In hypertension, the association between APOE-ε4 and executive function was also only significant in participants with lower CO2 vasoreactivity (P = .005 for APOE by CO2 vasoreactivity).
In ApoE4+ women, CIMT was significantly higher in those with poor metabolic phenotype compared with healthy (p = 0.0003) and high blood pressure (p = 0.001) phenotypes.
In CAAH, APOE epsilon 2 may interact with putative risk factors for hemorrhage, including antiplatelet/anticoagulant medication, minor head trauma, and hypertension.
In conclusion, in Slovene women risk genotypes of the apoE gene polymorphism are not associated with premature CAD; a metabolic clustering of diabetes, HDL, triglycerides and arterial hypertension is frequently present in Caucasian women with premature CAD.
In conclusion, we present evidence that combinations of SNPs in APOE and LPL identify subgroups of individuals at substantially increased risk of IHD beyond that associated with smoking, diabetes and hypertension.
In exploratory analyses, significant deleterious effects were found for CIG (p=0.001), DM (p=0.03), and HTN (p=0.05) in APOE ε4 carriers only that remained significant only for CIG after correction for multiple comparisons.
In men only, ApoE E4 associated with CVD (adjusted OR (aOR)=1.46, 95%CI 0.76, 2.80) and with 18-year mortality (adjusted HR (aHR) =1.47, 95%CI 0.95, 2.26), adjusting for age, ethnicity, physical activity, hypertension, diabetes, LDL-cholesterol, HDL-cholesterol, triglycerides and lipid-lowering medications.
In multivariate, random-effects linear models adjusted for age, education, gender, and race, the risk factors diabetes and APOE epsilon4 genotype were independently associated with a decline in performance on the DSS test (both P < .005), whereas hypertension and stroke were not.
In pairings of APOE*4 with hypertension (HTN) and congestive heart failure (CHF), the variables contributed independently and additively to all-cause dementia risk.
In this population, we analyzed the relationship between background risk factors [age, gender, the G1691A polymorphisms of factor V gene, the C677T polymorphisms of the methylenetetrahydrofolate reductase (MTHFR) gene, the 844ins68bp polymorphisms of the cystathionine-beta-synthase (CBS) gene, and the apolipoprotein E (APOE) polymorphisms] and environmental risk factors, both atherogenic (smoke, hypertension, diabetes, dyslipidemia, obesity) and thrombogenic (smoke, homocysteine, fibrinogen) by a Markov block-recursive modeling approach.
Multiple logistic regression analysis created a model of significant MARCD predictors, including age (odds ratio [OR], 1.1 per year), hypertension (OR, 3.4), and the apoE epsilon 2/epsilon 3 genotype (OR, 3.0).
Our data show an association between apolipoprotein E genotype and hypertension and support the hypothesis that the apolipoprotein set membership, vertical bar on horizontal stroke 4 allele is a susceptibility locus for systolic hypertension and carotid artery atherosclerosis.
Our results not only demonstrated potential interactions of APOE epsilon2/epsilon3/epsilon4 and LDLR C1773T polymorphisms with risk of having ischemic stroke, but also added the evidence of independent role of hypertension and APOE epsilon2/epsilon3/epsilon4 polymorphism in the development of this disorder in Northern Han Chinese.
Persons with higher age (OR 1.08, 95% CI 1.01-1.16), ApoE epsilon4 allele carriers (OR 2.04, 95% CI 1.15-3.64) and persons with medicated hypertension (OR 1.86, 95% CI 1.05-3.29) were more likely to convert to MCI than those individuals of lower age and without an ApoE epsilon4 allele or medicated hypertension.
Predictors of MCI were APOE ε4 allele (hazard ratio [HR] 1.89; p = 0.008), current depressive symptoms (HR 1.78; p = 0.02), midlife onset of hypertension (HR 2.43; p = 0.005), increasing number of vascular diseases (HR 1.13; p = 0.02), and chronic conditions from the Charlson Comorbidity Index (HR 1.08; p = 0.006).