Longstanding atrial fibrillation causes depletion of atrial natriuretic peptide in patients with advanced congestive heart failure.
BACKGROUND
Congestive heart failure (CHF) is characterized by neurohormonal activation, including increased plasma concentrations of atrial natriuretic peptide (ANP) and N-terminal ANP (N-ANP). Onset of atrial fibrillation (AF) further increases these peptides, but it may be hypothesized that concentrations decrease during longstanding AF due to inherent atrial degeneration.


OBJECTIVE
We sought to investigate the relation between neurohormonal activation in patients with CHF and the duration of concomitant AF.


METHODS
The study group comprised 60 patients (age 70 +/- 8 years) with advanced CHF due to left ventricular systolic dysfunction (left ventricular ejection fraction (LVEF) < 0.35) and chronic AF (duration 21 (1-340) months). Plasma neurohormone concentrations were measured, and multiple regression analysis was performed to identify their clinical predictors.


RESULTS
Median plasma neurohormone concentrations were: ANP 113 pmol/l, N-ANP 1187 pmol/l, norepinephrine 496 pg/ml, renin 127 micro units/l, aldosterone 128 pg/ml and endothelin 8.1 pg/ml. Norepinephrine, renin, aldosterone and endothelin were not significantly related to the duration of AF. In contrast, ANP decreased along with the duration of AF (P = 0.03), while the same trend was observed for N-ANP (P = 0.10). However, for these peptides a first order interaction with LVEF was present, which was not observed in the other neurohormones. In patients with LVEF > 0.25 ANP and N-ANP increased along with the duration of AF, whereas in patients with LVEF < or = 0.25 an inverse relation between ANP (P = 0.02) and N-ANP (P = 0.04) and the duration of AF was present, longer-standing AF being associated with lower concentrations.


CONCLUSIONS
In patients with advanced CHF with low LVEF plasma ANP and N-ANP concentrations decrease during longstanding AF. This finding agrees with the concept that longstanding AF leads to impaired ability of the atria to produce these neurohormones due to inherent degenerative changes.
van den Berg
Maarten P
MP
Department of Cardiology, Thorax Center, University Hospital Groningen, P.O. Box 30.001, 9700 RB Groningen, Hanzeplein 1, 9713 GZ, Groningen, The Netherlands. m.p.van.den.berg@thorax.azg.nl
Tjeerdsma
Geert
G
Jan de Kam
Pieter
P
Boomsma
Frans
F
Crijns
Harry J G M
HJ
van Veldhuisen
Dirk J
DJ
D000368:Aged; D000450:Aldosterone / Q000097:blood; D000704:Analysis of Variance; D001281:Atrial Fibrillation / Q000097:blood* / Q000503:physiopathology; D009320:Atrial Natriuretic Factor / Q000096:biosynthesis* / Q000097:blood; D005260:Female; D006333:Heart Failure / Q000097:blood* / Q000503:physiopathology; D006801:Humans; D008297:Male; D009638:Norepinephrine / Q000097:blood; D011498:Protein Precursors / Q000097:blood; D012083:Renin / Q000097:blood; D013318:Stroke Volume / Q000502:physiology; D013997:Time Factors; D018487:Ventricular Dysfunction, Left / Q000503:physiopathology
C099254:N-terminal proatrial natriuretic peptide; D011498:Protein Precursors; D000450:Aldosterone; D009320:Atrial Natriuretic Factor; D012083:Renin; D009638:Norepinephrine