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Transcript
MYOCARDIAL STIFFNESS IN ANGINA/Bourdillon et al.
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41. McCans JL, Parker JO: Left ventricular pressure-volume relationship during myocardial ischemia in man. Circulation 48: 775, 1973
42. Sasayama S, Franklin D, Ross J Jr, Kemper WS, McKown D:
Dynamic changes in left ventricular wall thickness and their use in
analysing cardiac function in conscious dogs. Am J Cardiol 38:
870, 1976
43. Sasayama S, Ross J Jr, Franklin D, Bloor CM, Bishop S, Dilley
RB: Adaptations of the left ventricle to chronic pressure overload.
Circ Res 38: 172, 1976
44. Osakada G, Sasayama S, Kawai C, Hirakawa A, Kemper WS,
Franklin D, Ross J Jr: The analysis of left ventricular wall thickness
and shear by an ultrasonic triangulation technique in the dog. Circ
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45. Yellin EL, Yoran C, Masatsugu H, Sonnenblick EH, Frater RWM:
Time constant of left ventricular relaxation in the filling and transiently non-filling (completely isovolumic) intact canine heart.
(abstr) Circulation 62 (suppl III): 111-205, 1980
46. Nayler WG, Williams A: Relaxation in heart muscle: some morphological and biochemical considerations. EurJ Cardiol 7 (suppl):
35, 1978
47. Nayler WG, Poole-Wilson PA, Williams A: Hypoxia and calcium.
J Mol Cell Cardiology 11: 683, 1979
48. Henry PD, Schuchleib R, David J, Weiss ES, Sobel BE: Myocardial contracture and accumulation of mitochondrial calcium in ischemic rabbit heart. Am J Physiol 233: H677, 1977
relaxation and passive diastolic properties in man. (abstr) Circulation 62 (suppl III): 111-205, 1980
Paulus WJ, Bourdillon PD, Serizawa T, Grossman W, Pasipoularides A, Mirsky 1: Altered passive mechanical properties of ischemic left ventricular myocardium after pacing tachycardia in dogs
with coronary stenoses. (abstr) Circulation 64 (suppl IV): IV-21 1,
1981
Gaasch WH, Battle WE, Oboler AA, Banac JS, Levine HJ: Left
ventricular stress and compliance in man. With special reference to
normalised left ventricular function curves. Circulation 45: 746,
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Flessas AP, Connelly GP, Hand S, Tilney CR, Kloster DK, Rimmer RH Jr, Keefe JF, Klein DM, Ryan TJ: Effects of isometric
exercise on the end-diastolic pressure volumes and function of the
left ventricle in man. Circulation 53: 839, 1976
Quinones MA, Gaasch WH, Waisser E, Alexander JK: Reduction
in the rate of diastolic descent of the mitral valve echogram in
patients with altered left ventricular diastolic pressure-volume relations. Circulation 49: 246, 1974
McCullough WH, Covell JW, Ross J Jr: Left ventricular dilatation
and diastolic compliance changes during chronic volume overloading. Circulation 45: 943, 1972
Mathey D, Bleifeld W, Franken G: Left ventricular relaxation and
diastolic stiffness in experimental myocardial infarction. Cardiovasc Res 8: 583, 1974
Effect of Rate on Left Ventricular Volumes and
Ejection Fraction During Chronic Ventricular Pacing
KENNETH A. NARAHARA, M.D.
,
AND
M. LOUIs BLETTEL P. A.
,
SUMMARY Resting left ventricular (LV) function was evaluated in 22 patients with permanent ventricular pacemakers. LVejection fraction and volume indexes were determined by gated blood pool scintigraphy
at ventricular pacing rates of 50-100 beats/min. In patients with a normal heart size, increases in pacing
rates resulted in significant linear decreases in stroke volume index and ejection fraction. However, endsystolic volume index and cardiac index did not change. Patients with cardiomegaly appeared to respond
differently. End-diastolic volume index decreased significantly as the pacing rate was increased from 50 to
100 beats/min. Ejection fraction was significantly reduced only at pacing rates of 90 and 100 beats/min.
Mean cardiac index was highest at ventricular pacing rates of 70-90 beats/min. Increases in cardiac index,
achieved by increasing the pacing rate, were maintained over a 4.3-month follow-up. Patients with underlying sinus rhythm had a 27% increase in cardiac output in association with an increase in ejection fraction
from 55% to 62% when sinus rhythm was compared to ventricular pacing at a rate of 60 beats/min.
