What is the clinical evidence from this study?

Study design: Observational. Population: Coronary artery disease undergoing elective coronary stent implantation (n=951). Intervention: Female gender vs. Male gender. Primary outcome: Composite of all-cause death, non-fatal myocardial infarction, definite stent thrombosis, and ischaemic stroke (OR 0.78, 95% CI 0.43-1.35, p=0.58).

September 6, 2011Open Access

Effect of gender difference on platelet reactivity

Resultado clave

Although women exhibited higher on-treatment platelet reactivity than men, the incidence of the composite clinical endpoint at 1 year was similar between genders (6.8% vs 8.6%, OR 0.78).

Diseño del estudio

Tipo

Observational (n=951)

PICO

Población

Coronary artery disease undergoing elective coronary stent implantation (n=951)

Intervención / comparador

Female gender vs Male gender

Resultado principal

Composite of all-cause death, non-fatal myocardial infarction, definite stent thrombosis, and ischaemic stroke — OR 0.78 (0.43-1.35), p=0.58

Resultado numérico

Estimación del efecto: OR 0.78 (95% CI 0.43-1.35)

Tasa de eventos absoluta: 6.8% vs 8.6%

valor p: p=0.58

Limitaciones

Magnitude of platelet reactivity was determined with a single assessment while patients were already on antiplatelet therapy, making it impossible to establish if differences were due to baseline reactivity or less response.
The role of hormonal influences remains unclear, as menopausal status and menstrual cycle were not assessed.

Resumen

BACKGROUND: Previous studies have suggested that women do not accrue equal therapeutic benefit from antiplatelet medication as compared with men. The physiological mechanism and clinical implications behind this gender disparity have yet to be established. METHODS: On-treatment platelet reactivity was determined in 717 men and 234 women on dual antiplatelet therapy, undergoing elective coronary stent implantation. Platelet function testing was performed using arachidonic acid and adenosine diphosphate-induced light transmittance aggregometry (LTA) and the VerifyNow P2Y12 and Aspirin assays. Also the incidence of all-cause death, non-fatal acute myocardial infarction, stent thrombosis and ischaemic stroke was evaluated. RESULTS: Women had higher baseline platelet counts than men. Women exhibited a higher magnitude of on-aspirin platelet reactivity using LTA, but not using the VerifyNow Aspirin assay. The magnitude of on-clopidogrel platelet reactivity was significantly higher in women as compared with men with both tests used. The cut-off value to identify patients at risk as well as the incidence of clinical endpoints was similar between women and men (16/2346.8% vs. 62/7178.6%, p = 0.38). CONCLUSION: Although the magnitude of platelet reactivity was higher in women, the absolute difference between genders was small and both the cut-off value to identify patients at risk and the incidence of the composite endpoint were similar between genders. Thus, it is unlikely that the difference in platelet reactivity accounts for a worse prognosis in women.

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