Jg. Motwani et al., PLASMA BRAIN NATRIURETIC PEPTIDE AS AN INDICATOR FOR ANGIOTENSIN-CONVERTING-ENZYME INHIBITION AFTER MYOCARDIAL-INFARCTION, Lancet, 341(8853), 1993, pp. 1109-1113
Brain natriuretic peptide (BNP) is a cardiac ventricular hormone that
may be a sensitive and specific marker of changes in ventricular funct
ion. In a prospective, randomised open trial with 16 patients followed
for 6 months after first Q wave anterior myocardial infarction we set
out to determine: whether BNP concentrations are raised acutely, the
effect on circulating BNP of angiotensin-converting enzyme (ACE) inhib
ition, how BNP and atrial natriuretic peptide (ANP) concentrations com
pared as correlates of left-ventricular ejection fraction, and whether
plasma BNP concentrations could distinguish patients with low (<40%)
and relatively preserved (>40%) ejection fractions. Plasma concentrati
ons of BNP measured on days 2, 7, 8, 42, and 180 postinfarction were s
ignificantly raised in patients compared with normal controls and to a
proportionately greater degree than ANP concentrations. Treatment wit
h placebo (n=8) or oral captopril (n=8) from day 8 resulted in signifi
cantly lower BNP concentrations at days 42 (p=0.05) and 180 (p<0.05) i
n the captopril-treated group. Compared with ANP, BNP concentrations w
ere much more strongly correlated with radionuclide-measured left-vent
ricular ejection fraction at days 2, 42, and 180. All 8 patients with
baseline (day 2) ejection fractions of 40% or above had plasma BNP con
centrations less than 10 pmol/L, whereas the 8 patients with ejection
fractions less than 40% had BNP concentrations greater than 10 pmol/L.
Our findings suggest that measurements of circulating BNP may identif
y those patients with significant left-ventricular dysfunction who hav
e been highlighted by the Survival and Ventricular Enlargement study a
s likely to benefit from long-term ACE inhibition after myocardial inf
arction.