title: Association of genetic polymorphisms with endothelial dysfunction in chronic heart failure.
abstract: OBJECTIVE
  Endothelial dysfunction can be shown very early in the cardiovascular disease. In the present study the association between congestive heart failure (CHF), endothelial function and 3 gene polymorphisms was investigated.
  
  
  METHODS
  In 104 healthy controls and 104 CHF patients, endothelial constitutive nitric oxide synthase (ecNOS), angiotensin converting enzyme (ACE) and angiotensin II type 1 receptor (AT1R) gene polymorphisms were assessed. The cause of CHF was ischemic in 68 patients and dilated cardiomyopathy (DCMP) in 36 patients. High resolution brachial artery ultrasound was used in 37 CHF patients and 37 healthy controls to assess the endothelial function. Endothelium-dependent vasodilation (EDD) and endothelium-independent vasodilation (EID) were determined.
  
  
  RESULTS
  There no was difference between controls and CHF patients for the ACE, ecNOS, and AT1R genotype frequencies. Compared to controls CHF patients had significantly impaired EDD (9.0+5% vs 16±7%, p < 0.001) and EID (13±6% vs 19+8%, p = 0.001). EDD (7±4% vs 12+6%, p = 0.005), but not EID, was significantly impaired in ischemic CHF as compared to DCMP patients. In the CHF group ecNOS a allele and AT1R C allele influence the EDD.
  
  
  CONCLUSIONS
  Endothelial dysfunction was present in CHF group and the presence of ecNOS a allele and AT1R C allele further impaired EDD.
authors.affiliation: Department of Internal Medicine, Istanbul University, Istanbul Faculty of Medicine, Istanbul, Turkey. doktortimur@gmail.com.
authors.forename: M
authors.initials: M
authors.lastname: Kose
authors.forename: T S
authors.initials: TS
authors.lastname: Akpinar
authors.forename: O K
authors.initials: OK
authors.lastname: Bakkaloglu
authors.forename: A
authors.initials: A
authors.lastname: Tufan
authors.forename: A
authors.initials: A
authors.lastname: Sumnu
authors.forename: S
authors.initials: S
authors.lastname: Emet
authors.forename: M
authors.initials: M
authors.lastname: Kocaaga
authors.forename: O
authors.initials: O
authors.lastname: Erk
authors.forename: M S
authors.initials: MS
authors.lastname: Kayacan
authors.forename: K
authors.initials: K
authors.lastname: Güler
authors.forename: A S
authors.initials: AS
authors.lastname: Demirel
mesh_terms: D000328:Adult; D000368:Aged; D001916:Brachial Artery / Q000000981:diagnostic imaging / Q000503:physiopathology; D004730:Endothelium, Vascular / Q000503:physiopathology; D005260:Female; D006333:Heart Failure / Q000235:genetics* / Q000503:physiopathology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D009154:Mutation; D052250:Nitric Oxide Synthase Type III / Q000235:genetics*; D007703:Peptidyl-Dipeptidase A / Q000235:genetics*; D011110:Polymorphism, Genetic; D044140:Receptor, Angiotensin, Type 1 / Q000235:genetics*; D014463:Ultrasonography; D014664:Vasodilation
chemical_list: D044140:Receptor, Angiotensin, Type 1; C496314:NOS3 protein, human; D052250:Nitric Oxide Synthase Type III; D007703:Peptidyl-Dipeptidase A