title: Chronic beta-blocker treatment in patients with advanced heart failure. Effects on neurohormones.
abstract: BACKGROUND
  To date, the use of beta-blockers in treating patients with chronic heart failure gains support, this since several large clinical trials reported reduced mortality after chronic beta-blockade. Part of these beneficial effects may result from inhibition of deleterious neurohormone activation that accompanies progression of chronic heart failure. The present study evaluates whether this neurohormone inhibition is preserved after chronic beta-blockade.
  
  
  METHODS
  In a retrospective analysis the neurohormonal profiles of patients with moderate to severe chronic heart failure were studied from three treatment subgroups: (1) Without beta-blockers or ACE-inhibitors (n=15), (2) without beta-blockers, with ACE-inhibitors (n=324), (3) with beta-blockers and ACE-inhibitors (n=31). Patients were on beta-blockers for an average period of 3.8 years. Plasma samples were obtained under controlled conditions.
  
  
  RESULTS
  Despite uneven group sizes, the groups were well matched for clinical characteristics. Plasma renin levels were significantly lower in patients treated adjunctively with beta-blockers. Plasma aldosterone and endothelin-I levels also tended to be lower after chronic beta-blockade, however, this did not reach statistical significance.
  
  
  CONCLUSIONS
  Chronic adjunctive beta-blocker treatment shows significantly lower plasma renin levels when compared to single ACE-inhibition. This persistent reduction of plasma neurohormone activation may concomitantly reduce the chance of neurohormones to escape from inhibition.
authors.affiliation: Department of Clinical Pharmacology, University of Groningen, Groningen, The Netherlands. cliphar@med.rug.nl
authors.forename: A C
authors.initials: AC
authors.lastname: Teisman
authors.forename: D J
authors.initials: DJ
authors.lastname: van Veldhuisen
authors.forename: F
authors.initials: F
authors.lastname: Boomsma
authors.forename: P J
authors.initials: PJ
authors.lastname: de Kam
authors.forename: G
authors.initials: G
authors.lastname: Tjeerdsma
authors.forename: Y M
authors.initials: YM
authors.lastname: Pinto
authors.forename: D
authors.initials: D
authors.lastname: de Zeeuw
authors.forename: W H
authors.initials: WH
authors.lastname: van Gilst
mesh_terms: D000319:Adrenergic beta-Antagonists / Q000494:pharmacology* / Q000627:therapeutic use; D000368:Aged; D000450:Aldosterone / Q000097:blood; D000704:Analysis of Variance; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology; D009320:Atrial Natriuretic Factor / Q000097:blood / Q000187:drug effects; D019332:Endothelin-1 / Q000097:blood / Q000187:drug effects; D005260:Female; D006333:Heart Failure / Q000097:blood / Q000188:drug therapy*; D006801:Humans; D016015:Logistic Models; D008297:Male; D009479:Neuropeptides / Q000097:blood / Q000187:drug effects*; D018377:Neurotransmitter Agents / Q000097:blood*; D009638:Norepinephrine / Q000097:blood; D012083:Renin / Q000097:blood / Q000187:drug effects; D012189:Retrospective Studies
chemical_list: D000319:Adrenergic beta-Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors; D019332:Endothelin-1; D009479:Neuropeptides; D018377:Neurotransmitter Agents; D000450:Aldosterone; D009320:Atrial Natriuretic Factor; D012083:Renin; D009638:Norepinephrine