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February 21, 2006
By: Jennifer Tartaglia MS
and Asher
Kimchi M.D.
Christchurch, New Zealand - Many epidemiological
studies have shown β-blockers reduce mortality in
heart failure (HF). Consequently, β-blockade is now
standard therapy for symptomatic HF. Acute and
chronic HF prognosis is indicated, in part, by
measuring levels of the B-type cardiac natriuretic
peptides, brain natriuretic peptide (BNP) and
N-terminal pro brain natriuretic peptide (NTproBNP).
These biomarkers appear to be good indicators of
diagnosis and cardiac function and have the
potential to be useful for cardiac diseases other
than heart failure. A study done by Mark E. Davis,
MBChB et al from the Christchurch School of Medicine
and Health Sciences in New Zealand reports that the
nonvasodilating β-blocker metoprolol causes a rise
in plasma BNP and NTproBNP in heart failure patients
that is unrelated to any clinical deterioration. The
study was published in the February 13, 2006 issue
of Circulation.
The study was randomized, balanced, controlled, and
parallel-grouped. Participants in the study were men under the
age of 80 with an ejection fraction <40% as determined by
echocardiography. After baseline values were determined,
patients were randomized to either the β-blockade group which
received 47.5 mg/d metoprolol succinate titrating to 190 mg/d
over a 6-week period, or to the control group which received no
change in medications. All patients were followed for 6 weeks.
Atrial natriuretic peptide (ANP) and BNP infusions were given
during baseline testing and at the end of the 6-week trial. With
the infusions, arterial blood pressure, heart rate, cardiac
output, and ANP and BNP levels were monitored.
The main study finding was a significantly increased
endogenous plasma BNP (P=0.001) and NTproBNP (P=0.012) in the
β-blockade group. In addition, metoprolol increased ANP
(P=0.008), N-terminal pro atrial natriuretic peptide (NTproANP;
P < 0.001), and second messenger urinary cGMP (P=0.062). Metoprolol
also increased the increments in plasma ANP during BNP infusion
(P=0.016) and increased the BNP increments during ANP infusion
(P=0.076).
These findings suggest that β-blockade enhances cardiac
secretion of ANP and BNP and possibly decreases their clearance
in the presence of infused ANP and BNP. Consequently, the
authors recommend that clinicians should keep in mind that the
increased level of BNP and NTproBNP seen in stable, mildly
symptomatic heart failure patients receiving a nonvasodilating
β-blocker may not reflect worsening heart failure or a poor
prognosis.
Co-authors: A. Mark Richards, MD; M. Gary Nicholls, MD;
Timothy G. Yandle, PhD; Christopher M. Frampton, PhD; Richard W.
Troughton, MD.
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