title: Exercise capacity after coarctation repair relates to the c.46A > G genomic polymorphism of the ss2-adrenoreceptor and the c.704T > C angiotensinogen polymorphism.
abstract: BACKGROUND
  Even after excellent repair of aortic coarctation without restenosis there are limitations in exercise capacity at long-term follow-up. This study was performed to assess the contribution of inherited genomic polymorphisms to exercise capacity in patients without restenosis.
  
  
  METHODS
  122 patients aged 17-72 years, 46 female, 76 male, seen 2-27 years after repair of aortic coarctation with a residual brachial-ankle-gradient ≤20 mmHg were investigated. Genomic polymorphism of angiotensin converting enzyme (ACE I/D), angiotensinogen (AGT, c.704C > T), angiotensin II receptor type 1 (AGTR1, c.1166A > C), endothelin 1 (EDN1, EDN1/ex5-c.5665G > T), G protein (GNB3, c.825C > T), and two polymorphisms each of the ß1-adrenoreceptor (ADRB1, c.145G > A and c.1165C > G), ß2-adrenoreceptor (ADRB2, c.46A > G and c.79C > G), and endothelial NO synthase (NOS3, intron 4 I/D and NOS3, c.894G > T) were determined by PCR amplification and fragment length analysis. Exercise capacity was determined by an upright bicycle exercise test.
  
  
  RESULTS
  Only the c.46A > G polymorphism of the ADRB2 (p = 0.024) and the c.704T > C AGT polymorphism (p = 0.042) were positively correlated with peak workload. Patients with one or especially two polymorphic alleles showed a significant higher exercise performance compared with those patients homozygous for the wild type.
  
  
  CONCLUSIONS
  In contrast to a previous study in heart failure patients, after coarctation repair adults had a better exercise capacity with the G allele of the ß2-receptor c.46A > G polymorphism. Therefore, the exercise capacity of coarctation patients does not profit from an enhanced down regulation of their beta receptors.
authors: Department of Pediatric Cardiology and Congenital Heart Disease, Deutsches Herzzentrum München, Technische Universität München, Lazarettstrasse 36, Munich, Germany. a-hager@web.de
authors: Alfred
authors: A
authors: Hager
authors: Judith
authors: J
authors: Bildau
authors: Joachim
authors: J
authors: Kreuder
authors: Christian
authors: C
authors: Schreiber
authors: Harald
authors: H
authors: Kaemmerer
authors: John
authors: J
authors: Hess
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000808:Angiotensinogen / Q000235:genetics; D001017:Aortic Coarctation / Q000235:genetics* / Q000503:physiopathology / Q000601:surgery; D015536:Down-Regulation; D005080:Exercise Test; D017079:Exercise Tolerance / Q000502:physiology*; D005260:Female; D020022:Genetic Predisposition to Disease; D006801:Humans; D006973:Hypertension / Q000235:genetics*; D008297:Male; D008875:Middle Aged; D007703:Peptidyl-Dipeptidase A / Q000235:genetics; D011110:Polymorphism, Genetic; D011446:Prospective Studies; D018343:Receptors, Adrenergic, beta-2 / Q000235:genetics*; D055815:Young Adult
chemical_list: D018343:Receptors, Adrenergic, beta-2; D000808:Angiotensinogen; D007703:Peptidyl-Dipeptidase A