628 
PHYSIOLOGY 
rate the relation between left ventricular end- 
diastolic pressure and stroke work was unaf- 
fected up to heart rates of 158 per minute and 
at rates of 180 and 200 per minute deviates only 
at the highest work value examined. 
They noted that as pacing rate was increased 
higher and higher above approximately 139 
beats per minute a larger and larger portion of 
atrial systole occurred prior to opening of the 
mitral valve, and of course ventricular diastole 
became shorter and shorter. These observations 
are not in agreement with those of Berglund, 
Borst, Duff and Schreiner^^ who found a close 
correlation between left ventricular end-dia- 
stolic pressure and left atrial mean pressure at 
both high and low heart rates. Finally, these in- 
vestigators observed that when stroke work 
was plotted against mean left atrial pressure 
the function curves showed a shift to the left as 
heart rate was increased by atrial pacing, how- 
ever, when these same stroke work values were 
plotted against left ventricular end-diastolic 
pressure, and vide infra end-diastolic ventricu- 
lar volume, no such shift was seen. The implica- 
tion was clear from these studies that 
myocardial contractility was not significantly al- 
tered by atrial pacing up to rates of approxi- 
mately 180 per minute. Looking at this another 
way, one might state that if there were changes 
in myocardial contractility these changes had 
little or no effect on their left ventricular func- 
tion curves. Several years later the studies of 
Covell, Ross, Sonnenblick, and Braunwald*^ 
clarified this point. For they showed that while 
force-velocity curves, simultaneously con- 
structed along with ventricular function curves 
(stroke work/left ventricular end-diastolic 
pressure), shifted definitely to the right with 
increased heart rates (produced by atrial pac- 
ing), the left ventricular function curve was 
unaffected. The changes in myocardial contrac- 
tility produced by right atrial pacing is admit- 
ted to be small, and these observations do imply 
some insensitivity of the left ventricular func- 
tion curves to small changes in myocardial nor- 
epinephrine concentration and/or contractil- 
ity. 
In 1969, Leighton, Zaron, Robinson and 
Weissler^- studied the effect of atrial pacing on 
hemodynamic data and systolic time intervals 
in 10 patients with heart disease, eight of whom 
had "left ventricular dysfunction" and the 
other two had mitral stenosis. They concluded 
that "during atrial pacing there was no signifi- 
cant alteration in cardiac output, minute work, 
left atrial or pulmonary wedge mean pressure, 
or duration of left ventricular pre-ejection pe- 
riod." They did observe as others have, how- 
ever, that aortic diastolic pressure rose while 
left ventricular end-diastolic pressure fell as the 
pacing rate was increased. They also noted a 
significant rise in peak dP/dt in three of the pa- 
tients with the increase in atrial pacing rate. In 
all these studies a moderate increase in heart 
rate (an average of 44 beats/min) was used. 
These authors also were impressed that the fall 
in left ventricular end-diastolic pressure, and 
vide infra end-diastolic volume, could not be 
simply explained by an ineffective atrial con- 
traction, at high heart rates, as claimed by oth- 
ers and supported by their own observation of 
fusion of the V and A waves seen in the left 
atrial pressure pulse. Rather they use the fact 
that mean left atrial pressure was unchanged to 
support their contention that "the diminished 
filling volume of the left ventricle must there- 
fore be accounted for by factors other than sys- 
tolic emptying such as decreased diastolic filling 
time or mistimed left atrial systole. . . ." Their 
argument is unacceptable to this reviewer. 
Linhart" has recently reported his studies in 
patients where he used atrial pacing to alter 
left ventricular end-diastolic pressure and 
stroke work in order to produce what he has 
termed "pacing" ventricular function curves. 
He chose to evaluate the merit of using these 
curves for comparison of patients with normal 
and abnormal left ventricular function. He 
showed that the character of the pacing ventric- 
ular function curves he obtained with atrial 
stimulation permitted a clear separation of nor- 
mal and abnormal responses, and that they 
were particularly useful in identifying patients 
with valvular disease (without insufficiency) 
with an associated decrease in myocardial func- 
tion. He noted, that as heart rate was increased 
with atrial pacing there was a decrease in left 
ventricular end-diastolic pressure in both the 
normal and abnormal ventricle. 
Parker, Khaja and Case^^ have recently 
