title: Role of the angiotensin II type 2 receptor gene (+1675G/A) polymorphism on left ventricular hypertrophy and geometry in treated hypertensive patients.
abstract: OBJECTIVE
  A genetic polymorphism in the angiotensin II type 2 receptor (AGTR2 +1675G/A) has been associated with left ventricular hypertrophy (LVH). We tested whether this polymorphism affects LVH and left ventricular geometry parameters in patients with essential hypertension and cardiovascular disease who are treated according to guidelines.
  
  
  METHODS
  We analyzed a cohort of 208 women and 1030 men with essential hypertension, associated cardiovascular disease and left ventricular ejection fractions 40% or more. Previous cardiac diseases included coronary heart disease (81%) and myocardial infarction (MI; 52%). Ten parameters of left ventricular mass, geometry and function were determined by echocardiography. Genotyping was performed by PCR. Due to the X chromosomal location of AGTR2, genotype-phenotype analysis was separated for women and men. Statistical analysis was performed by univariate and multivariate analysis accounting for confounding factors.
  
  
  RESULTS
  The mean age was 58.4 +/- 10 years. In the overall cohort, mean left ventricular mass index was 54 +/- 23.6 g/h without significant differences between patients with and without MI. The frequency of LVH (49% overall) was also similar in patients with or without MI. In men, AGTR2 +1675G/A had no influence on echocardiographic parameters. Similar findings were obtained in women, with the exception that the thickness of the interventricular septum was significantly lower in A allele carriers (-11%) in both crude (P = 0.002) and multivariate analysis (P = 0.044).
  
  
  CONCLUSIONS
  In treated patients with arterial hypertension, cardiac disease and preserved left ventricular systolic function AGTR2 (+1675G/A) exhibits only a minor effect on left ventricular geometry in women and none in men.
authors.affiliation: Institute of Clinical Pharmacology and Toxicology, Charité Centrum für Therapieforschung, Charité - Universitätsmedizin Berlin, Berlin, Germany.
authors.forename: Matthias
authors.initials: M
authors.lastname: Huber
authors.forename: Heinz
authors.initials: H
authors.lastname: Völler
authors.forename: Stefanie
authors.initials: S
authors.lastname: Jakob
authors.forename: Rona
authors.initials: R
authors.lastname: Reibis
authors.forename: Van
authors.initials: V
authors.lastname: Do
authors.forename: Juliane
authors.initials: J
authors.lastname: Bolbrinker
authors.forename: Irina
authors.initials: I
authors.lastname: Zergibel
authors.forename: Roland E
authors.initials: RE
authors.lastname: Schmieder
authors.forename: Andras
authors.initials: A
authors.lastname: Treszl
authors.forename: Karl
authors.initials: K
authors.lastname: Wegscheider
authors.forename: Reinhold
authors.initials: R
authors.lastname: Kreutz
mesh_terms: D000368:Aged; D005260:Female; D005838:Genotype; D006239:Haplotypes; D006801:Humans; D006973:Hypertension / Q000188:drug therapy / Q000235:genetics* / Q000503:physiopathology; D017379:Hypertrophy, Left Ventricular / Q000235:genetics* / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D044139:Receptor, Angiotensin, Type 2 / Q000235:genetics*
chemical_list: D044139:Receptor, Angiotensin, Type 2