These data suggest that patients with cardiomegaly have a narrow range of optimal pacing rates at rest.
PROGRAMMABLE PACEMAKERS are widely
available. Pacing rate and other pacemaker functions
can be altered easily and noninvasively. Investigations
of the role of pacing rate on cardiac function have
From the Cardiovascular Section, Medical Service and Nuclear
Medicine Service of the Veterans Administration Medical Center, and
the Department of Intemal Medicine, Southwestern Medical School,
University of Texas Health Sciences Center, Dallas, Texas.
Supported in part by the Medical Research Service of the Veterans
Administration.
Performed during Dr. Narahara's tenture as a research associate of
the Veterans Administration.
Presented in part at the 28th Annual Meeting of the Society of Nuclear
Medicine, Las Vegas, June 1981.
Address for correspondence: Kenneth A. Narahara, M.D., Cardiology Division (Box 7), Harbor-UCLA Medical Center, 1000 West Carson
Street, Torrance, California 90509.
Received April 30, 1982; revision accepted July 30, 1982.
Circulation 67, No. 2, 1983.
produced varying results. Many investigationsl4 suggest that patients will have little or no change in cardiac
output when the ventricular pacing rate is altered.
However, Sowton5 and Samet et al.6 reported marked
increases in cardiac output when pacing rate is increased in selected patients. In addition, there are
occasional reports of patients with congestive heart
failure and severe bradycardia who have responded
favorably to ventricular pacing.7'
The cardiac response to changes in pacing rate may
be related to the degree of cardiac compensation.5 6
However, few data are available regarding left ventricular ejection fraction or ventricular volumes during
alterations in ventricular pacing rate. This study was
undertaken to evaluate resting left ventricular function
in patients with chronically implanted ventricular
pacemakers and to define alterations that might be
produced by changes in pacing rate.
324
CIRCULATION
Materials and Methods
Twenty-two male patients with a diagnosis of complete atrioventricular block were enrolled in the study.
All patients had ventricular inhibited, rate-adjustable
pacemakers (Medtronic Inc. models 5994, 5995, 5984
and 5985). The mean duration of ventricular pacing
was 5.2 years (range 1-9 years). Nineteen patients had
transvenous pacing leads implanted in the right ventricular apex and three had left ventricular epicardial
leads. The patients were 48-78 years old and had a
variety of underlying cardiac disorders (table 1).
Patients were initially categorized as having a normal heart size or an abnormal heart size. An abnormal
TABLE 1. Clinical Data
Duration
of
Age pacing
Pt
(years) (years)
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Normal heart size
1
65
2
62
3
78
4
60
4
8
3
6
7
60
65
63
4
6
6
8
48
5
9
10
73
65
9
8
S
Diagnosis
Idiopathic conduction system disease
Aortic stenosis
Coronary artery disease
Idiopathic conduction system disease,
hypertension
Coronary artery disease
Idiopathic conduction system disease
Idiopathic conduction system disease,
hypertension
Idiopathic conduction system disease,
hypertension
Idiopathic conduction system disease
Post aortic valve replacement for
aortic stenosis
Cardiomegaly
73
7
Idiopathic conduction system disease,
compensated CHF, normal coronary
2
57
9
3
62
8
4
60
8
Idiopathic conduction system disease,
compensated CHF
Post aortic valve replacement for
aortic insufficiency, compensated
CHF, normal coronary arteries
Coronary artery disease, prior
myocardial infarction, compensated
5
60
5
Idiopathic conduction system disease,
6
55
4
Idiopathic conduction system disease,
congestive cardiomyopathy, normal
7
66
1
Idiopathic conduction system disease,
hypertension
arteries
CHF
congestive cardiomyopathy
coronary
arteries
Underlying sinus rhylthm
66
61
66
76
72
Abbreviation:
3
4
5
heart size was defined as a cardiothoracic ratio greater
than 0.50.
Seventeen of the patients had no intrinsic cardiac
activity at a pacing rate of 50 beats/min. Further testing
of these patients revealed that none had an unpaced
cardiac rhythm during exercise stress. During the
course of the investigation, five of the patients with a
prior diagnosis of complete atrioventricular block were
noted to have an underlying sinus bradycardia with
ventricular rates of 52-60 beats/min.
