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Neurohormonal activation in heart failure after acute myocardial infarction treated with beta-receptor antagonists

Hans Persson1, Karin Andréasson, Thomas Kahan

  • 1Section of Cardiology, Division of Internal Medicine, Karolinska Institutet Danderyd Hospital, S-182 88, Stockholm, Sweden. hans.persson@med.ds.sll.se

European Journal of Heart Failure
|January 29, 2002
PubMed

Insights

Beta-receptor antagonists like metoprolol decreased neurohormonal activity in heart failure patients post-myocardial infarction. Elevated NPY-LI and N-ANF levels at discharge predicted long-term cardiovascular mortality.

Area of Science:

  • Cardiology
  • Pharmacology
  • Biochemistry

Background:

  • Limited research exists on neurohormonal activation post-myocardial infarction (MI) with heart failure (HF) treated by beta-receptor antagonists.
  • Investigating the impact of beta(1) receptor antagonists versus agonists on neurohormonal markers is crucial for HF management.

Purpose of the Study:

  • To describe neurohormonal activity in HF patients after MI.
  • To compare the effects of metoprolol (beta(1) antagonist) and xamoterol (partial beta(1) agonist) on neurohormonal markers.

Main Methods:

  • A double-blind, randomized trial compared metoprolol (n=74) and xamoterol (n=67) in post-MI HF patients.
  • Plasma levels of catecholamines, neuropeptide Y-like immunoreactivity (NPY-LI), renin activity, and N-terminal pro-atrial natriuretic factor (N-ANF) were measured.
  • Clinical and echocardiographic data were collected at baseline and 3 months.

Main Results:

  • N-terminal pro-atrial natriuretic factor (N-ANF) correlated closely with HF severity indicators.
  • Metoprolol and xamoterol reduced catecholamines, dopamine, and renin activity.
  • Metoprolol increased NPY-LI and N-ANF, while xamoterol decreased N-ANF.

Conclusions:

  • Beta-receptor antagonists reduced sympathetic nervous system and renin-angiotensin system activity in HF patients post-MI.
  • Elevated NPY-LI and N-ANF at discharge were associated with increased long-term cardiovascular mortality.
  • Changes in N-ANF may relate to cardiac preload, renal function, and beta-receptor mediated effects.
Abstract

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