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European Heart Journal 1995 16(6):770-778;
Copyright © 1995 by the European Society of Cardiology.
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© 1995 The European Society of Cardiology

Neurohormonal changes after acute myocardial infarction

Relationships with haemodynamic indices and effects of ACE inhibition

S. G. Foy, I. G. CROZLER, A. M. RICHARDS, M. G. NICHOLLS, J. G. TURNER*, C. M. FRAMPTON and H. IKRAM

Department of Cardiology, Christchurch Hospital Christchurch, New Zealand
*Department of Nuclear Medicine, Christchurch Hospital Christchurch, New Zealand

revised 11 August 1994; accepted 26 September 1994.

Correspondence. Dr Hamid Ikram, Deptrtment of Cardiology, Christchurch Hospital, Private Bag 4710. Christchurch, New Zealand

Abstract

To determine the neurohormonal response to angiotensin-converting enzyme (ACE) inhibition after acute myocardial infarction, 36 patients presenting within 6 h of the onset of chest pain were studied in a single regional cardiology service. In this double-blind study, 13 patients ;were randomized to receive captopril, 12 patients received enalapril, and 11 patients received placebo, for 12 months.

In patients receiving placebo, acute myocardial infarction was associated with activation of the renin-angiotensin-aldosterone and sympathetic nervous systems, and stimulation of plasma brain natriuretic peptide and atrial natriuretic peptide levels. ACE inhibition did not significantly alter circulating levels of norepinephrine, brain natriuretic peptide or atrial natriuretic peptide. Compared with placebo, enalapril induced a steep decline in plasma ACE activity, and plasma angiolensin II levels were reduced by both ACE inhibitors.

Using grouped data, circulating levels of brain natriuretic peptide at the zero sampling time were significantly higher than atrial natriuretic peptide values. Brain natriuretic peptide levels at 72 h were significantly correlated with the radionuclide left ventricular ejection fraction measured 5 days and 3 months after infarction. Similar associations were observed for atrial natriuretic peptide and norepinephrine.

We confirm activation of the renin-angiotensin-aldosterone and sympathetic nervous systems after acute myocardial infarction. The atrial nairiuretic peptide and brain natriuretic peptide and sympathetic nervous system responses to acute myocardial infarction were not significantly modified by ACE inhibition. Brain natriuretic peptide and atrial natriuretic peptide levels were sign correlated with the left ventricular ejection fraction measured 5 days and again 3 months after myocardial infarction, and may prove a useful prognostic index.

Key Words: Myocardial infarction • renin-angiotensin system • sympathetic system • angiotensin-converting enzyme inhibitors • natriuretic peptides


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