Table 2

Polymorphisms associated with the incidence of stroke and validated in the SWiTCH and HUSTLE cohorts

GeneSNP IDMinor alleleHUSTLE (n = 206), %SWiTCH (n = 260), %Genetic modelPOdds ratio95% CI
ADCY9 rs2238432 33.0 22.3 Dominant .003 0.47 0.28-0.79 
ANXA2 rs11853426 34.9 44.6 Recessive .007 2.70 1.25-5.84 
TEK rs489347 35.9 46.9 Recessive .016 2.16 1.11-4.23 
TGFBR3 rs284875 7.8 13.5 Dominant .005 2.53 1.28-4.99 
HbA2 rs63751476 Δ3.7 17.0 8.8 Dominant .009 0.45 0.24-0.84 
GeneSNP IDMinor alleleHUSTLE (n = 206), %SWiTCH (n = 260), %Genetic modelPOdds ratio95% CI
ADCY9 rs2238432 33.0 22.3 Dominant .003 0.47 0.28-0.79 
ANXA2 rs11853426 34.9 44.6 Recessive .007 2.70 1.25-5.84 
TEK rs489347 35.9 46.9 Recessive .016 2.16 1.11-4.23 
TGFBR3 rs284875 7.8 13.5 Dominant .005 2.53 1.28-4.99 
HbA2 rs63751476 Δ3.7 17.0 8.8 Dominant .009 0.45 0.24-0.84 

The minor allele and the minor allele frequency are given for each SNP. Significance between the control (HUSTLE) and stroke (SWiTCH) groups was tested using Fisher exact test under the dominant or recessive genetic models. All SNPs matched the published orientation of association with stroke risk (increased or decreased risk) and were tested by a one-tailed Fisher exact test. The HbA2 polymorphism is the Δ3.7-kb α-thalassemia single gene deletion.

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