Objectives

To characterize the rs1042034 allele distribution in Vietnamese adults with untreated hypercholesterolemia and evaluate its impact on baseline lipid profiles and the early lipid-lowering response to rosuvastatin 20 mg.

Materials and Methods

In this cross-sectional exploratory study, 79 adults with low-density lipoprotein cholesterol [LDL-C] ≥ 3.4 mmol/L were enrolled and treated with rosuvastatin 20 mg plus lifestyle advice for 3 months. Genotypes were determined by TaqMan real-time PCR with Sanger sequencing validation. Baseline and 3-month lipid panels (LDL-C, high-density lipoprotein cholesterol [HDL-C], total cholesterol, non-HDL-C, triglycerides) were measured. Between-group comparisons used Kruskal–Wallis/ANOVA as appropriate; analysis of covariance (ANCOVA) models adjusted for baseline values assessed genotype (TT vs. CT + CC) effects on posttreatment lipids. Multivariable linear regression examined age, sex, and body-mass index as predictors; false discovery rate correction was applied.

Results

Baseline lipid concentrations did not differ significantly by genotype (overall LDL-C 4.37 ± 0.62 mmol/L; total cholesterol 6.62 ± 0.77 mmol/L). After three months, LDL-C reductions differed markedly by genotype (P < .001): median absolute reductions were −0.47 mmol/L (TT; fractional −9.7%), −1.12 mmol/L (CT; −28.1%) and −1.28 mmol/L (CC; −29.8%). HDL-C change also differed (P = .049) with medians 0.09, 0.24 and 0.15 mmol/L for TT, CT and CC, respectively. ANCOVA (adjusting for baseline) showed the TT genotype was independently associated with higher posttreatment LDL-C (β = 0.758; P = .001), lower posttreatment HDL-C (β = −0.121; P = .004), and higher TC (β = 0.482; P = .026) and non-HDL-C (β = 0.566; P = .007); TG was not affected (P = .751).

Conclusions

This study provides preliminary evidence that APOB rs1042034 polymorphism significantly influences rosuvastatin efficacy in Vietnamese patients with hypercholesterolemia.