title: The impact of the AMPD1 gene polymorphism on exercise capacity, other prognostic parameters, and survival in patients with stable congestive heart failure: a study in 686 consecutive patients.
abstract: BACKGROUND
  Previous studies have demonstrated that the adenosine monophosphate deaminase 1 (AMPD1) C34T polymorphism may be associated with survival in cardiac populations with a protective effect of the T allele. However, these studies included limited number of patients with few cardiovascular events.
  
  
  METHODS
  We prospectively analyzed the impact of the C34T polymorphism of the AMPD1 gene in 686 unrelated white patients with stable congestive heart failure related to left ventricular systolic dysfunction. Patients underwent echocardiography, radionuclide angiography, and a cardiopulmonary exercise test. Blood samples were drawn for standard and hormonal determinations and for genetic analysis.
  
  
  RESULTS
  There were 517 (75%) CC homozygotes, 155 (23%) CT heterozygotes, and 14 (2%) TT mutated homozygotes. We did not demonstrate any impact of this polymorphism on clinical, biologic, echocardiographic, radionuclide, and exercise parameters in the whole population and in ischemic and nonischemic subgroups of patients. During a median follow-up period of 3 years, there were 145 cardiac-related deaths and 6 urgent transplantations. There was no impact of this polymorphism on survival.
  
  
  CONCLUSIONS
  In our population, we did not demonstrate any effect of the C34T polymorphism of the AMPD1 gene on major congestive heart failure parameters and on survival.
authors.affiliation: Service de Cardiologie C, Hôpital Cardiologique, Centre Hospitalier Régional et Universitaire de Lille, Boul Prof J Leclercq, 59037 Lille cedex, France. pdegroote@chru-lille.fr
authors.forename: Pascal
authors.initials: P
authors.lastname: de Groote
authors.forename: Nicolas
authors.initials: N
authors.lastname: Lamblin
authors.forename: Nicole
authors.initials: N
authors.lastname: Helbecque
authors.forename: Frédéric
authors.initials: F
authors.lastname: Mouquet
authors.forename: Xavier
authors.initials: X
authors.lastname: Hermant
authors.forename: Philippe
authors.initials: P
authors.lastname: Amouyel
authors.forename: Jean
authors.initials: J
authors.lastname: Dallongeville
authors.forename: Christophe
authors.initials: C
authors.lastname: Bauters
mesh_terms: D000659:AMP Deaminase / Q000235:genetics*; D000225:Adenine; D000328:Adult; D000368:Aged; D003596:Cytosine; D005260:Female; D005838:Genotype; D006333:Heart Failure / Q000209:etiology / Q000235:genetics* / Q000503:physiopathology; D006801:Humans; D007527:Isoenzymes / Q000235:genetics; D008297:Male; D008875:Middle Aged; D010807:Physical Endurance / Q000235:genetics*; D011110:Polymorphism, Genetic; D011379:Prognosis; D011446:Prospective Studies; D016019:Survival Analysis; D013599:Systole; D018487:Ventricular Dysfunction, Left / Q000150:complications
chemical_list: D007527:Isoenzymes; D003596:Cytosine; D000659:AMP Deaminase; C514117:AMPD1 protein, human; D000225:Adenine