorylation (VASP) assay, multiple electrode aggregometry (MEA), cone and platelet analyser (CPA) and platelet function analyser (PFA-100) were performed in 416 patients undergoing percutaneous coronary intervention. The rates of events were recorded during a 12-month follow-up. RESULTS: Platelet aggregation by MEA predicted stent thrombosis (2.4%) better (c-index = 0.90; P < 0.001; sensitivity = 90%; specificity = 83%) than the VASP assay, CPA or PFA-100 (c-index < 0.70; P > 0.05; sensitivity < 70%; specificity < 70% for all) or even the CYP2C19*2 polymorphism (c-index < 0.56; P > 0.05; sensitivity = 30%; specificity = 71%). Survival analysis indicated that patients classified as poor responders by MEA had a substantially higher risk of developing stent thrombosis or MACE than clopidogrel responders (12.5% vs. 0.3%, P < 0.001, and 18.5% vs. 11.3%, P = 0.022, respectively), whereas poor metabolizers (CYP2C19*1/*2 or *2/*2 carriers) were not at increased risks (stent thrombosis, 2.7% vs. 2.5%, P > 0.05; MACE, 13.5% vs. 12.1%, P = 0.556). The incidence of major bleedings (2.6%) was numerically higher in patients with an enhanced vs. poor response to clopidogrel assessed by MEA (4% vs. 0%) or in ultra-metabolizers vs. regular metabolizers (CYP2C19*17/*17 vs. CYP2C19*1/*1; 9.5% vs. 2%). The classification tree analysis demonstrated that acute coronary syndrome at hospitalization and diabetes mellitus were the best discriminators for clopidogrel responder status. CONCLUSIONS: Phenotyping of platelet response to clopidogrel was a better predictor of stent thrombosis than genotyping.
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Siller‐Matula et al. (2012) conducted a cohort in percutaneous coronary intervention (n=416). Poor response to clopidogrel assessed by multiple electrode aggregometry (MEA) vs. Clopidogrel responders by MEA was evaluated on Stent thrombosis (p=<0.001). Poor responders to clopidogrel identified by multiple electrode aggregometry had a significantly higher risk of stent thrombosis compared to responders (12.5% vs. 0.3%, P<0.001).
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