title: Left ventricular hypertrophy, cardiac remodeling and asymmetric dimethylarginine (ADMA) in hemodialysis patients.
abstract: BACKGROUND
  The endogenous inhibitor of nitric oxide (NO), asymmetric dimethylarginine (ADMA), is a strong predictor of adverse cardiovascular outcomes in patients with end-stage renal disease (ESRD).
  
  
  METHODS
  Since arterial and cardiac remodeling is associated with altered endothelial microcirculatory responses to forearm ischemia (a NO-dependent response), interference of ADMA with the NO system may be important for the pathogenesis of left ventricular hypertrophy (LVH) in these patients. This study sought to identify the relationship between plasma ADMA and LV geometry and function in a cohort of 198 hemodialysis patients.
  
  
  RESULTS
  Plasma ADMA was significantly higher (P = 0.008) in patients with LVH (median 3.00 micromol/L, inter-quartile range 1.73 to 3.97 micromol/L) than in those without this alteration (1.88 micromol/L, 1.15 to 3.56 micromol/L) and was significantly related to left ventricular (LV) mass (r = 0.26, P < 0.001). Interestingly, ADMA was much higher (P < 0.001) in patients with concentric LVH (3.60 micromol/L, 2.90 to 4.33 micromol/L) than in patients with eccentric LVH (2.17 micromol/L, 1.47 to 3.24 micromol/L) or normal LV mass (1.76 micromol/L, 1.13 to 2.65 micromol/L). Furthermore, plasma ADMA was higher (P = 0.02) in patients with systolic dysfunction (3.52 micromol/L, 2.08 to 5.87 micromol/L) than in those with normal LV function (2.58 micromol/L, 1.53 to 3.84 micromol/L) and inversely related to ejection fraction (EF; r = -0.25, P < 0.001). The link between ADMA and LV mass and EF was confirmed by multivariate analysis (ADMA vs. LVMI, beta = 0.17, P = 0.006; ADMA vs. EF, beta = -0.24, P < 0.001).
  
  
  CONCLUSIONS
  Overall, this study indicates that raised plasma concentration of ADMA is associated to concentric LVH and LV dysfunction. Intervention studies are needed to see whether the link between ADMA and concentric LVH remodeling and LV dysfunction is a causal one.
authors.affiliation: CNR, Division of Nephrology, Centre of Clinical Physiology and Renal Unit, Via Sbarre Inferiori 39, 89131 Reggio Calabria, Italy. carmine.zoccali@tin.it
authors.forename: Carmine
authors.initials: C
authors.lastname: Zoccali
authors.forename: Francesca
authors.initials: F
authors.lastname: Mallamaci
authors.forename: Renke
authors.initials: R
authors.lastname: Maas
authors.forename: Francesco A
authors.initials: FA
authors.lastname: Benedetto
authors.forename: Giovanni
authors.initials: G
authors.lastname: Tripepi
authors.forename: Lorenzo S
authors.initials: LS
authors.lastname: Malatino
authors.forename: Alessandro
authors.initials: A
authors.lastname: Cataliotti
authors.forename: Ignazio
authors.initials: I
authors.lastname: Bellanuova
authors.forename: Rainer
authors.initials: R
authors.lastname: Böger
mesh_terms: D000328:Adult; D000368:Aged; D001120:Arginine / Q000031:analogs & derivatives* / Q000097:blood*; D004452:Echocardiography; D004730:Endothelium, Vascular / Q000502:physiology; D005260:Female; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000097:blood / Q000209:etiology*; D007676:Kidney Failure, Chronic / Q000150:complications / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D009569:Nitric Oxide / Q000096:biosynthesis; D006435:Renal Dialysis; D014664:Vasodilation; D018487:Ventricular Dysfunction, Left / Q000097:blood / Q000209:etiology*
chemical_list: D009569:Nitric Oxide; C018524:N,N-dimethylarginine; D001120:Arginine