Association of ABCB1 G2677T polymorphism with atorvastatin lipid efficacy and extended prognosis in patients with cerebral ischemic stroke

To investigate the association between ABCB1 (2677T > G) (rs2032582) polymorphism and lipid-lowering efficacy of atorvastatin with long-term prognosis in patients with cerebral ischemic stroke (CIS). A prospective cohort of 127 CIS patients admitted to Xuchang Central Hospital from January to December 2021 was consecutively enrolled. ABCB1 (2677T > G) genotypes were determined using digital fluorescence molecular hybridization technology, categorizing patients into GG (n = 48), GT (n = 49), and TT (n = 30) groups. All patients received oral atorvastatin 20 mg/day. Lipid profile changes (pre-treatment vs. 2-month post-treatment) were analyzed via analysis of covariance (ANCOVA). Treatment efficacy was defined as achieving serum LDL-C < 1.8 mmol/L, and binary logistic regression analysis was used to explore the impact of ABCB1(2677T > G) gene polymorphism on the lipid-lowering efficacy of atorvastatin. All patients were followed up for 36 months post-discharge to compare differences in long-term prognosis among the three groups. Genotype distribution followed Hardy-Weinberg equilibrium (χ² = 3.225, P = 0.199). In both the additive and recessive models with age as a covariate, significant differences were observed among the three groups in ΔLDL-C, ΔLDL-C/LDL-C, Δ(LDL-C/HDL-C), and Δ(LDL-C/HDL-C)/(LDL-C/HDL-C) (additive model: F_ΔLDL-C = 4.198, P = 0.001; F_{ΔLDL-C/LDL-C} = 3.042, P = 0.013; F_{Δ(LDL-C/HDL-C)} = 3.870, P = 0.003; F_{Δ(LDL-C/HDL-C)/(LDL-C/HDL-C)} = 2.551, P = 0.031. Recessive model: F_ΔLDL-C = 5.142, P = 0.002; F_{ΔLDL-C/LDL-C} = 3.539, P = 0.017; F_{Δ(LDL-C/HDL-C)} = 5.938, P = 0.001; F_{Δ(LDL-C/HDL-C)/(LDL-C/HDL-C)} = 4.312, P = 0.006). In the dominant model with age as a covariate, ABCB1(2677T > G) gene polymorphism significantly affected Δ(LDL/HDL) (F = 3.571, P = 0.016), but had no significant effect on ΔLDL-C, ΔLDL-C/LDL-C, or Δ(LDL-C/HDL-C)/(LDL-C/HDL-C) (all P > 0.05). Binary logistic regression analysis showed that ABCB1(2677T > G) genotype was an independent risk factor affecting the lipid-lowering efficacy of atorvastatin. In the additive model, GG carriers exhibited 3.181-fold higher efficacy than TT (OR = 3.181, 95%CI:1.159 ~ 8.730, P = 0.025).In the recessive model, GG genotype showed 3.141-fold superiority over T-allele carriers (OR = 3.141, 95%CI:1.397 ~ 7.061, P = 0.006). Nighttime sleep deprivation independently compromised lipid-lowering efficacy (P < 0.001). No statistically significant differences in long-term clinical outcomes were observed among the three groups during the 36-month follow-up period (χ² = 1.465, P = 0.481). The ABCB1 (2677T > G) polymorphism is significantly associated with interindividual variability in the lipid-lowering efficacy of atorvastatin among patients CIS. Specifically, CIS patients carrying the GG genotype demonstrate superior lipid-lowering responses to atorvastatin therapy compared to wild-type T allele carriers. However, this genetic variation does not appear to influence long-term prognostic outcomes in this patient population.