Circulation, Vol 74, 1075-1084, Copyright © 1986 by American Heart Association
PW Armstrong, TP Stopps, SE Ford and AJ de Bold
We examined rapid ventricular cardiac pacing as a means of inducing heart
failure in the dog to establish the sequence and nature of physiologic
compensation in this preparation. Seven animals paced at 250 beats/min for
3 weeks (VP1 group) showed an increase in cardiac size from 78.5 +/-
9.5(SD) to 105.8 +/- 13.0 cm2, a reduction in mean arterial pressure from
149 +/- 7 to 130 +/- 21 mm Hg, a fall in cardiac index from 196 +/- 57 to
125 +/- 37 ml/kg/min, and an increase in left ventricular filling pressure
from 6 +/- 5 to 22 +/- 9 mm Hg and in right atrial pressure from 2 +/- 2 to
5 +/- 3 mm Hg. An additional series of six animals (VP2 group) was paced
until a clear biologic end point for heart failure was reached (average 5.3
+/- 1.9 weeks) and they showed similar but more advanced changes compared
with the VP1 group. The changes in cardiac size and hemodynamics in the VP1
and VP2 groups were significantly different from those in parallel studies
of 10 sham-operated animals. Plasma norepinephrine and renin activity were
unchanged in sham-operated animals, whereas in the VP1 group, plasma
norepinephrine rose from 338 +/- 118 to 764 +/- 567 pg/ml (p less than
.05), but plasma renin activity did not change. In the VP2 group
norepinephrine rose from 471 +/- 285 to 999 +/- 425 pg/ml (p less than
.025) and plasma renin rose from 2.1 +/- 1.5 to 8.0 +/- 7.1 ng/ml/hr (p
less than .05). There was an excellent correlation between plasma
norepinephrine and renin activity before the animals were killed in both
the VP1 and VP2 groups (r = .88, p less than .001). No change was evident
in atrial natriuretic factor content, as determined by bioassay, in
sham-operated or VP1 group animals. However, there was a significant
reduction in atrial natriuretic activity from the right atrium that was
inversely correlated with the level of right atrial pressure in the VP2
group.
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Rapid ventricular pacing in the dog: pathophysiologic studies of heart failure
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