Key result
Smoking was significantly associated with an increased risk of lacunar infarcts (OR 1.87; 95% CI 1.05-3.31) and death at 15 months, with effects amplified by the GpIIb/IIIa Pl(A2) allele.
Why the study?
Does the interaction between smoking and the GpIIb/IIIa Pl(A1/A2) polymorphism affect the risk of lacunar stroke and midterm survival in patients with ischemic stroke?
Cohort (n=486)
Does the interaction between smoking and the GpIIb/IIIa Pl(A1/A2) polymorphism affect the risk of lacunar stroke and midterm survival in patients with ischemic stroke?
Effect estimate: OR 1.87 (95% CI 1.05-3.31)
p-value: p=0.033
Prothrombotic genetic factors like the GpIIb/IIIa Pl(A1/A2) polymorphism may interact with smoking to increase the risk of lacunar stroke and reduce midterm survival.
May increase lacunar infarct and mortality risk via Pl(A2) interaction; hypothesis-generating for gene-environment effects, needing prospective validation.
BACKGROUND AND PURPOSE: Smoking, increased fibrinogen levels, and platelet activation are related to the risk of ischemic stroke. The platelet fibrinogen receptor glycoprotein (Gp) IIb/IIIa Pl(A1/A2) polymorphism affects the binding of platelets to fibrinogen and is suggested to interact with smoking. METHODS: We explored the association of smoking and the Pl(A1/A2) polymorphism with ischemic stroke and survival in the Stroke Aging Memory cohort, comprising 486 consecutive patients (55 to 85 years old) who were analyzed 3 months after an ischemic stroke and followed up for 15 months. Stroke subtype determined by magnetic resonance imaging and GpIIb/IIIa Pl(A1/A2) genotype data were available for 272 patients. RESULTS: In multivariate analysis, smoking was the only factor related to the risk of lacunar infarcts (odds ratio [OR]=1.87, 95% CI=1.05 to 3.31; P=0.033), and it was also a predictor of death (n=24, 8.8%) at 15 months (OR=5.13, 95% CI=1.61 to 16.36; P=0.006), along with age (OR=1.10, 95% CI=1.01 to 1.19; P=0.008). The GpIIb/IIIa Pl(A1/A2) polymorphism alone showed no association with stroke subtype or survival. However, there was a smoking-by-genotype association with the risk of lacunar infarcts (OR=2.10, 95% CI=0.90 to 4.89; P=0.087) and with survival (OR=2.78, 95% CI=0.89 to 8.61; P=0.077). Among younger (55 to 69 years) stroke patients, smokers carrying the Pl(A2) allele were at a higher (OR=5.81, 95% CI=1.26 to 26.80; P=0.024) risk of lacunar infarcts than noncarrier smokers (OR=3.12, 95% CI=1.06 to 9.24; P=0.039). The effect of Pl(A2) and smoking combined on survival was also stronger (OR=8.86, 95% CI=1.68 to 46.55; P=0.010) than the effect of smoking alone (OR=5.06, 95% CI=1.20 to 21.35; P=0.027). CONCLUSIONS: Our results indicate that prothrombotic genetic factors may interact with smoking by modifying the stroke phenotype and affecting midterm survival.
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Oksala et al. (2006) conducted a cohort in Ischemic stroke (n=486). Smoking and GpIIb/IIIa Pl(A1/A2) polymorphism vs. Non-smokers and non-carriers was evaluated on Risk of lacunar infarcts (OR 1.87, 95% CI 1.05-3.31, p=0.033). Smoking was significantly associated with an increased risk of lacunar infarcts (OR 1.87; 95% CI 1.05-3.31) and death at 15 months, with effects amplified by the GpIIb/IIIa Pl(A2) allele.
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