Chronic beta-blocker treatment in patients with advanced heart failure. Effects on neurohormones.
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.
Teisman
A C
AC
Department of Clinical Pharmacology, University of Groningen, Groningen, The Netherlands. cliphar@med.rug.nl
van Veldhuisen
D J
DJ
Boomsma
F
F
de Kam
P J
PJ
Tjeerdsma
G
G
Pinto
Y M
YM
de Zeeuw
D
D
van Gilst
W H
WH
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
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