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

20Citations
Citations of this article
38Readers
Mendeley users who have this article in their library.

Abstract

Background: Few studies have described how neurohormonal activation is influenced by treatment with beta-receptor antagonists in patients with heart failure after acute myocardial infarction. The aims were to describe neurohormonal activity in relation to other variables and to investigate treatment effects of a beta1 receptor-antagonist compared to a partial beta1 receptor-agonist. Methods: Double-blind, randomized comparison of metoprolol 50-100 mg b.i.d. (n = 74), and xamoterol 100-200 mg b.i.d (n = 67). Catecholamines, neuropeptide Y-like immunoreactivity (NPY-LI), renin activity, and N-terminal pro-atrial natriuretic factor (N-ANF) were measured in venous plasma before discharge and after 3 months. Clinical and echocardiographic variables were assessed. Results: N-ANF showed the closest correlations to clinical and echocardiographic measures of heart failure severity, e.g. NYHA functional class, furosemide dose, exercise tolerance, systolic and diastolic function. Plasma norepinephrine, dopamine and renin activity decreased after 3 months on both treatments, in contrast to a small increase in NPY-LI which was greater (by 3.9 pmol/1, 95% CI 1.2-6.6) in the metoprolol group. N-ANF increased on metoprolol, and decreased on xamoterol (difference: 408 pmol/1, 95% CI 209-607). Increase above median of NPY-LI (> 25.2 pmol/1, odds ratio 2.8, P = 0.0050) and N-ANF (> 1043 pmol/1, odds ratio 2.8, P = 0.0055) were related to long term (mean follow-up 6.8 years) cardiovascular mortality. Conclusions: Decreased neurohormonal activity, reflecting both the sympathetic nervous system and the renin-angiotensin system, was found 3 months after an acute myocardial infarction with heart failure treated with beta-receptor antagonists. The small increase in NPY-LI may suggest increased sympathetic activity or reduced clearance from plasma. The observed changes of N-ANF may be explained by changes in cardiac preload, renal function, and differences in beta-receptor mediated inhibition of atrial release of N-ANF. NPY-LI, and N-ANF at discharge were related to long term cardiovascular mortality. © 2002 European Society of Cardiology. All rights reserved.

Cite

CITATION STYLE

APA

Persson, H., Andréasson, K., Kahan, T., Eriksson, S. V., Tidgren, B., Hjemdahl, P., … Erhardt, L. (2002). Neurohormonal activation in heart failure after acute myocardial infarction treated with beta-receptor antagonists. European Journal of Heart Failure, 4(1), 73–82. https://doi.org/10.1016/S1388-9842(01)00196-9

Register to see more suggestions

Mendeley helps you to discover research relevant for your work.

Already have an account?

Save time finding and organizing research with Mendeley

Sign up for free