Cardiovascular disease remains the leading cause of death worldwide. In this review, we briefly summarize new insights on the modulation of genetic cardiovascular risk by host factors such as sex and age and lifestyle factors such as salt intake. As phenotypes (genotypes) of interest, we considered left ventricular structure and function (ADD1 Gly460Trp; AGTR2 G1675A; ACE D/I), the incidence of heart failure (ADD1 Gly460Trp), heart rate variability (CYP11B2 C-344T; AGTR1 A1166C), carotid distensibility (IL6 G-174C), and serum lipid levels (APOE e{open} 2/ e{open} 3/ e{open} 4; APOA1 A 75G). In each case, the associations with the genetic cardiovascular risk factor were modulated by sex, age, sodium intake, or a combination thereof. These interactions highlight that genetic risk factors and phenotype-genotype associations can only be interpreted within their ecogenetic context. Perhaps a better understanding of these phenomena will lead researchers to target in a more specific way the pathophysiologic mechanisms operating within each individual. © 2008 Current Medicine Group LLC.
Modulation of genetic cardiovascular risk by age and lifestyle
Tikhonoff Valerie;
2008
Abstract
Cardiovascular disease remains the leading cause of death worldwide. In this review, we briefly summarize new insights on the modulation of genetic cardiovascular risk by host factors such as sex and age and lifestyle factors such as salt intake. As phenotypes (genotypes) of interest, we considered left ventricular structure and function (ADD1 Gly460Trp; AGTR2 G1675A; ACE D/I), the incidence of heart failure (ADD1 Gly460Trp), heart rate variability (CYP11B2 C-344T; AGTR1 A1166C), carotid distensibility (IL6 G-174C), and serum lipid levels (APOE e{open} 2/ e{open} 3/ e{open} 4; APOA1 A 75G). In each case, the associations with the genetic cardiovascular risk factor were modulated by sex, age, sodium intake, or a combination thereof. These interactions highlight that genetic risk factors and phenotype-genotype associations can only be interpreted within their ecogenetic context. Perhaps a better understanding of these phenomena will lead researchers to target in a more specific way the pathophysiologic mechanisms operating within each individual. © 2008 Current Medicine Group LLC.Pubblicazioni consigliate
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