High platelet reactivity on clopidogrel was associated with similar stent thrombosis risk in both sexes, but reduced clinically relevant bleeding only in women (HR 0.54; 95% CI 0.40-0.74; P<0.001).
Cohort (n=8,448)
Does high platelet reactivity on clopidogrel differentially impact clinical outcomes (stent thrombosis and bleeding) in women versus men after percutaneous coronary intervention with drug-eluting stents?
High platelet reactivity on clopidogrel after PCI with drug-eluting stents increases stent thrombosis risk similarly in both sexes, but is associated with significantly reduced bleeding only in women.
Effect estimate: HR 0.54 (95% CI 0.40-0.74)
Absolute Event Rate: 5.3% vs 9.8%
p-value: p=<0.001
Background— Sex differences in the outcomes after percutaneous coronary intervention with drug-eluting stents and in the response to clopidogrel therapy have been reported; however, the differential risk of high platelet reactivity (HPR) on clopidogrel in women versus men is unknown. Methods and Results— We compared 8448 patients enrolled in the ADAPT-DES study (Assessment of Dual Antiplatelet Therapy With Drug-Eluting Stents) according to sex and the presence/absence of HPR on clopidogrel (defined as P2Y12 reactivity units >208). Study end points were definite and probable stent thrombosis (ST), clinically relevant bleeding, all-cause mortality, myocardial infarction, and major adverse cardiac events (comprising mortality, myocardial infarction, and target lesion revascularization). HPR was more common among women (1118/2163, 51.7%) than men (2491/6285, 39.6%). HPR was associated with a roughly double risk of 1-year ST in both women and men (women with versus without HPR: 1.4% versus 0.7%; hazard ratio HR, 2.02; 95% confidence interval CI, 0.82–4.95; P =0.12; and men: 1.2% versus 0.5%; HR, 2.42; 95% CI, 1.36–4.30; P =0.002; P interaction =0.73). HPR was associated with almost half the rate of clinically relevant bleeding in women (women: HPR versus no HPR, 5.3% versus 9.8%; HR, 0.54; 95% CI, 0.40–0.74; P <0.001), whereas men had similar rates of bleeding regardless of HPR status (men: HPR versus no HPR, 5.7% versus 5.9%; HR, 0.96; 95% CI, 0.78–1.18; P =0.70; P interaction =0.003). In propensity-adjusted models, HPR was an independent predictor of ST and myocardial infarction in men; although both associations were nonsignificant among women, no interaction was observed in the associations between HPR and either ST or myocardial infarction. Conversely, HPR was an independent predictor of reduced bleeding only in women (women: adjusted HR, 0.58; 95% CI, 0.41–0.82; P =0.002; and men: adjusted HR, 0.83; 95% CI, 0.65–1.04; P =0.11; P interaction =0.01). Conclusions— In the current analysis, the associated risk of HPR for ST was similar in both sexes. However, HPR was associated with significantly reduced bleeding only among women. Clinical Trial Registration— URL: http://www.clinicaltrials.gov . Unique identifier: NCT00638794.
Yu et al. (Wed,) conducted a cohort in High platelet reactivity after percutaneous coronary intervention with drug-eluting stents (n=8,448). High platelet reactivity (HPR) on clopidogrel vs. No high platelet reactivity was evaluated on Clinically relevant bleeding in women (HR 0.54, 95% CI 0.40-0.74, p=<0.001). High platelet reactivity on clopidogrel was associated with similar stent thrombosis risk in both sexes, but reduced clinically relevant bleeding only in women (HR 0.54; 95% CI 0.40-0.74; P<0.001).