title: Association of left ventricular mass with the AGTR1 A1166C polymorphism.
abstract: BACKGROUND
  The A1166C polymorphism is located within the microRNA-155 binding site of the human angiotensin II (Ang II) type-1 receptor (AGTR1) gene. The C allele interferes with the base-pairing complementariness between AGTR1 mRNA and microRNA-155 and thereby increases AGTR1 protein expression in vitro. We hypothesized that left ventricular (LV) mass is associated with the AGTR1 A1166C polymorphism.
  
  
  METHODS
  Among 708 individuals (mean age, 49.4 years; 51.8% women) randomly recruited in a white European population, we measured LV structure by two-dimensional guided M-mode echocardiography, the AGTR1 A1166C polymorphism and the 24-h urinary aldosterone. We applied a mixed model to assess phenotype-genotype associations while adjusting for covariables and accounting for relatedness.
  
  
  RESULTS
  The AA (49.1%), AC (42.8%), and CC (8.1%) genotypes were in Hardy-Weinberg equilibrium. Using a recessive model, CC homozygotes compared to A-allele carriers showed significant increases (P < 0.021) in LV mass index (+5.78 ± 2.25 g/m(2)), mean wall thickness (MWT) (+0.48 ± 0.15 mm), interventricular septum (IVS) (+0.60 ± 0.18 mm) and posterior wall thickness (PWT) (+0.34 ± 0.15 mm), but lower 24-h urinary aldosterone excretion (geometric mean, 22.4 vs. 19.0 nmol; P = 0.050). Sensitivity analyses in 552 participants untreated for hypertension were confirmatory.
  
  
  CONCLUSIONS
  LV mass index is associated with the AGTR1 A1166C polymorphism. Further research should clarify to what extent this association might be mediated via different expression of AGTR1 as modulated by microRNA-155.
authors.affiliation: Studies Coordinating Centre, Division of Hypertension and Cardiovascular Rehabilitation, Department of Cardiovascular Diseases, University of Leuven, Belgium.
authors.forename: Yu
authors.initials: Y
authors.lastname: Jin
authors.forename: Tatiana
authors.initials: T
authors.lastname: Kuznetsova
authors.forename: Lut
authors.initials: L
authors.lastname: Thijs
authors.forename: Boris
authors.initials: B
authors.lastname: Schmitz
authors.forename: Yanping
authors.initials: Y
authors.lastname: Liu
authors.forename: Kei
authors.initials: K
authors.lastname: Asayama
authors.forename: Stefan-Martin
authors.initials: SM
authors.lastname: Brand
authors.forename: Stephane
authors.initials: S
authors.lastname: Heymans
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; D000368:Aged; D000369:Aged, 80 and over; D000450:Aldosterone / Q000652:urine; D004452:Echocardiography; D005260:Female; D006352:Heart Ventricles / Q000503:physiopathology; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000235:genetics*; D008875:Middle Aged; D020641:Polymorphism, Single Nucleotide; D044140:Receptor, Angiotensin, Type 1 / Q000235:genetics*
chemical_list: D044140:Receptor, Angiotensin, Type 1; D000450:Aldosterone