title: Evaluation of cardiac sympathetic nerve activity and aldosterone suppression in patients with acute decompensated heart failure on treatment containing intravenous atrial natriuretic peptide.
abstract: OBJECTIVE
  Aldosterone prevents the uptake of norepinephrine in the myocardium. Atrial natriuretic peptide (ANP), a circulating hormone of cardiac origin, inhibits aldosterone synthase gene expression in cultured cardiocytes. We evaluated the effects of intravenous ANP on cardiac sympathetic nerve activity (CSNA) and aldosterone suppression in patients with acute decompensated heart failure (ADHF).
  
  
  METHODS
  We studied 182 patients with moderate nonischemic ADHF requiring hospitalization and treated with standard therapy containing intravenous ANP and 10 age-matched normal control subjects. ANP was continuously infused for >96 h. In all subjects, delayed total defect score (TDS), heart to mediastinum ratio, and washout rate were determined by 123I-metaiodobenzylguanidine (MIBG) scintigraphy. Left ventricular (LV) end-diastolic volume, end-systolic volume, and ejection fraction were determined by echocardiography. All patients with acute heart failure (AHF) were examined once within 3 days and then 4 weeks after admission, while the control subjects were examined only once (when their hemodynamics were normal). Moreover, for 62 AHF patients, plasma aldosterone concentrations were measured at admission and 1 h before stopping ANP infusion.
  
  
  RESULTS
  123I-MIBG scintigraphic and echocardiographic parameters in normal subjects were more favorable than those in patients with AHF (all p < 0.001). After treatment, all these parameters improved significantly in AHF patients (all p < 0.001). We also found significant correlation between percent changes of TDS and aldosterone concentrations (r = 0.539, p < 0.001) in 62 AHF patients.
  
  
  CONCLUSIONS
  The CSNA and LV performance were all improved in AHF patients. Furthermore, norepinephrine uptake of myocardium may be ameliorated by suppressing aldosterone production after standard treatment containing intravenous ANP.
authors.forename: Shu
authors.initials: S
authors.lastname: Kasama
authors.forename: Takuji
authors.initials: T
authors.lastname: Toyama
authors.forename: Toshiya
authors.initials: T
authors.lastname: Iwasaki
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Sumino
authors.forename: Hisao
authors.initials: H
authors.lastname: Kumakura
authors.forename: Kazutomo
authors.initials: K
authors.lastname: Minami
authors.forename: Shuichi
authors.initials: S
authors.lastname: Ichikawa
authors.forename: Naoya
authors.initials: N
authors.lastname: Matsumoto
authors.forename: Tomoaki
authors.initials: T
authors.lastname: Nakata
authors.forename: Masahiko
authors.initials: M
authors.lastname: Kurabayashi
mesh_terms: D019797:3-Iodobenzylguanidine; D061605:Administration, Intravenous; D000368:Aged; D000450:Aldosterone / Q000097:blood / Q000378:metabolism*; D009320:Atrial Natriuretic Factor / Q000008:administration & dosage / Q000494:pharmacology* / Q000627:therapeutic use; D005260:Female; D006333:Heart Failure / Q000000981:diagnostic imaging* / Q000188:drug therapy / Q000378:metabolism / Q000503:physiopathology*; D006352:Heart Ventricles / Q000187:drug effects / Q000294:innervation / Q000473:pathology; D006801:Humans; D008297:Male; D008875:Middle Aged; D020097:Natriuretic Peptide, Brain / Q000097:blood; D009929:Organ Size / Q000187:drug effects; D011877:Radionuclide Imaging; D013564:Sympathetic Nervous System / Q000187:drug effects* / Q000503:physiopathology*
chemical_list: D020097:Natriuretic Peptide, Brain; D019797:3-Iodobenzylguanidine; D000450:Aldosterone; D009320:Atrial Natriuretic Factor