Study Design
Each patient gave informed consent. Gated blood
pool scintigraphy was performed and left ventricular
ejection fraction and volume indexes were determined
at ventricular rates of 50, 60, 70, 80, 90 and 100 beats/
min. The five patients with an underlying sinus bradycardia mechanism were studied while in sinus rhythm
as well as at ventricular pacing rates of 60, 70, 80, 90,
and 100 beats/min. One of the five patients had a sinus
rate of 60 beats/min. In this patient, the lowest ventricular pacing rate resulting in 100% capture was 61
beats/min. Acquisition of scintillation data required 510 minutes at each pacing rate. Cuff blood pressure
recordings were obtained at the end of each scintigraphic collection period. At least 10 minutes were
allowed between a change in pacing rate and the commencement of scintigraphic data acquisition.
To evaluate the stability of rate-induced changes in
left ventricular function, the pacing rate was programmed from 70 beats/min to rates of 80 or 90 beats/
min in six patients. These patients were restudied scintigraphically an average of 4.3 months afterwards to
evaluate serial changes in left ventricular function.
Scintigraphic Studies
1
1
2
VOL 67, No 2, FEBRUARY 1983
4
1
Idiopathic conduction system disease
Idiopathic conduction system disease,
hypertension
7
Coronary artery disease
3
Coronary artery disease
4
Idiopathic conduction system disease
CHF = congestive heart failure.
The scintigraphic studies were obtained using in
vivo labeled red blood cells. Unlabeled stannous pyrophosphate (Phosphotel, Squibb) was administered intravenously. Thirty minutes later, 25 mCi of technetium-99m sodium pertechnetate were administered.
Scintigraphic data collection was performed with a
mobile gamma camera (Ohio Nuclear Sigma 420)
equipped with high-resolution, parallel-hole collimator interfaced to a dedicated computer system (Ohio
Nuclear VIP 450). The cardiac cycle was divided into
32 equal segments and approximately 180,000 counts/
frame were collected. Left ventricular volumes were
calculated by the method of Dehmer et al.,9 with an
operator-chosen background around the left ventricle.
Left ventricular isotope activity was related to isotope
activity per milliliter of peripheral venous blood and
converted to volumes by a regression equation after
correction for isotope decay.
Radionuclide ventriculography in this laboratory
was compared with contrast ventriculography using
the single-plane Kennedy regression equation.10 A
comparison of 24 patients not included in this study
demonstrated that the correlation coefficient for the
ejection fraction between contrast and radionuclide left
ventriculography was 0.95 (SEE = 2.7 ejection fraction percentage points). The correlation coefficient for
325
EFFECT OF PACING RATE/Narahara and Blettel
left ventricular volumes between contrast angiography
and radionuclide ventriculography was 0.94 (SEE =
16.3 ml over a volume range of 20-378 ml).
At least two radionuclide ventriculograms were performed at the same pacing rate on the same day in 15
patients. For example, if a patient initially had a pacing
rate of 70 beats/min, an initial study at a pacing rate of
70 beats/min was performed. After other pacing rates
had been tested, another study was performed at a rate
of 70 beats/min. The standard error of the estimate for
the ejection fraction when the two studies at the same
rate were compared was 2.1 ejection fraction percentage points. The standard error of the estimate for endsystolic and end-diastolic volumes was 10.7 ml when
the two scintigraphic studies were compared.
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Statistical Methods
Left ventricular ejection fraction and volume indexes, systolic blood pressure and double product were
evaluated in each patient group. These variables were
evaluated using Duncan's multiple-range test for variable response. A Student-Newman-Keul test was then
applied, and a p value < 0.05 was considered statistically significant.'1 All values are mean + SEM.
Results
In patients with cardiomegaly by conventional chest
x-ray, end-diastolic volume index at a pacing rate of 50
beats/min was substantially above the upper limits of
normal, with a mean of 149 ± 21.3 ml/m2. Enddiastolic volume index fell significantly at each incremental increase in pacing rate (fig. 1), and at a pacing
rate of 100 beats/min, had fallen to 1 12 + 17.4 mI/m2.
