Ge. Newton et al., DIGOXIN REDUCES CARDIAC SYMPATHETIC ACTIVITY IN SEVERE CONGESTIVE-HEART-FAILURE, Journal of the American College of Cardiology, 28(1), 1996, pp. 155-161
Objectives. This study evaluated the effect of digoxin on cardiac symp
athetic activity in patients with congestive heart failure. Background
. Digoxin favorably alters autonomic tone in heart failure. Whether it
reduces cardiac sympathetic drive in the setting of heart failure is
unknown. Methods. Digoxin (0.25 mg intravenously) was administered to
12 patients with severe heart failure and elevated left ventricular en
d-diastolic pressure (>14 mm Hg, Group A), 5 patients with less severe
heart failure who had normal left ventricular end diastolic pressure
(less than or equal to 14 mm Hg, Group B) and 6 patients with normal v
entricular function. Seven additional patients with heart failure were
studied as a time control group. Cardiac and total body norepinephrin
e spillover, systemic arterial pressure, left ventricular filling pres
sure and peak positive first derivative of left ventricular pressure w
ere all assessed before and 30 min after administration of digoxin. Re
sults. In Group A there were no changes in hemodynamic variables or to
tal body norepinephrine spillover after digoxin administration; howeve
r, there was a significant reduction in cardiac norepinephrine spillov
er (263 +/- 70 to 218 +/- 62 pmol/min, mean +/- SEM, p < 0.001). In co
ntrast, in Group B, digoxin caused a significant increase in cardiac n
orepinephrine spillover that was not associated with any hemodynamic c
hanges or a change in total body spillover. There were no hemodynamic
or spillover changes in the time control or normal ventricular functio
n group. Conclusions. Digoxin, in the absence of detectable inotropic
or hemodynamic effects, caused a reduction in cardiac norepinephrine s
pillover in patients with heart failure who had elevated filling press
ures. This finding suggests a potentially beneficial primary autonomic
action of digoxin in patients with severe heart failure.