title: Angiotensin I-converting enzyme and chymase gene polymorphisms - relationship to left ventricular mass in type 2 diabetes patients.
abstract: BACKGROUND
  Type 2 diabetic patients are at increased risk for cardiovascular morbidity and mortality. Increased left ventricular mass also predicts a higher incidence of cardiovascular events. Angiotensin II is a potent mediator of myocardial growth, and angiotensin II can be produced in the heart by angiotensin I-converting enzyme (ACE) and heart chymase (CMA). The aim of this study was to establish the role of ACE gene insertion/deletion (I/D) and CMA gene CMA/B polymorphisms in determining left ventricular mass in type 2 diabetic patients.
  
  
  METHODS
  Echocardiographic measurements, ACE gene I/D and CMA/B genotypes were determined in 154 type 2 diabetic patients.
  
  
  RESULTS
  Mean LVMI was higher among DD homozygotes compared to heterozygotes and II homozygotes (128.9 g/m2 vs. 120.5 g/m2 and 120.4 g/m2, respectively), but the difference was not statistically significant (ANOVA P=0.12). A similar effect was observed for the CMA/B polymorphism, where mean LVMI were 126.6 g/m2, 122.1 g/m2 and 118.2 g/m2, for carriers of AA, AG and GG genotype, respectively (not statistically significant, P=0.33). ACE I/D and CMA/B polymorphism were also analyzed jointly, and carriers of both DD and AA genotypes were found to have significantly higher LVMI values (P=0.05) than non-carriers (133.0 g/m2 and 121.2 g/m2, for 21 DD and AA carriers vs. 133 non-carriers). In multivariate analysis, the presence of DD and AA genotypes was independently associated with LVMI (P=0.04).
  
  
  CONCLUSIONS
  Our results may suggest the additive effect of ACE and CMA gene polymorphisms on the increase in left ventricular mass in NIDDM patients.
authors.affiliation: Department of Internal Medicine, Diabetology and Nephrology, Silesian Medical University, Zabrze, Poland. jgumprecht@slam.katowice.pl
authors.forename: Janusz
authors.initials: J
authors.lastname: Gumprecht
authors.forename: Marcin
authors.initials: M
authors.lastname: Zychma
authors.forename: Władysław
authors.initials: W
authors.lastname: Grzeszczak
authors.forename: Beata
authors.initials: B
authors.lastname: ŁAcka
authors.forename: Wacław
authors.initials: W
authors.lastname: Burak
authors.forename: Mariusz
authors.initials: M
authors.lastname: Mosur
authors.forename: Jacek
authors.initials: J
authors.lastname: Kaczmarski
authors.forename: Ireneusz
authors.initials: I
authors.lastname: Otulski
authors.forename: Tomasz
authors.initials: T
authors.lastname: Stokłosa
authors.forename: Piotr
authors.initials: P
authors.lastname: Czank
mesh_terms: D000368:Aged; D053818:Chymases; D003924:Diabetes Mellitus, Type 2 / Q000235:genetics* / Q000473:pathology; D004452:Echocardiography; D005260:Female; D020022:Genetic Predisposition to Disease; D005838:Genotype; D006352:Heart Ventricles / Q000000981:diagnostic imaging / Q000201:enzymology / Q000473:pathology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D009929:Organ Size; D007703:Peptidyl-Dipeptidase A / Q000235:genetics*; D011110:Polymorphism, Genetic; D012697:Serine Endopeptidases / Q000235:genetics*
chemical_list: D007703:Peptidyl-Dipeptidase A; D012697:Serine Endopeptidases; D053818:Chymases