title: Can angiotensin II +1675 G/A type 2 receptor gene polymorphism be a marker of left ventricular hypertrophy in patients with aortic stenosis?
abstract: OBJECTIVE
  Activation of the angiotensin II type 2 receptor (AT2R) gene lowers blood pressure, inhibits endothelial and smooth muscle proliferation, and modifies left ventricular hypertrophy (LVH) and fibrosis. Recently, several studies on the presence and importance of AT2R polymorphism for cardiovascular pathology have been reported. The study aim was to investigate any relationship between +1675 G/A AT2R polymorphism and the degree of LVH in patients with aortic stenosis (AS).
  
  
  METHODS
  The influence of +1675 G/A AT2R gene polymorphism on AS severity, degree of LVH and systolic function was analyzed in 308 patients (185 men, 123 women; mean age 61.5 +/- 10 years) with significant AS.
  
  
  RESULTS
  Due to chromosome X localization of the AT2R gene, the analysis was performed separately in males and females. The prevalence of genotypes was 32.8% for AA, 40.8% for AG, and 26.4% for GG in females; and 52.9% and 47.1% for the A and G alleles, respectively, in males. No correlation was found between +1675 G/A AT2R polymorphism and LVH. The only significant difference was a lower left ventricular ejection fraction (LVEF) and a greater end-systolic LV dimension in males carrying the A allele as compared to allele G carriers. The A allele was more frequently observed in patients with LVEF < 40%. In the multivariate analysis, presence of the A allele was significantly related to LVEF (adjusted for age, hypertension, coronary artery disease), although the impact was of borderline statistical significance (p = 0.04) and explained only 2% of LVEF variance.
  
  
  CONCLUSIONS
  The study results indicate that the +1675 G/A AT2R gene polymorphism cannot be considered as a marker of LVH in patients with AS, but its negative influence on LVEF in A allele carriers may be considered as a marker of premature left ventricular decompensation in males.
authors.affiliation: Department of Valvular Heart Diseases, National Institute of Cardiology, Warsaw, Poland. eorlowska@ikard.pl
authors.forename: Ewa
authors.initials: E
authors.lastname: Orlowska-Baranowska
authors.forename: Grzegorz
authors.initials: G
authors.lastname: Placha
authors.forename: Rafal
authors.initials: R
authors.lastname: Baranowski
authors.forename: Piotr
authors.initials: P
authors.lastname: Michalek
authors.forename: Jarosław
authors.initials: J
authors.lastname: Gora
authors.forename: Zbigniew
authors.initials: Z
authors.lastname: Gaciong
authors.forename: Janina
authors.initials: J
authors.lastname: Stepinska
mesh_terms: D000368:Aged; D000483:Alleles; D001024:Aortic Valve Stenosis / Q000150:complications* / Q000235:genetics; D015415:Biomarkers; D015331:Cohort Studies; D005260:Female; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000175:diagnosis / Q000235:genetics* / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D011110:Polymorphism, Genetic / Q000235:genetics*; D044139:Receptor, Angiotensin, Type 2 / Q000235:genetics*; D012720:Severity of Illness Index; D012727:Sex Characteristics; D013318:Stroke Volume / Q000502:physiology; D018487:Ventricular Dysfunction, Left / Q000503:physiopathology
chemical_list: D015415:Biomarkers; D044139:Receptor, Angiotensin, Type 2