NEUROHORMONAL CHANGES AFTER ACUTE MYOCARDIAL-INFARCTION - RELATIONSHIPS WITH HEMODYNAMIC INDEXES AND EFFECTS OF ACE-INHIBITION

Citation
Sg. Foy et al., NEUROHORMONAL CHANGES AFTER ACUTE MYOCARDIAL-INFARCTION - RELATIONSHIPS WITH HEMODYNAMIC INDEXES AND EFFECTS OF ACE-INHIBITION, European heart journal, 16(6), 1995, pp. 770-778
Citations number
53
Categorie Soggetti
Cardiac & Cardiovascular System
Journal title
ISSN journal
0195668X
Volume
16
Issue
6
Year of publication
1995
Pages
770 - 778
Database
ISI
SICI code
0195-668X(1995)16:6<770:NCAAM->2.0.ZU;2-3
Abstract
To determine the neurohormonal response to angiotensin-converting enzy me (ACE) inhibition after acute myocardial infarction, 36 patients pre senting 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 o f the renin-angiotensin-aldosterone and sympathetic nervous systems, a nd stimulation of plasma brain natriuteric peptide and atrial natriure tic peptide levels. ACE inhibition did not significantly alter circula ting levels of norepinephrine, brain natriuretic peptide or atrial nat riuretic peptide. Compared with placebo, enalapril induced a steep dec line in plasma ACE activity, and plasma angiotensin II levels were red uced by both ACE inhibitors. Using grouped data, circulating levels of brain natriuretic peptide at the zero sampling time were significantl y higher; than atrial natriuretic peptide values. Brain natriuretic pe ptide levels at 72 h were significantly correlated with the radionucli de left ventricular ejection fraction measured 5 days and 3 months aft er infarction. Similar associations were observed for atrial natriuret ic peptide and norepinephrine. We confirm activation of the renin-angi otensin-aldosterone and sympathetic nervous systems after acute myocar dial infarction. The atrial natriuretic peptide and brain natriuretic peptide and sympathetic nervous system responses to acute myocardial i nfarction were not significantly modified by ACE inhibition. Brain nat riuretic peptide and atrial natriuretic peptide levels were significan tly correlated with the left ventricular ejection fraction measured 5 clays and again 3 months after myocardial infarction, and may prove a useful prognostic index.