Subject(s)
ABO Blood-Group System/genetics , Coronary Artery Disease/genetics , Genetic Predisposition to Disease , Genome-Wide Association Study , Myocardial Infarction/genetics , Coronary Artery Disease/blood , Coronary Artery Disease/complications , Humans , Myocardial Infarction/blood , Myocardial Infarction/complicationsABSTRACT
Published studies investigating the role of APOE gene on lipid response (total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C) and triglycerides) to statin treatment have reported inconsistent results. A meta-analysis was conducted to estimate the lipid response to statin treatment among APOE genetic variants (e2 carriers, e3e3 homozygotes and e4 carriers). Twenty-four studies were included in the meta-analyses. The pooled mean reduction (Delta mu) in TC from baseline was significant for all variants (e2 carriers: Delta mu=-27.7% (-32.5 to -22.8%), e3e3: Delta mu=-25.3% (-28.0 to -22.6%) and e4 carriers: Delta mu=-25.1% (-29.3 to -21.0%)). Significant changes in LDL-C, HDL-C and triglyceride levels were also noted for all genotypes, although these changes did not differ significantly among genotypic groups. There was significant heterogeneity among the studies. Given these non-significant effects of APOE genotypes on lipid responses, there is little reason to consider the use of APOE genetic testing for guiding treatment with statins.