In general, gene frequencies observed in this study were similar to those reported by other authors. Concerning an association between blood pressure and ApoE genotypes, some studies have shown an association between systolic blood pressure and E4E4 and E3E4 genotypes, suggesting that ApoE polymorphism can be a silent factor influencing the increase in blood pressure 31. Other studies, however, did not show this association 32,34. In our study, an inverse association was observed: high diastolic blood pressure in the E3E3 elderly. However, no reference was found about this possible association in the literature. This suggests that a correlation between blood pressure levels and ApoE polymorphism may exist, even though no causal genotype-phenotype relation was observed in regard to blood pressure, indicating that other not yet identified genetic-environmental interactions may exist.

Individuals and variables of the lipid profile assessed by simple logistic regression and their respective odds ratio Variables X2 P Odds ratio 95% CI LDL-cholesterol (130 mg/dL) 5.82 0.013 2.61 1.04-6.56 Uric acid (6 mg/dL) 6.05 0.007 0.09 0.10-0.78 Fibrinogen (300 mg/dL) 12.21 0.042 2.07 1.20-7.88 Total cholesterol (240 mg/dL) 3.58 0.060 1.23 2.77-5.43 X2- chi-square; CI - confidence interval

Surprisingly, individuals with the E3E4 genotype had a significantly higher mean age than E3E3 individuals did in our results. Differences in ApoE frequencies and longevity strongly suggest that relations between certain genotypes and longevity are also influenced by other variables, such as environmental factors and the interaction with other genetic factors (Fig.1). This variation could be responsible for the difficulty in defining a biological and clinical profile strongly correlated with risk factors for cardiovascular diseases at advanced ages (>80 years). Therefore, we believe that this may have contributed to the result obtained.

Studies showed higher mortality in the group of individuals with low blood pressure (both systolic and diastolic) than that in the group of individuals with higher-than-expected blood pressure 35. This result was later confirmed in similar studies, including the Framingham Study, in which participants were divided into two groups (<75 and 75 years). A substantial increase in the mortality rate was observed both in males and females with systolic blood pressure <120 mmHg. As we do not yet know precisely which role hypertension plays in the elderly, and the results here obtained showed an association between high diastolic blood pressure and E3E3 genotype, we cannot consider that the relation represents an additional risk in individuals with the referred genotype. Future studies on mortality follow-up in the elderly with different genotypes may clarify whether this relation is beneficial, neutral, or bad.

In several biological variables studied, body mass index and diastolic blood pressure showed significant differences among the most frequent ApoE genotypes. In this case, individuals with E3E3According to ethnic group, an association between the E3E4 genotype and acute myocardial infarction at an early age of 31 was observed. An association between the E4 allele and myocardial ischemia was also noted at 34. Among studies where no consistent association between ApoE genotypes and cardiovascular diseases was found, longitudinal studies on the relation between genotypes and coronary lesions lasting 4 to 6 years can be cited at 37. In one study conducted in Italy with 15,000 individuals, no association between cardiovascular diseases and differential ApoE genotypes was found at 33. It is still early to confirm or deny the association between the ApoE gene and cardiovascular diseases because the relation between ApoE and cardiovascular diseases is still controversial. We can infer that if this relation exists, it is not causal (direct) and may be associated with other factors, both genetic and environmental 1-4.

Unlike LDL-c, no correlation was observed between ApoE genotypes and HDL-c, mainly in regard to the presence of the E4 allele. This finding was also reported in other population studies, such as that by Pablos-Mendez et al at 36. Population studies have suggested the association between an increase in the frequency of hypertriglyceridemia (type IV HLP) in individuals with the E2 allele and individuals with the E4E4 genotype; a lower frequency of the E2 allele associated with dyslipidemia IIa; and an increase in the frequency of type IIb dyslipidemia in individuals with at least one E4 allele in their genotype at 32. However, the association of the effect of hypocholesterolemia and the E2 allele was stronger than the association of hypercholesterolemia and the E4 allele at 32.

Other findings of our study that were not reported in studies published about the subject were the relation between high fibrinogen levels and the E3E4 genotype and the relation between more elevated levels of uric acid and the E3E3 genotype. In regard to the former, it is worth noting that elevated fibrinogen levels are associated with cardiovascular diseases at 22. However, despite the differences observed between the two genotypes, the fibrinogen levels observed are within the reference levels (< 400 mg/dL) for both groups. Only one individual in the entire sample had fibrinogen levels higher than 400 mg/dL. In regard to the second finding, considering that high uric acid levels may increase the risk of cardiovascular diseases at 38, this association could reduce the benefits related to the E3E3 genotype in regard to atherogenesis.