Key result
High-risk gene-gene interactions among TXA2R rs1131882, P2Y1 rs1371097, and GPIIIa rs2317676 independently increased the risk of symptomatic carotid stenosis in ischemic stroke patients (OR 2.72).
Why the study?
Genetic risk factors for carotid stenosis are not fully understood, prompting investigation into platelet activation-relevant gene variants in ischemic stroke patients.
Does the interaction among TXA2R rs1131882, P2Y1 rs1371097, and GPIIIa rs2317676 increase the risk of carotid stenosis in patients with ischemic stroke?
Case-Control (n=614)
Yes
Does the interaction among TXA2R rs1131882, P2Y1 rs1371097, and GPIIIa rs2317676 increase the risk of carotid stenosis in patients with ischemic stroke?
Effect estimate: OR 2.72 (95% CI 1.28-7.82)
p-value: p=0.001
Gene-gene interactions among TXA2R rs1131882, P2Y1 rs1371097, and GPIIIa rs2317676 are synergistically associated with an increased risk of symptomatic carotid stenosis in patients with ischemic stroke.
Gene interactions associated with higher carotid stenosis risk in stroke; hypothesis-generating and requires prospective validation before clinical use.
BACKGROUND: The genetic risk factors for carotid stenosis are not fully understood. The aim of this study is to investigate the relationship between variants in platelet activation-relevant genes and carotid stenosis in patients with ischemic stroke (IS). METHODS: Eleven variants of platelet activation-relevant genes, aggregates of platelet-leukocyte, and platelet aggregation were examined in 236 IS patients with carotid stenosis and 378 patients without carotid stenosis. High-resolution B-mode ultrasound was used to assess carotid stenosis. Generalized multifactor dimensionality reduction (GMDR) methods were applied in analyzing gene-gene interactions to determine whether there was any interactive role of assessed variants in affecting risk of carotid stenosis. RESULTS: Platelet aggregation and aggregates of platelet-leukocyte showed higher value in patients with carotid stenosis, compared with patients without carotid stenosis. Excluding potential disturbance variables, these 11 variants were not associated with carotid stenosis. However, according to the GMDR analysis, gene-gene interactions among TXA2R rs1131882, P2Y1 rs1371097 and GPIIIa rs2317676 had a synergistic influence on carotid stenosis. The high-risk interactions between the three variants showed a relationship with higher platelet activation, and have independent associations with risk of carotid stenosis (OR = 2.72, 95% CI: 1.28-7.82, P = 0.001). CONCLUSION: The interactions among rs1131882, rs1371097 and rs2317676 perhaps increase the risk of symptomatic carotid stenosis, and maybe a potential marker for carotid stenosis. In this study, the combinatorial analysis made good use in elucidating complex risk factors in the heredity of carotid stenosis.
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Yi et al. (2019) conducted a case-control in Ischemic stroke with or without carotid stenosis (n=614). High-risk gene-gene interactions (TXA2R rs1131882, P2Y1 rs1371097, GPIIIa rs2317676) vs. Low-risk gene-gene interactions was evaluated on Symptomatic carotid stenosis (≥ 50%) (OR 2.72, 95% CI 1.28-7.82, p=0.001). High-risk gene-gene interactions among TXA2R rs1131882, P2Y1 rs1371097, and GPIIIa rs2317676 independently increased the risk of symptomatic carotid stenosis in ischemic stroke patients (OR 2.72).
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