F. KRAFT-HUNTER AND E. W. HAWTHORNE 
627 
nal stroke work than when the atrium was 
stimulated at the same frequency. This was be- 
lieved to be largely because the ventricle was 
deprived of the atrial contribution to ventricu- 
lar filling during ventricular pacing. These 
investigators also suggested that electrical stim- 
ulation of the left ventricle, in contrast to stimu- 
lation by a normally propogated impulse, re- 
sulted in the ventricle producing less stroke 
work from any given end-diastolic pressure, 
largely because of a less synchronous ventricu- 
lar contraction. On the contrary, Benchimol and 
Liggett" found no significant difi'erences be- 
tween artificial stimulation of the right atrium 
and right ventricle at rates between 80 and 180 
beats per minute. They observed no significant 
differences for cardiac index, stroke volume, 
mean arterial pressure, ventricular power and 
ejection time when the effect of atrial pacing 
was compared to ventricular pacing at any 
given rate between 80 and 180 beats per minute 
in normal subjects and in patients with either 
compensated heart disease or heart failure. 
They concluded that the contribution of atrial 
systole to cardiac function was minimal in nor- 
mal subjects. 
All studies show that end-diastolic volume de- 
creases with increase in pacing rate. In 1966 
Glick, Williams, Harrison, Morrow and Braun- 
wald^i sutured Roentgen opaque markers to 
the surfaces of one or both ventricles in 
nine patients at the time of corrective cardiac 
surgery. Post operative cineradiograms were 
obtained and the changes in the distances be- 
tween the markers were measured at regular 
periods throughout several heart cycles. When 
heart rate was increased by atrial pacing (by 
an average of 56 beats/min), they noted that 
right ventricular end-diastolic and end-systolic 
dimensions decreased by averages of 7.2 and 
4.9%, respectively. Left ventricular end-dia- 
stolic length decreased an average of 6.0%. 
These observed effects of heart rate on ven- 
tricular size are of course not new revelations. 
Since the beginning of this century it has been 
appreciated that heart rate may modify the size 
of the ventricles. Yandell Henderson in 1906=^ 
using a cardiometer placed about an open chest 
dog's heart observed that both the end-diastolic 
and end-systolic size of the whole heart de- 
creased as heart rate was increased. Further- 
more, he found that end-diastolic size decreased 
more than did end-systolic size for any given 
heart rate increase. Patterson, Piper and 
Starling'3 using their now famous heart-lung 
preparation and Wiggers and Katz-^ observed 
that slowing the heart rate by vagal stimulation 
increased both end-diastolic size and stroke vol- 
ume. This greater fall in end-diastolic size 
than end-systolic (and therefore decrease in 
stroke volume) was also observed in 1960 by 
Chapman^s and by Miller, Gleason, Whalen, 
Morris and Mcintosh"*' in 1962 in studies in- 
volving the use of cineangiographic techniques. 
Rushmer^'^ noted that the left ventricular ex- 
ternal diameter of conscious dogs decreased 
with each increase in rate of right atrial stimu- 
lation. Bristow, Ferguson, Mintz and Rapa- 
port,^'' have measured left ventricular end-dia- 
stolic and end-systolic volumes in anesthetized 
dogs and showed a decrease in these vol- 
umes with increases in right atrial pacing 
rate. 
Rusfcmer's studies^'^'^s on conscious dogs 
emphasize the significant differences in effect on 
ventricular function between a heart rate in- 
crease resulting from atrial or ventricular pac- 
ing and the rate increase associated with the ex- 
ercise response in conscious dogs. He noted that 
during exercise although heart rate increased 
markedly, stroke volume was either unchanged 
or slightly increased. Stroke work increased 
slightly and peak dP/dt was significantly in- 
creased. In contrast atrial pacing routinely 
caused a decrease in stroke volume and stroke 
work. Peak dP/dt was only insignificantly in- 
creased. The maintenance of stroke volume dur- 
ing exercise was apparently associaed with an 
increased ejection fraction resulting from in- 
creased cardiac sympathetic nerve activity. 
Mitchell, Gilmore, and Sarnoff^° studied the 
effect of increasing heart rate by right atrial 
pacing on the relation between mean left atrial 
pressure and left ventricular end-diastolic pres- 
sure. They observed that as the heart rate was 
increased in progressive steps up to 236 per 
minute the mean left atrial pressure became 
progressively higher than left ventricular end- 
diastolic pressure. When left ventricular func- 
tion curves were constructed for each atrial 
