Apolipoprotein A1 polymorphisms and risk of coronary artery disease: a meta-analysis

Abstract

A b s t r a c tIntroduction: It has been reported that APOA1 -75G/A polymorphism might be associated with susceptibility to coronary artery disease (CAD). Owing to mixed and inconclusive results, we conducted a meta-analysis to systematically summarize and clarify the association between APOA1-75G/A polymorphism and the risk of CAD. Material and methods: A systematic search of studies on the association of single nucleotide polymorphisms (SNP) with susceptibility to CAD was conducted. A total of 9 case-control studies (1864 cases and 1196 controls) on the APOA1-75G/A polymorphism were included. Results: We observed no statistically significant association between APOA1 -75G/A polymorphism and risk of CAD under the dominant genetic model (AA + AG vs. GG: OR = 1.03, 95% CI: 0.65-1.66), allelic contrast (A vs. G: OR = 0.88, 95% CI: 0.58-1.32), heterozygote model (AG vs. GG: OR = 1.24, 95% CI: 0.81-1.89) or homozygote model (AA vs. GG: OR = 0.52, 95% CI: 0.26-1.05). Significant heterogeneity between individual studies appears in all five models, but a strong association under the recessive genetic model (AA vs. AG + GG: OR = 0.51, 95% CI: 0.28-0.92). In the subgroup analysis by Hardy-Weinberg equilibrium (HWE; the presence or absence of HWE in controls), significantly decreased CAD risk and no significant heterogeneity were observed among controls consistent with HWE. Overall, the APOA1 A allele is one of the protective factors of CAD. A stronger association between APOA1-75G/A polymorphisms and CAD risk was present in the studies consistent with HWE. Conclusions: The minor allele of the APOA1-75G/A polymorphism is a protective factor for CAD, especially in the studies consistent with HWE.

Association of ficolin-2 (FCN2) functional polymorphisms and protein levels with rheumatic fever and rheumatic heart disease: relationship with cardiac function

“…First, cases with severe heart failure showed a decrease in ficolin-3 levels, and these low levels of ficolin-3 are a consequence of consumption after binding to altered self-structures in the myocardial cell wall, with subsequent complement activation, leading to inflammation and tissue damage. Xu et al [42] reported that the minor allele of the apolipoprotein A1 -75G/A polymorphism is a protective factor for coronary artery disease, especially in the studies consistent with HWE.…”

Metabolic and genetic profiling of young adults with and without a family history of premature coronary heart disease (MAGNETIC). Study design and methodology

“…Studies of subjects with an FH of premature CAD showed a higher frequency of lipid disorders, elevated lipoprotein a and homocysteine levels in this group of patients [21–25].…”

The Effects of Linoleic Acid Consumption on Lipid Risk Markers for Cardiovascular Disease in Healthy Individuals: A Review of Human Intervention Trials

“…These events subsequently lead to the development of atherosclerosis, heart disease, and myocardial infarction [9,10]. However, there are various mechanisms that increase the risk of CHD, such as high blood pressure, thrombosis, arrhythmia, inflammation, endothelial dysfunction, insulin resistance, oxidative stress, cigarette smoking, family history, obesity, and overall dietary patterns, among others [10,25]. Lipid levels are another such mechanism that have been suggested to be "strong" risk factors for CVD and mortality, such as high cholesterol, triglycerides (TGs), low-density lipoprotein cholesterol (LDL-C), lipoprotein(a) (Lp(a)), very-low-density lipoprotein cholesterol (VLDL-C), and low high-density lipoprotein cholesterol (HDL-C) [10,26].…”