In contrast, patients with a normal-sized heart on conventional chest x-ray had an end-diastolic volume index of 81 + 5.3 ml/m2 at a pacing rate of 50 beats/min
(range 54-97 ml/m2) (fig. 2). Although there was a
trend toward decreasing end-diastolic volume index
with increasing pacing rate, the increments that
reached statistical significance were at pacing rates of
70 and 90 beats/min. Pacing rates of 70 and 90 beats/
min yielded progressively smaller end-diastolic volume indexes than rates of 50 and 60 beats/min. Values
at pacing rates of 80 and 100 beats/min were not significantly different from those at 90 beats/min.
End-systolic volume index was not significantly altered by changes in ventricular pacing rate in either
group of patients. End-systolic volume index was 94
± 22.8 ml/m2 in the patients with cardiomegaly and
fell to 79 ± 18.2 mI/m2 at a pacing rate of 100 beats/
min. This decrease was not significant at any point in
the pacing range. Similarly, end-systolic volume index
in the patients with a normal heart size was 35 ± 2.4
ml/m2 at a pacing rate of 50 beats/min and fell only
slightly, to 33 ± 2.2 ml/m2, at a pacing rate of 100
beats/min.
Since end-systolic volume index was essentially unchanged in both groups and end-diastolic volume index tended to decrease with increases in pacing rate,
(ml /M2)
1401
-140
120-
-120
STROKE
VOLUME
INDEX
100
END
80 - DIASTOLIC
t100
80
VOLUME
INDEX
60-
.60
40-
END
SYSTOLIC 40
VOLUME
INDEX
20-
-20
PACING RATE
EF
Cl (I/M )
SBP
DP
50
43
2.8
121
61
60
42
70
41
3.1*
3.3*
121
123
80
40
3.4
126
101*
90
38*
3.4
124
112*
100
35*
3.2
126
126*
73*
86*
FIGURE 1. Ejectionfraction (EF) and volume indexes in patients with cardiomegaly. End-diastolic volume index
at a pacing rate of 60 beatslmin is less than that at 50 beatslmin. Pacing at 80 beatslmin results in a lower value
than at 60 beats/min, but is not differentfrom that at 70 beatslmin. EF is reduced only at 90 and 100 beatslmin.
Maximal cardiac index (CI) occurs at pacing rates of 70 to 90 beats/min. Brackets indicate the SEM. *Significantly
different (p < 0.05)from all values at lower pacing rates. tSignificantly different (p < 0.05)from pacing rates
that are greater than 10 beats lower. SBP = systolic blood pressure; DP = double product.
326
VOL 67, No 2, FEBRUARY 1983
CIRCULATION
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stroke volume index fell in both groups. Stroke volume
index in the patients with cardiomegaly was 55 + 4.2
ml/m2 at a pacing rate of 50 beats/min, and it fell
significantly, to 33 ± 1.8 ml/m2, at a pacing rate of
100 beats/min. The mean values of estimated stroke
volume index at each of the six pacing rates were
significantly different (p < 0.05) (fig. 3). Similar
values, were recorded in patients with a normal heart
size in whom stroke volume index was 46 + 3. 1 mI/m2
at a pacing rate of 50 beats/min and decreased to 25 +
1.8 ml/m2 at a pacing rate of 100 beats/min. The values
for stroke volume index at each of the six ventricular
pacing rates in this group were also significantly different from each other (fig. 4).
Mean cardiac index in patients with cardiomegaly
was 2.8 + 0.2 1/min/m2 at a pacing rate of 50 beats/
min. There were small but statistically significant increases in cardiac index at ventricular pacing rates of
both 60 and 70 beats/min (3.1 ± 0.2 and 3.3 ± 0.2 1/
min/m2, respectively). Cardiac indexes at pacing rates
of 80 and 90 beats/min were not significantly different
from those recorded at 70 beats/min. However, there
was a small but significant decrease in cardiac index at
a ventricular pacing rate of 100 beats/min (3.2 ± 0.2
1/min/m2). The mean value for cardiac index at a pacing rate of 100 was not significantly different from
those at 50 and 60 beats/min.
The maximum cardiac index in this group of patients
was recorded at a ventricular pacing rate of 70 beats/
min in two patients, 80 beats/min in two, 90 beats/min
in two and 100 beats/min in one patient. In comparing
the highest cardiac indexes in these patients with the
values at a ventricular pacing rate of 50 beats/min, the
average increase was 0.8 + 1. 1/min/m2 (27%). In
contrast, changes in the ventricular pacing rate had no
significant effect on estimated cardiac index in patients
with a normal heart size.
