Dual nonresponsiveness to aspirin and clopidogrel after PCI was associated with a higher risk of MI, revascularization, stent thrombosis, or cardiac death (31.6% vs 12.3%; HR 2.9, 95% CI 1.17-7.2).
Cohort (n=182)
Does dual antiplatelet drug resistance increase the risk of cardiovascular events in patients after percutaneous coronary intervention?
Dual nonresponsiveness to aspirin and clopidogrel is an independent risk factor for adverse cardiovascular events following PCI, suggesting a need for intensified antiplatelet therapy in this high-risk subgroup.
Hazard Ratio: 2.9 (95% CI 1.17–7.2)
Absolute Event Rate: 31.6% vs 12.3%
p-value: p=0.02
BACKGROUND: Nonresponsiveness to clopidogrel and acetylsalicylic acid (ASA), a frequent result of platelet aggregometry studies, has unclear clinical and prognostic significance. METHODS: We performed impedance aggregometry in 182 patients 12-24 h after percutaneous coronary intervention (PCI) and a 600-mg loading dose of clopidogrel, adding 5 micromol/L ADP and 1 mg/L collagen to diluted whole blood to determine platelet inhibition by clopidogrel and ASA, respectively. Samples from nonresponders were incubated in vitro with methyl-S-adenosine monophosphate or ASA to distinguish between pharmacodynamic and pharmacokinetic types of resistance. We assessed a combined primary endpoint of myocardial infarction, target vessel revascularization, late stent thrombosis, or cardiac death. RESULTS: Nineteen patients (10.4%) were dual nonresponders (nonresponsive to both ASA and clopidogrel), and 163 patients (89.6%) were designated responders. The latter group also included 15 and 14 single nonresponders (responsive to either clopidogrel or ASA, respectively), who exhibited endpoint frequencies comparable to those of full responders (n = 134). Pharmacokinetic resistance was most prevalent. Primary endpoints occurred more frequently in dual nonresponders (n = 6, 31.6%) than in responders (n = 20, 12.3%) (relative risk 2.57; 95% CI 1.18-5.61; log-rank P = 0.03). Multivariate analysis confirmed dual nonresponsiveness (hazard ratio 2.9; 95% CI 1.17-7.2; P = 0.02) as an independent risk factor. CONCLUSIONS: Dual nonresponders carry a high cardiovascular risk after PCI and should obtain intensified antiplatelet therapy and follow-up.
Ivandic et al. (2009) conducted a cohort in Post-percutaneous coronary intervention (PCI) (n=182). Dual nonresponsiveness to clopidogrel and acetylsalicylic acid (ASA) vs. Responders (responsive to either or both clopidogrel and ASA) was evaluated on Combined primary endpoint of myocardial infarction, target vessel revascularization, late stent thrombosis, or cardiac death (HR 2.9, 95% CI 1.17-7.2, p=0.02). Dual nonresponsiveness to aspirin and clopidogrel after PCI was associated with a higher risk of MI, revascularization, stent thrombosis, or cardiac death (31.6% vs 12.3%; HR 2.9, 95% CI 1.17-7.2).
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: