B-type natriuretic peptide infusions in acute myocardial infarction.
BACKGROUND
Natriuretic peptides have actions likely to ameliorate cardiac dysfunction. B-type natriuretic peptide (BNP) is indicated as treatment for decompensated cardiac failure.


OBJECTIVE
To determine the utility of BNP in acute myocardial infarction (MI).


METHODS
Double-blind randomised placebo-controlled trial.


METHODS
Tertiary hospital coronary care unit.


METHODS
28 patients with acute MI with delayed or failed reperfusion and moderate left ventricular dysfunction.


METHODS
Infusion of BNP or placebo for 60 hours after MI.


METHODS
Neurohormonal activation and renal function in response to BNP infusion, secondary end points of echocardiographic measures of left ventricular function and dimension.


RESULTS
BNP infusion resulted in a significant rise in BNP (276 pg/l vs 86 pg/l, p = 0.001). NT-proBNP levels were suppressed by BNP infusion (p = 0.002). Atrial natriuretic peptide (ANP) and NT-proANP levels fell with a significant difference in the pattern between BNP infusion and placebo during the first 5 days (p<0.005). C-type natriuretic peptide (CNP) and NT-proCNP levels rose during the infusion with higher levels than placebo at all measurements during the first 3 days (p<0.01). Cyclic guanosine monophosphate (cGMP) was raised during the infusion period showing a peak of 23 pmol/l on day 2 (placebo 8.9 pmol/l, p = 0.002), with a correlation between BNP and cGMP levels (p<0.001). Glomerular filtration rate (GFR) fell with BNP infusion but was not significantly lower than with placebo (71.0 (5.6) vs 75.8 (5.4) ml/min/1.73 m2, p = 0.62). Patients receiving nesiritide exhibited favourable trends in left ventricular remodelling.


CONCLUSIONS
Nesiritide, given soon after MI, induced increments in plasma cGMP and CNP and decrements in other endogenous cardiac peptides with a neutral effect on renal function and a trend towards favourable ventricular remodelling.
Hillock
R J
RJ
Christchurch Cardioendocrine Research Group, Christchurch School of Medicine and Health Sciences and Christchurch Hospital, Christchurch, New Zealand.
Frampton
C M
CM
Yandle
T G
TG
Troughton
R W
RW
Lainchbury
J G
JG
Richards
A M
AM
D000368:Aged; D009320:Atrial Natriuretic Factor / Q000097:blood; D003324:Coronary Artery Disease / Q000097:blood / Q000188:drug therapy*; D006152:Cyclic GMP / Q000378:metabolism*; D004305:Dose-Response Relationship, Drug; D004311:Double-Blind Method; D018619:Echocardiography, Doppler, Pulsed / Q000379:methods; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D007668:Kidney / Q000187:drug effects; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood / Q000188:drug therapy*; D045283:Natriuretic Agents / Q000008:administration & dosage*; D020097:Natriuretic Peptide, Brain / Q000008:administration & dosage* / Q000097:blood; D010446:Peptide Fragments / Q000097:blood; D017461:Receptors, Atrial Natriuretic Factor / Q000008:administration & dosage* / Q000097:blood
D045283:Natriuretic Agents; D010446:Peptide Fragments; C058930:brain natriuretic peptide receptor; C109794:pro-brain natriuretic peptide (1-76); D020097:Natriuretic Peptide, Brain; D009320:Atrial Natriuretic Factor; D017461:Receptors, Atrial Natriuretic Factor; D006152:Cyclic GMP