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Metoprolol Increases Plasma Cardiac Natriuretic Peptide Levels in Patients with Heart Failure

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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