Abstract
BackgroundIncreased apolipoprotein (apo) B level (hyperapoB) is a strong predictor of cardiovascular disease (CVD), even in patients who achieve recommended LDL-Cholesterol (LDL-C) goals. ApoB level, an important correlate of metabolic syndrome (MetS), is influenced by several gene-environment interactions. Some of them are rare and can explain a large proportion of apoB variance, whereas others more common have variable effects. The aim of this study was to evaluate the association of interaction between smoking and common hyperapoB gene variants (PPARα-L162V, lipoprotein lipase loss-of function mutation, apo e4 allele or apo E2/2 genotype) with plasma apoB concentrations, according to the expression of MetS.MethodsThis study was performed among 1798 subjects. Smoking was defined as non/mild smokers vs. moderate-to-heavy smokers. ApoB levels were determined using nephelometry. Logistic regression models were used to document interactions between smoking habits and the presence of hyperapoB gene variants on the relative odds to exhibit increased plasma apoB concentrations.ResultsAround 29% of individuals with a low-risk lipid profile without MetS component had hyperapoB. Smoking and the presence of hyperapoB gene variants tended to be associated with higher plasma apoB levels even in presence of low-LDL-C. There was a significant interaction (P = 0.04) between the presence of ≥1 gene variants and smoking on the risk to exhibit hyperapoB among subjects with low risk profile in primary prevention.ConclusionsCombination of life habits assessment and some common genes variants may detect a significant proportion of patients with increased apoB levels, and therefore a higher risk of CVD, who could have been initially perceived as low-risk.
Highlights
Increased apolipoprotein B level is a strong predictor of cardiovascular disease (CVD), even in patients who achieve recommended LDL-Cholesterol (LDL-C) goals
The aim of this study was to evaluate the association of interactions between smoking and common gene variants affecting apoB catabolic pathways (PPARα-L162V, heterozygous loss-of function lipoprotein lipase (LPL) mutation, apo e4 allele or apo E2/2 genotype) with plasma apoB concentrations, according to the expression of metabolic syndrome (MetS)
Increase in the number of MetS components is associated with an Odds ratio (OR) of 1.8 (P < 0.001) to exhibit plasma apoB > 0.9 mmol/L among subjects with LDL-C < 3.5 mmol/L, whereas the relation between both variables is nonsignificant in subjects with LDL-C ≥ 3.5 mmol/L (OR = 1.1; P = 0.58)
Summary
Increased apolipoprotein (apo) B level (hyperapoB) is a strong predictor of cardiovascular disease (CVD), even in patients who achieve recommended LDL-Cholesterol (LDL-C) goals. The aim of this study was to evaluate the association of interaction between smoking and common hyperapoB gene variants (PPARα-L162V, lipoprotein lipase loss-of function mutation, apo e4 allele or apo E2/2 genotype) with plasma apoB concentrations, according to the expression of MetS. ApoE gene polymorphisms, the peroxisome proliferator-activated receptor (PPAR)α-L162V mutation, as well as loss-of-function (LoF) lipoprotein lipase (LPL) gene mutations, are examples of common variants modulating apoB-containing lipoprotein metabolism. APOE2, in the homozygous state, is associated with a reduced very-low-density lipoprotein (VLDL)-remnants clearance, an increased number of intermediatedensity lipoprotein (IDL) particles (β-VLDL) and a higher concentration of IDL-apoB, increasing the risk of dysbetalipoproteinemia and CVD [9]
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