Key result
Metabolic syndrome in PCI patients is linked to a ~20-point higher rate of clopidogrel resistance.
Why the study?
Despite the proven benefits of combined clopidogrel and aspirin therapy for CAD, patients with metabolic syndrome still tend to experience coronary thrombotic events, prompting an investigation into the influence of metabolic risk factors on clopidogrel efficacy during PCI.
Cohort (n=336)
Does not support changing clopidogrel regimens based on metabolic syndrome alone; extends observational data on resistance predictors.
BACKGROUND: Despite the proven benefits of clopidogrel combined aspirin therapy for coronary artery disease (CAD), CAD patients with metabolic syndrome (MS) still tend to have coronary thrombotic events. We aimed to investigate the influence of metabolic risk factors on the efficacy of clopidogrel treatment in patients with CAD undergoing percutaneous coronary intervention (PCI). METHODS: Cohorts of 168 MS and 168 non-MS subjects with CAD identified by coronary angiography (CAG) were enrolled in our study. MS was defined by modified Adult Treatment Panel III criteria. All subjects had taken 100 mg aspirin and 75 mg clopidogrel daily for more than 1 month, and administered loading doses of 600 mg clopidogrel and 300 mg aspirin before PCI. Blood samples were taken 24 h after the loading doses of clopidogrel and aspirin. Platelet aggregation was measured using light transmittance aggregometry (LTA) and thrombelastography (TEG). Clopidogrel resistance was defined as more than 50% adenosine diphosphate (ADP) induced platelet aggregation as measured by TEG. RESULTS: Platelet aggregation inhibition rate by ADP was significantly lower in patients with MS as measured both by TEG (55% ± 31% vs. 68% ± 32%; P < 0.001) and LTA (29% ± 23% vs. 42% ± 29%; P < 0.001). In the multivariate analysis, elderly [OR (95% CI): 1.483 (1.047-6.248); P = 0.002], obesity [OR (95% CI): 3.608 (1.241-10.488); P = 0.018], high fasting plasma glucose level [OR (95% CI): 2.717 (1.176-6.277); P = 0.019] and hyperuricemia [OR (95% CI): 2.583 (1.095-6.094); P = 0.030] were all statistically risk factors for clopidogrel resistance. CAD patients with diabetes and obesity were more likely to have clopidogrel resistance than the CAD patients without diabetes and obesity [75% (61/81) vs. 43% (67/156); P < 0.001]. CONCLUSIONS: CAD patients with MS appeared to have poorer antiplatelet response to clopidogrel compared to those without MS. Obesity, diabetes and hyperuricemia were all significantly associated with clopidogrel resistance.
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Wu et al. (2015) conducted a cohort in Coronary artery disease undergoing percutaneous coronary intervention (n=336). Metabolic syndrome vs. No metabolic syndrome was evaluated on Clopidogrel resistance defined as >=50% ADP-induced platelet aggregation measured by thrombelastography (TEG) (p=0.001). Metabolic syndrome in CAD patients undergoing PCI was associated with a higher rate of clopidogrel resistance (63% vs 43%, P=0.001) and lower ADP-induced platelet inhibition (55% vs 68%, P<0.001).
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