The patients with cardiomegaly had their pacemakers programmed to the rate that provided the highest
resting cardiac index. These patients were restudied an
average of 4.3 months later. No significant changes
were noted between values recorded during the initial
study and the later study at the same rate.
Resting left ventricular ejection fraction in the patients with cardiomegaly was depressed (average 43 +
6.7%). The only significant changes in ejection fraction in this group occurred when ventricular pacing
rates of 90 and 100 beats/min were programmed. The
left ventricular ejection fraction at a rate of 90 beats/
min was 38 ± 6.3%, significantly less than the ejection fraction at a rate of 80 beats/min and less. The
ejection fraction at 100 beats/min fell further, to 35 +
5.7%, which was also significantly less than that at 90
beats/min and less. In patients with a normal heart
size, the left ventricular ejection fraction fell significantly with each 10-beat increase in pacing rate.
(mu/M2)
80-
80
~/1
70
70
'
Xt-
60
1
.7]-
5040
-60
STROKE -50
VOLUME
INDEX
-40
/
END
DIASTOLIC
VOLUME
INDEX
4
30
-30
END
SYSTOLICC -20
VOLUME
INDEX
-10
20
10
PACING RATE
2
EF
50
59
2.3
134
67
60
57*
70*
54
2.5
136
80*
52
90
49*
100
45*
2.5
2.5
2.4
2.5
Cl (I/M2)
SBP
135
136
135
135
DP
82*
95*
108*
122*
135*
FIGURE 2. Ejection fraction (EF) and volume indexes in patients with a normal heart size. Symbols and
abbreviations are as in figure 1. Significant decreases in end-diastolic volume are noted at pacing rates of 70 and
90 beatslmin. Significant decreases in EF are noted with each increase in ventricular pacing rate, but cardiac
index (CI) and end-systolic volume index are unchanged.
EFFECT OF PACING RATE/Narahara and Blettel
(I/M2 )
(I/M2)
4
4-
CARDIAC
INDEX
327
3-
[3
2-
.2
CARDIAC
INDEX
=*- 4
3
3
t
2-
(rml / M2)
50-
-2
-50
( mI/M,)
-60
60-
STROKE
VOLUME
INDEX
50
-40
40-
30PACING RATE
EF
L30
50
43
60
42
70
41
80
40
90
38
100
35*
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FIGURE 3. Cardiac index (CI) and stroke volume index in
patients with cardiomegaly. The CI is higher at rates of 60 and
70 beatslmin than at 50 beatslmin. Pacing at a rate of 1 00 beats!
min results in a CI that is lower than at 80 beatslmin and that is
not significantly differentfrom that recorded at 60 and 50 beatsl
min. EF = ejection fraction.
Patients with Intrinsic Sinus Rhythm
Five patients were noted to have sinus rhythm de-
spite a diagnosis of complete atrioventricular block.
Their average sinus rate was 55 ± 2 beats/min (range
52-60 beats/min). All had a normal heart size.
Estimated end-diastolic volume index with the patient in sinus rhythm was 95 + 10.3 ml/m2, which fell
significantly, to 81 ± 9.7 ml/m2, when ventricular
pacing was initiated at a rate of 60 beats/min (fig. 5).
End-diastolic volume index at a pacing rate of 100
beats/min was significantly less (66 ± 6.5 ml/m2) than
-40
STROKE 40VOLUME
INDEX
3020PACING RATE
EF
-30
-20
50
59
60
57*
70*
54
80
90
52*
49*
100
45*
FIGURE 4. Cardiac index (CI) and stroke volume index (SVI)
in patients with a normal heart size. SVI decreases with increasing pacing rate. However, the SVI is sufficient to maintain
a stable CI. No significant changes in CI are noted at any
pacing rate from 50 to 100 beatslmin. EF = ejection fraction.
the value recorded at a pacing rate of 80 beats/min.
There were no significant changes in estimated endsystolic volume index when the patients were in sinus
rhythm or at any of the pacing rates from 60 to 100
beats/min. Stroke volume index in sinus rhythm was
56 5.3 ml/m2 (fig. 6). This fell to 43 5.0 ml/m2 at
a pacing rate of 60 beats/min (p < 0.05). Increasing
pacing rates further to 70 and 80 beats/min had no
effect on stroke volume index. However, at a pacing
rate of 90 beats/min, stroke volume index decreased to
33
2.4 ml/m2 (p < 0.05) and decreased further, to
29 1.9 ml/m2 (p < 0.05), when the pacing rate was
increased to 100 beats/min.
