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Apolipoprotein E phenotypes, serum lipoproteins and apolipoproteins in angiographically assessed coronary heart
P M Stuyt1, B J Brenninkmeijer, P N Demacker
1Department of Medicine, University of Nijmegen, The Netherlands.
Insights
Apolipoprotein E (apoE) phenotype does not directly increase coronary artery disease (CAD) risk. However, apoE polymorphism influences lipoprotein levels, indirectly affecting CAD risk when other factors are considered.
Area of Science:
- Cardiovascular Genetics
- Lipid Metabolism
- Medical Research
Background:
- Apolipoprotein E (apoE) plays a crucial role in lipid metabolism.
- The influence of apoE polymorphism on coronary artery disease (CAD) risk and associated lipid profiles requires further clarification.
Purpose of the Study:
- To investigate the association between apoE polymorphism and the incidence of CAD.
- To examine the impact of apoE phenotypes on serum lipid, lipoprotein, and apolipoprotein levels.
Main Methods:
- Study included 145 CAD patients and 153 controls, excluding individuals with specific comorbidities.
- Covariance and logistic regression analyses were performed, adjusting for age, sex, smoking, and body weight.
- ApoE phenotypes were analyzed in relation to CAD risk and lipid profiles.
Main Results:
- No significant direct association was found between apoE phenotypes and cardiovascular disease risk.
- CAD patients exhibited higher levels of total cholesterol, triglycerides, VLDL-cholesterol, LDL-cholesterol, and apoB, with lower HDL-cholesterol and apoA-I.
- The apoE E3/E2 phenotype was linked to lower cholesterol, LDL-cholesterol, and apoB, and higher apoE levels compared to E3/E3 and E4/E3 phenotypes.
- Lipid profiles, including LDL-cholesterol, apoA-I, and VLDL-cholesterol, were effective predictors of cardiovascular disease.
Conclusions:
- ApoE phenotype is not an independent risk factor for CAD when other risk factors are accounted for.
- ApoE polymorphism influences lipoprotein levels, potentially mediating an indirect effect on CAD risk.
- Understanding these genetic influences on lipid metabolism is key to assessing cardiovascular risk.
Abstract:
To determine the influence of the apolipoprotein E polymorphism on the occurrence of coronary artery disease (CAD) and on serum lipids, lipoproteins and apolipoproteins we studied 145 patients with angiographically defined CAD and compared them with 153 control subjects without history or complaints of vascular disease and with 35 subjects without significant stenosis on coronary arteriography. Subjects with hypertension, diabetes mellitus and endocrine or metabolic disorders were excluded. Covariance analysis and logistic regression analysis were performed with adjustment for age, sex, smoking habits and relative body weight. There were no significant differences for the apoE phenotypes on risk of cardiovascular disease. The CAD group had significantly higher mean values of serum cholesterol and triglycerides, very-low-density lipoprotein (VLDL)-cholesterol and VLDL-triglycerides, low-density lipoprotein (LDL)-cholesterol and apoprotein B; they had lower high-density lipoprotein (HDL)-cholesterol and apo A-I. The combination of LDL-cholesterol, apoA-I and VLDL-cholesterol was the best model in predicting cardiovascular disease. ApoE phenotype group E3/E2 had significantly lower values for serum cholesterol, LDL-cholesterol, and apoB and higher levels of apoE in comparison with the phenotype groups E3/E3 and E4/E3. The combination of LDL-cholesterol, cholesterol, apoE and VLDL-triglycerides was the best model in predicting the apoE phenotype. Thus, taking other risk factors into account, the apoE phenotype is not an independent risk factor for CAD; the apoE polymorphism influences lipoprotein levels and possibly, in that way, indirectly also the risk for CAD.