Low response to clopidogrel assessed with MEA was associated with a higher risk of definite stent thrombosis at 30 days compared with normal response (2.2% vs 0.2%; OR 9.4; 95% CI 3.1-28.4; p<0.0001).
Cohort (n=1,608)
Does high platelet reactivity (low response) to clopidogrel assessed with point-of-care multiple electrode aggregometry predict early drug-eluting stent thrombosis in patients undergoing PCI?
Point-of-care assessment of clopidogrel response using multiple electrode aggregometry can effectively identify patients at high risk for early drug-eluting stent thrombosis.
Odds Ratio: 9.4 (95% CI 3.1–28.4)
Absolute Event Rate: 2.2% vs 0.2%
p-value: p=< 0.0001
OBJECTIVES: The aim of this prospective trial was to assess whether platelet reactivity to clopidogrel assessed with multiple electrode platelet aggregometry (MEA) correlates with the risk of early drug-eluting stent thrombosis (ST). BACKGROUND: Studies using light transmission aggregometry (LTA) have shown that insufficient suppression of platelet reactivity to adenosine diphosphate (ADP) after clopidogrel treatment is associated with an increased risk of adverse cardiovascular events after percutaneous coronary intervention (PCI). However, LTA is time- and labor-intensive and inconvenient for the routine. A point-of-care assay with similar predictive power would be of great value. METHODS: Between February 2007 and April 2008, a total of 1,608 consecutive patients with coronary artery disease and planned drug-eluting stent implantation were enrolled. Before PCI, all patients received 600 mg clopidogrel. Blood was obtained directly before PCI. The ADP-induced platelet aggregation was assessed in whole blood with MEA on a Multiplate analyzer (Dynabyte, Munich, Germany). The primary end point was definite ST at 30 days. RESULTS: The upper quintile of patients according to MEA measurements (n = 323) was defined as clopidogrel low responders. Compared with normal responders (n = 1,285), low responders had a significantly higher risk of definite ST within 30 days (2.2% vs. 0.2%; odds ratio OR: 9.4; 95% confidence interval CI: 3.1 to 28.4; p < 0.0001). Mortality rates were 1.2% in low versus 0.4% in normal responders (OR: 3.2; 95% CI: 0.9 to 11.1; p = 0.07). The composite of death or ST was higher in low versus normal responders (3.1% vs. 0.6%; OR: 5.1; 95% CI: 2.2 to 11.6; p < 0.001). CONCLUSIONS: Low response to clopidogrel assessed with MEA is significantly associated with an increased risk of ST. Further studies are warranted to evaluate the ability of MEA to guide antiplatelet therapy in patients undergoing PCI.
“We're still not measuring [platelet reactivity] in patients as a standard of care. We're not moving the needle.”
Sibbing et al. (Sun,) conducted a cohort in coronary artery disease (n=1,608). Low response to clopidogrel vs. Normal response to clopidogrel was evaluated on definite ST at 30 days (OR 9.4, 95% CI 3.1 to 28.4, p=< 0.0001). Low response to clopidogrel assessed with MEA was associated with a higher risk of definite stent thrombosis at 30 days compared with normal response (2.2% vs 0.2%; OR 9.4; 95% CI 3.1-28.4; p<0.0001).
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