title: Relationship between ACE gene polymorphism and ischemic chronic heart failure in Turkish population.
abstract: BACKGROUND
  Angiotensin-converting enzyme (ACE) gene insertion/deletion (I/D) polymorphism has been associated with the development of left ventricular hypertrophy, myocardial infarction, and remodeling. However, little is known about its role in ischemic chronic heart failure (CHF). We investigated the relationship between ACE gene I/D polymorphism and ischemic CHF and its influence on exercise capacity.
  
  
  METHODS
  ACE gene I/D polymorphism was analyzed in 209 Turkish patients with coronary artery disease (CAD) undergoing coronary angiography. ACE genotype distributions were examined in 84 consecutive patients with ischemic CHF, functional capacity class II-IV to New York Heart Association and left ventricular ejection fraction (LVEF) < 40% and 125 consecutive patients with stable angina pectoris and LVEF > or = 40%. Furthermore the results of the cardiopulmonary exercise testing (CPX) in each ACE genotype were compared in medically treated ischemic CHF patients (n = 84).
  
  
  RESULTS
  ACE genotype distributions were similar between the patients with and without symptomatic CHF in CAD. The odds ratios were 0.95 for D homozygotes (p > 0.05) and 0.98 for the D allele (p > 0.05). In patients with ischemic CHF the differences in CPX findings were statistically not significant in ACE D/D, I/D and I/I genotypes (peak oxygen consumptions 13.7 +/- 4.6; 14.6 +/- 5.1 and 14.5 +/- 5.0 ml/kg/min, respectively (p >0.05).
  
  
  CONCLUSIONS
  In this study population, there was no evidence that ACE gene I/D polymorphism plays a role in the development of CHF in CAD or any influence on exercise capacity in treated patients with ischemic CHF.
authors.affiliation: Siyami Ersek Cardiovascular and Thoracic Surgery Center, Cardiology Department, Istanbul, Turkey.
authors.forename: T
authors.initials: T
authors.lastname: Akbulut
authors.forename: T
authors.initials: T
authors.lastname: Bilsel
authors.forename: S
authors.initials: S
authors.lastname: Terzi
authors.forename: F
authors.initials: F
authors.lastname: Ciloglu
authors.forename: S
authors.initials: S
authors.lastname: Unal Dayi
authors.forename: N
authors.initials: N
authors.lastname: Sayar
authors.forename: I
authors.initials: I
authors.lastname: Peker
authors.forename: K
authors.initials: K
authors.lastname: Yesilcimen
mesh_terms: D000368:Aged; D003324:Coronary Artery Disease; D005260:Female; D005787:Gene Frequency; D005838:Genotype; D006333:Heart Failure / Q000453:epidemiology* / Q000235:genetics*; D006801:Humans; D008297:Male; D008875:Middle Aged; D017202:Myocardial Ischemia / Q000453:epidemiology* / Q000235:genetics*; D007703:Peptidyl-Dipeptidase A / Q000235:genetics* / Q000378:metabolism; D011110:Polymorphism, Genetic; D014421:Turkey / Q000453:epidemiology
chemical_list: D007703:Peptidyl-Dipeptidase A