title: Left ventricular hypertrophy and endothelial dysfunction in chronic hemodialysis patients.
abstract: BACKGROUND
  Endothelial dysfunction (ED), which is a risk factor for atherosclerosis, has been reported recently in chronic hemodialysis (CHD) patients. In this study, we aim to investigate the association of ED and presence of left ventricular hypertrophy (LVH) in CHD patients.
  
  
  METHODS
  One hundred four CHD patients (47 men, 57 women; mean age, 45 +/- 12 years) and 49 age- and sex-matched controls were included. Mean time on dialysis therapy was 62 months. Echocardiographic examination and flow-mediated endothelium-dependent (EDD) and endothelium-independent dilatation (EID) of the brachial artery, measured by high-resolution ultrasonography, a noninvasive method for assessing endothelial function, were performed on a nondialysis day.
  
  
  RESULTS
  LVH was detected in 72 CHD patients (69%). Patients with LVH had a lower EDD (9.3% +/- 6.1% versus 12.1% +/- 8.3%; P = 0.06), but the difference was not significant. Mean EID was significantly lower in CHD patients with LVH (13.6% +/- 7.6% versus 18.6% +/- 9.8%; P = 0.008). Left ventricular mass index (LVMI) correlated with both EDD (r = -0.22; P = 0.03) and EID (r = -0.32; P = 0.002). Patients with LVH had a greater rate of hypertension (35 of 72 versus 7 of 32 patients; P = 0.02) and lower hemoglobin levels (11.0 +/- 1.8 versus 11.8 +/- 1.6 g/dL [110 +/- 18 versus 118 +/- 16 g/L]; P = 0.05). CHD patients had a lower EDD (10.2% +/- 6.9% versus 20.9% +/- 7.6%; P < 0.001) and EID (15.0% +/- 8.5% versus 27.8% +/- 8.5%; P < 0.001) compared with controls. In linear regression analysis for predicting LVMI, presence of hypertension, hemoglobin level, and EID, but not EDD, were found to be independent variables.
  
  
  CONCLUSIONS
  EID, which may reflect decreased elasticity of arteries, contributes to the development of LVH in CHD patients, in addition to hypertension and anemia.
authors.affiliation: Department of Internal Medicine, Division of Nephrology, Istanbul School of Medicine, Istanbul, Turkey. alaattiny@hotmail.com
authors.forename: Alaattin
authors.initials: A
authors.lastname: Yildiz
authors.forename: Huseyin
authors.initials: H
authors.lastname: Oflaz
authors.forename: Hamdi
authors.initials: H
authors.lastname: Pusuroglu
authors.forename: Fehmi
authors.initials: F
authors.lastname: Mercanoglu
authors.forename: Hakan
authors.initials: H
authors.lastname: Genchallac
authors.forename: Vakur
authors.initials: V
authors.lastname: Akkaya
authors.forename: T Alp
authors.initials: TA
authors.lastname: Ikizler
authors.forename: Mehmet S
authors.initials: MS
authors.lastname: Sever
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D001916:Brachial Artery / Q000000981:diagnostic imaging / Q000503:physiopathology; D016022:Case-Control Studies; D003430:Cross-Sectional Studies; D004452:Echocardiography / Q000379:methods; D004730:Endothelium, Vascular / Q000000981:diagnostic imaging / Q000503:physiopathology*; D005260:Female; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000209:etiology* / Q000503:physiopathology; D007676:Kidney Failure, Chronic / Q000503:physiopathology / Q000628:therapy; D008297:Male; D008875:Middle Aged; D012039:Regional Blood Flow / Q000502:physiology; D006435:Renal Dialysis / Q000009:adverse effects*; D014664:Vasodilation / Q000502:physiology