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
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.