title: Left ventricular structure in relation to the human SAH gene in the European Project on Genes in Hypertension.
abstract: Earlier studies showed association of the human SAH (Spontaneously hypertensive rat-clone A-Hypertension associated) gene with hypertension and obesity. Left ventricular mass index (LVMI) increases with blood pressure and body mass index. In a family-based population study (54.5% women; mean age, 43.1 years), we measured LVMI, mean wall thickness (MWT) and the left ventricular internal diameter (LVID) at end-diastole in 699 non-Slavic and 493 Slavic participants. In multivariable-adjusted analyses, we investigated phenotype-genotype associations (SAH G-1606A and -962ins/del polymorphisms), while accounting for confounders and relatedness. Non-Slavic -1606GG homozygotes had a slightly greater LVID than -1606A allele carriers (48.6 vs. 48.0 mm; P=0.08). However, the between-family component of the variance in LVID was significant (P=0.005), suggesting that population stratification might explain the latter finding. Non-Slavic -962del carriers had higher LVMI (91.1 vs. 88.5 g m(-2); P=0.03) and MWT (9.61 vs. 9.44 mm; P=0.03) than -962ins homozygotes. Transmission of the -962del to non-Slavic offspring was also associated with higher MWT (P=0.03). In Slavic participants, in the absence of population stratification (P>or=0.69), -1606GG homozygotes had lower LVMI (96.5 vs. 102.3 g m(-2); P=0.004) and lower MWT (10.1 vs. 10.5 mm; P=0.003) than -1606A carriers. Sensitivity analyses showed that the latter associations were confined to founders. Transmission of the -962del allele to Slavic offspring was associated with lower MWT (P=0.007). In conclusion, LVMI and MWT, two phenotypes that are jointly influenced by blood pressure and obesity, might be related to variation in the human SAH gene.
authors.affiliation: Studies Coordinating Centre, Division of Hypertension and Cardiovascular Research, Department of Cardiovascular Diseases, University of Leuven, Leuven, Belgium.
authors.forename: Yu
authors.initials: Y
authors.lastname: Jin
authors.forename: Tatiana
authors.initials: T
authors.lastname: Kuznetsova
authors.forename: Valérie
authors.initials: V
authors.lastname: Tikhonoff
authors.forename: Lutgarde
authors.initials: L
authors.lastname: Thijs
authors.forename: Sandra
authors.initials: S
authors.lastname: Hasenkamp
authors.forename: Veronika
authors.initials: V
authors.lastname: Bäumer
authors.forename: Katarzyna
authors.initials: K
authors.lastname: Stolarz-Skrzypek
authors.forename: Andrew
authors.initials: A
authors.lastname: Ryabikov
authors.forename: Tom
authors.initials: T
authors.lastname: Richart
authors.forename: Sofia
authors.initials: S
authors.lastname: Malyutina
authors.forename: Yuri
authors.initials: Y
authors.lastname: Nikitin
authors.forename: Edoardo
authors.initials: E
authors.lastname: Casiglia
authors.forename: Kalina
authors.initials: K
authors.lastname: Kawecka-Jaszcz
authors.forename: Agnieszka
authors.initials: A
authors.lastname: Olszanecka
authors.forename: Stefan-Martin
authors.initials: SM
authors.lastname: Brand-Herrmann
authors.forename: Eva
authors.initials: E
authors.lastname: Brand
authors.forename: Robert
authors.initials: R
authors.lastname: Fagard
authors.forename: Jan A
authors.initials: JA
authors.lastname: Staessen
mesh_terms: D000293:Adolescent; D000328:Adult; D003066:Coenzyme A Ligases / Q000235:genetics* / Q000502:physiology*; D004247:DNA / Q000235:genetics; D004452:Echocardiography; D005060:Europe / Q000453:epidemiology; D005190:Family; D005260:Female; D005787:Gene Frequency; D005838:Genotype; D006321:Heart / Q000502:physiology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D010641:Phenotype; D020641:Polymorphism, Single Nucleotide; D016277:Ventricular Function, Left / Q000235:genetics*; D055815:Young Adult
chemical_list: D004247:DNA; C487181:ACSM3 protein, human; D003066:Coenzyme A Ligases