title: Association of angiotensin converting enzyme and angiotensin II type 1 receptor genotypes with left ventricular function and mass in patients with angiographically normal coronary arteries.
abstract: OBJECTIVE
  To analyse the potential association of the angiotensin converting enzyme (ACE) and angiotensin II type 1 receptor (AT1R) gene polymorphisms on left ventricular function and mass in patients with normal coronary arteries.
  
  
  METHODS
  Consecutive sample.
  
  
  METHODS
  University hospital.
  
  
  METHODS
  141 consecutive white patients referred for coronary angiography and with angiographically normal coronary arteries. Patients with valvar diseases, cardiomyopathies, or a history of myocardial infarction were excluded.
  
  
  METHODS
  Left ventricular variables were measured for all patients. The ACE and AT1R genotypes were determined with a polymerase chain reaction based protocol using DNA prepared from white blood cells. A general linear model was used to compare data according to the ACE and to the AT1R genotypes.
  
  
  RESULTS
  A strong association was observed between left ventricular mass and systemic hypertension (mean (SD) hypertension: 114 (31) g/m2; no hypertension 98 (23) g/m2; P < 0.003). However, no influence of ACE and AT1R polymorphisms on left ventricular mass was found, regardless of systemic hypertension. The subjects homozygous for the AT1R CC mutation had a significantly lower ejection fraction than those with allele A (AC+AA) (mean (SD) 62(12)% and 68(10)%, respectively, P < 0.05). No synergistic interaction of ACE and AT1R gene polymorphisms on left ventricular function and mass was found.
  
  
  CONCLUSIONS
  These data do not support an association of the ACE and AT1R genotypes on left ventricular hypertrophy in white patients with normal coronary arteries.
authors.affiliation: Service de Cardiologie B et Hémodynamique, Hôpital Cardiologique, CHRU de Lille, France.
authors.forename: M
authors.initials: M
authors.lastname: Hamon
authors.forename: C
authors.initials: C
authors.lastname: Amant
authors.forename: C
authors.initials: C
authors.lastname: Bauters
authors.forename: F
authors.initials: F
authors.lastname: Richard
authors.forename: N
authors.initials: N
authors.lastname: Helbecque
authors.forename: E
authors.initials: E
authors.lastname: McFadden
authors.forename: J M
authors.initials: JM
authors.lastname: Lablanche
authors.forename: M
authors.initials: M
authors.lastname: Bertrand
authors.forename: P
authors.initials: P
authors.lastname: Amouyel
mesh_terms: D000804:Angiotensin II; D017023:Coronary Angiography; D005260:Female; D017353:Gene Deletion; D005838:Genotype; D006321:Heart / Q000503:physiopathology; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000000981:diagnostic imaging / Q000235:genetics* / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D007703:Peptidyl-Dipeptidase A / Q000235:genetics*; D011110:Polymorphism, Genetic; D011945:Receptors, Angiotensin / Q000235:genetics*
chemical_list: D011945:Receptors, Angiotensin; D000804:Angiotensin II; D007703:Peptidyl-Dipeptidase A