Cardiac index was 3.1 ± 0.3 1/min/m2 when pa-
( m1/M')
100
100-
80
80-
ST-ROKE
VO)LUME
60- IINqDEX
-60
END
-40
DIASTOLIC
VOLUME
INDEX
L20
40END
20-1 SYSTOLIC
VOLUME
INDEX
PACING RATE (SINUS)
62
EF
CI (I/min/M2) 3.1
144
SBP
80
DP
60*
55
2.6*
134*
81
70
53
2.7
135
95*
80
54
2.9
136
1 09*
90
52
3.0t
135
121*
100
49t
2.9
135
135*
FIGURE 5. Ejection fraction (EF) and volume indexes in patients with underlying sinus rhythm. Initiation of
ventricular pacing at a rate of 60 beatslmin results in a marked decrease in end-diastolic volume index. Pacing at a
rate of 100 beats/min results in an end-diastolic volume index less than that at 80 beats/min and below. EF is
reduced by pacing at 60 beatslmin compared with sinus rhythm. EF at a pacing rate of 100 beatslmin is less than at
a rate of 80 beatslmin or less. CI = cardiac index; SBP = systolic blood pressure; DP = double product.
CIRCULATION
328
(I/min/M2)
o
3-
o
2
*
2
(ml/M2)
55
50-
-55
-50
E 40-
-40
X
z
-J
0
W
30
30-
0
ir
C')
VOL 67, No 2, FEBRUARY 1983
conventional chest x-ray, there were no significant
differences in estimated cardiac index at any ventricular pacing rate from 50 to 100 beats/min. There were
small, significant linear decreases in stroke volume
index and ejection fraction with increasing pacing
rates. These changes with increasing pacing rates may
reflect decreased diastolic filling time. Alternatively,
the decrease may represent a normal compensatory
mechanism to maintain a stable cardiac index. Endsystolic volume index, an important estimate of left
ventricular contractile state,'2 was unchanged at ventricular pacing rates of 50-100 beats/min.
Patients with Enlarged Hearts
20PACING
EF
(SINUS)
62
-
60.
55
70
53
80
54
90
52
100
49t
20
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FIGURE 6. Ejection fraction (EF) and volume indexes in patients with underlying sinus rhythm. A significant decrease in
cardiac index and stroke volume index are noted when ventricular pacing at a rate of 60 beatslmin supplants sinus rhythm.
Stroke volume index decreases at rates of 90 and 100 beatslmin.
Cardiac index at a pacing rate of 90 beats/min is greater than
that at 70 beatslmin.
tients were in sinus rhythm and fell significantly, to
2.6 ± 0.3 ml/m2, when pacing at 60 beats/min was
instituted (fig. 6). Cardiac index was unchanged at
pacing rates of 70 and 80 beats/min; however, pacing
at 90 beats/min resulted in an estimated cardiac index
of 3.0 + 0.2 1/min/m2, which was significantly higher
than that at a ventricular rate of 60 beats/min.
Ventricular pacing decreased the ejection fraction
from 62 1.6% in sinus rhythm to 55 ± 1.2% when
ventricular pacing at a rate of 60 beats/min was initiated. A ventricular pacing rate of 100 beats/min further
decreased ejection fraction to 48 ± 2.5%, which was
significantly less than that at a pacing rate of 80 beats/
min (54 + 2.2%).
Discussion
Ventricular pacemakers are often used to treat
chronic or intermittent bradyarrhythmias. The widespread availability of rate-programmable pacemakers
provides the possibility of optimizing ventricular pacing rate for arrhythmia control, the preservation of
sinus rhythm in patients with rare episodes of bradycardia, and potential increases in cardiac output. Resolution or improvement of congestive heart failure has
been reported when patients with complete atrioventricular block were paced from the ventricle at rates of
50-75 beats/min. In addition, studies performed by
Samet and co-workers' and Sowton5 indicate that acute
increases in ventricular pacing rate from 50 to 125
beats/min may be associated with an incremental increase in resting cardiac output in selected patients.
This investigation demonstrates that changes in ventricular pacing rate can alter values of resting left ventricular function, which may be clinically significant.
