Association of polymorphisms of ApoE, ApoA1, PCSK9 with LDL-C modification following Atorvastatin therapy in dyslipidemic patients.

Dyslipidemia, a risk factor for atherosclerotic cardiovascular disease, is primarily managed by statins. Single-nucleotide polymorphisms (SNPs) may influence LDL-C reduction variability seen with statins. Treatment-naïve adult dyslipidemic patients prescribed Atorvastatin (40/80mg) were enrolled in a 12-week observational study. Lipid profiles were estimated at baseline & follow-up (week 1, 2, 4, 12), serum ApoA1, ApoE & PCSK9 were estimated at baseline and week 12. Six SNPs were genotyped at baseline. LDL-C reduction of ≥50% was compared with SNP variants. In 55 patients who completed follow-up, a decrease in LDL-C, total cholesterol, triglycerides, and ApoE was 54.55%, 40.60%, 53.1%, and 40.46%, respectively. Meanwhile, HDL-C, ApoA1 & PCSK9 levels increased by 8.76%, 17.29% &12.35% respectively. Reduction in LDL-C levels was associated with variants of rs429358(T>C) [p= 0.05], rs7412(C>T) & rs429358(T>C) combined [p= 0.13], and rs7412(C>T), rs429358(T>C), rs5069(G>A) & rs505151(G>A) combined [p= 0.18]. Genotype-based therapy may improve treatment outcomes for atorvastatin in dyslipidemia.