Patients with Normal Heart Size
In patients with
a
normal heart size, defined from
In the patients with cardiomegaly, a different pattern
emerged. Estimated cardiac index improved as ventricular pacing rates were increased from 50 to 60 and
70 beats/min. A further increase to 100 beats/min resulted in a decrease in cardiac index for the group.
End-systolic volume index did not change significantly, although there appeared to be a downward trend as
heart rate increased. End-diastolic volume index decreased with increasing pacing rate, and the absolute
differences were greater than that in patients with a
normal heart size. However, the percent changes in
end-diastolic volume index were similar in both
groups.
One interpretation of the data in this group of patients is that maximal resting cardiac index can be
obtained from a specific ventricular pacing rate between 70 and 90 beats/min. In this range of heart rates,
all but one patient demonstrated his peak cardiac index. Significant decreases in left ventricular ejection
fraction occurred at pacing rates of 90 and 100 beats/
min. Thus, the increases in pacing rate in the patients
with cardiomegaly did not produce the same alterations in left ventricular function as in patients with
normal hearts. The reduced cardiac index noted at rates
of 50 and 60 beats/min could be interpreted to mean
that low pacing rates in this patient population exposes
an insufficient contractile reserve for maintenance of a
stable cardiac index. Conversely, high pacing rates
may also lead to a decreased cardiac index through
insufficient diastolic filling time in an enlarged noncompliant ventricle. Increases in cardiac index associated with increased pacing rates appeared to be sustained for as along as 4 months.
Patients with Sinus Rhythm
Unexpectedly, five patients in this study had underlying sinus rhythm despite a previous diagnosis of
complete atrioventricular block. The data presented
are consistent with multiple studies that emphasize the
importance of atrial contraction in augmenting stroke
volume.'1- 1' Their estimated end-systolic volume index was the same during sinus rhythm as during pacing
at a rate of 60-100 beats/min. The major volume
change noted in this group of patients was a marked
increase in end-diastolic and stroke volumes during
sinus rhythm. Atrial contraction during sinus rhythm at
a rate of 51-60 beats/min resulted in a 27% increase in
329
EFFECT OF PACING RATE/Narahara and Blettel
cardiac index compared with ventricular pacing at a
rate of 60 beats/min (with asynchronous atrial
contractions).
Clinical Implications
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Ventricular pacing in normal animals may result in
either no change or a decrease in left ventricular contractility. Badke and co-workers'4 noted a decrease in
systolic shortening in the canine left ventricle when
ventricular pacing was substituted for right atrial pacing. Others have reported similar results'5 and suggest
that the altered synchronization created by pacing results in a less efficient contraction. The data from our
patients with a normal heart size indicate that global
left ventricular function as measured by the ejection
fraction is negatively affected by an increase in ventricular pacing rate. However, in these presumably more
normal left ventricles, such decrements in ejection
fraction were not associated with negative effects on
end-systolic volume index or resting cardiac index,
and may represent a normal physiologic response.
In patients with cardiomegaly, ventricular pacing
and pacing rate may be more important. This group of
patients had lower ejection fractions at all pacing rates
than patients who had a normal heart size. Ventricular
pacing'at rates below 70 beats/min was associated with
significantly lower cardiac indexes owing to an inability to increase stroke volume appropriately. To preserve resting cardiac index, optimal pacing rates appeared to be 70-90 beats/min. Neither the end-systolic
volume index nor ejection fraction were significantly
altered between pacing rates of 50 and 80 beats/min.
Hence, diastolic filling time may be more critically
rate-related in these patients. However, the number of
patients with cardiomegaly examined in this study is
small, and these findings must be confirmed in larger
groups of patients.
Scintigraphic ejection fractions and volumes are
independent of geometric considerations. Therefore,
this technique may be ideally suited for evaluating the
asynchronous left ventricular contraction that occurs in
patients with pacemakers. In the patient with a marginal cardiac reserve, such studies may be useful for determining which rate is most applicable at rest.
Acknowledgment
The authors express their gratitude to Alvis Walls and Robert Butsch
for their technical assistance and to Grace Fredrickson for her meticulous secretarial support. Dr. Gregory Dehmer's assistance in the application of the left ventricular volume analysis and Dr. J. Michael Criley's
thoughtful review are appreciated.
References
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Effect of rate on left ventricular volumes and ejection fraction during chronic ventricular
pacing.
K A Narahara and M L Blettel
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Circulation. 1983;67:323-329
doi: 10.1161/01.CIR.67.2.323
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