Download Increases Left-to-Right Ventricular Systolic Interaction

720
Pacing-Induced Dilated Cardiomyopathy
Increases Left-to-Right
Ventricular Systolic Interaction
David J. Farrar, PhD; John C. Woodard, PhD; Edna Chow, PhD
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Background. The right ventricle (RV) receives part of its systolic pumping force from the left ventricle
through systolic ventricular interaction. The purpose of this study was to determine the effects of dilated
cardiomyopathy on left ventricular to right ventricular (LV-to-RV) systolic interaction.
Methods and Results. Studies were performed in six normal pigs and in six pigs in which dilated
cardiomyopathy resulting in congestive heart failure (CHF) was produced with rapid ventricular pacing
at 230 beats per minute for 1 week. In all pigs, we rapidly withdrew blood from the LV apex into a
prosthetic ventricle in a single beat, which reduced LV systolic pressure without changing RV or LV
end-diastolic pressure, and the resultant instantaneous changes in RV systolic pressure and pulmonary
artery flow were determined. The LV-to-RV mean systolic interaction gain was calculated as the change
from a normal beat to the instantaneous unloaded beat in mean RV systolic pressure divided by the
change in mean LV systolic pressure. Mean systolic pressure gain was approximately 2½2 times greater
(P<.05) in the CHF animals (0.103±0.018 mm Hg/mm Hg) than in the normal pigs (0.040±0.011
mm Hg/mm Hg).
Conclusions. These data demonstrate that left-to-right ventricular systolic interaction is significantly
greater in dilated cardiomyopathy compared with the normal heart, indicating that the contribution of the
left ventricle to RV systolic pressure generation has increased. This is consistent with decreased elastance
of the interventricular septum resulting in increased coupling between the ventricles. (Circulation
1993;88:720-725)
KEY WORDs * ventricular interdependence * septal compliance
V entricular interactions during systole and diastole are important determinants of ventricular
function.'-36 Various terms have been used to
describe these phenomena, including ventricular interference,6 cross talk,3 interdependence,13'22'28 and ventricular interaction.7'12,21,35 Diastolic ventricular interaction is due to the volume of one ventricle impinging on
the volume of the contralateral ventricle."6'10'12'31 On
the other hand, systolic ventricular interaction, rather
than impairing the contralateral ventricle, is responsible
for transmission of systolic forces from one ventricle to
the other479112022232529-36 resulting in an increase in
the "effective contractility" of the contralateral ventricle over and above its native contractility.31 This is
especially important for the low-pressure right ventricle,
which is assisted during ejection by forces from the left
ventricle transmitted mainly through the interventricular septum and the common muscle fibers of the free
walls.31,33-36
The role of systolic interaction in various forms of
heart disease has not been fully studied. Little et al,'8 in
studies of right ventricular (RV) pressure-overload hypertrophy, and Slinker et al,23 in studies of left ventricReceived November 4, 1992; revision accepted March 30, 1993.
From the Department of Cardiac Surgery and Research Institute, California Pacific Medical Center, San Francisco.
Correspondence to Dr Farrar, Department of Cardiac Surgery,
California Pacific Medical Center, 2351 Clay St, Room S637, San
Francisco, CA 94115.
ular (LV) pressure-overload hypertrophy, have found
that RV-to-LV ventricular interaction decreases during
hypertrophy, which is attributed to a stiffening of the
interventricular septum. We hypothesize that the opposite occurs during dilated cardiomyopathy, that ventricular interaction increases and becomes an increasingly
important determinant of cardiac function, especially
for the right ventricle. We test this hypothesis by
comparing LV-to-RV isolated systolic ventricular interaction gains in the normal intact porcine heart with
gains measured in a pacing-induced dilated heart failure
model.
Methods
Surgical and instrumentation protocols have been
described previously for the pacing-induced model of
dilated heart failure37'38 and for determining isolated
systolic ventricular interaction gains.35 The present
study consists of ventricular interaction measurements
obtained in 12 new experimental pigs divided equally
into two groups: a normal group and congestive heart
failure (CHF) group. The six normal pigs (average body
weight, 41.6+2.1 kg) proceeded directly to the instrumentation and data collection protocols. The six CHF
pigs (weight, 44.2+1.7 kg) underwent rapid ventricular
pacing for 1 week before data collection. These protocols are briefly reviewed here.
Farrar et al Ventricular Interaction With Cardiomyopathy
721
removal of the usual mechanical inflow and outflow
valves, and the outflow port was blocked off. A 12-mm
id wire-wrapped cannula was inserted into the LV apex
via a stab incision, and the cannula was connected to the
VAD inflow port. The VAD pneumatic control console
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FIG 1. Diagram of experimental preparation showing the
method of transiently unloading the left ventricle with a
modified ventricular assist device (VAD), which removes
blood from the left ventricle during a single systole through a
cannula in the left ventricular apex. Left (LVP) and right
(RVP) ventricular pressures were measured with high-fidelity
catheters. PA, pulmonary artery; AoP, aortic pressure.
Model of Congestive Heart Failure
After anesthesia with ketamine (20 mg/kg IM for
preinduction) and intravenous injections of thiamylal
sodium (4.5 mg/kg initial bolus and 2.5 mg/kg maintenance doses every 15 to 20 minutes), the six pigs from
this group were intubated and connected to an artificial
ventilator. Respiratory rate, tidal volume, and FiO2 were
adjusted as necessary to maintain acid-base equilibrium. A Medtronic unipolar sutureless pacing lead was
attached to the LV apex through a small opening in the
diaphragm under the xiphoid process and connected to
a Medtronic pacemaker (modified model SX-5985)
implanted in a subcutaneous abdominal pocket. After
recovery from anesthesia, the pigs were returned to a
chronic care facility, where they received a standard
diet, free access to water, and an antibiotic regimen of
penicillin-G. The pacemaker was then programmed at a
rate of 230 beats per minute. Seven days later, the
animals were brought back to the laboratory for the
acute experiment. Before induction of general anesthesia, the pacemaker was turned off. The chest was
opened, and the heart was instrumented as described
below.
Instrumentation
In the six CHF pigs and the six normal pigs, the heart
was exposed through a median sternotomy and implanted with a modified Thoratec (Berkeley, Calif)
ventricular assist device (VAD), which is a sac-type
prosthetic ventricle (Fig 1). The VAD was modified by
was also modified to create single-cycle operation, in
which there is rapid filling of the VAD and therefore
rapid unloading of the left ventricle upon command in a
single beat immediately after the R wave of the ECG.
Left and right ventricular pressures (LVP, RVP) were
measured with high-fidelity Millar microtip catheters
(Millar Instruments, Inc, Houston, Tex). These transducers were zeroed in blood at body temperature before
insertion and checked at the end of the experiment.
Aortic pressure (AoP) was measured with a standard
fluid-filled catheter positioned in the carotid artery and
was connected to a pressure transducer (Statham, Oxnard, Calif). An electromagnetic flow probe (Carolina
Medical Electronics, Inc, King, NC) was placed around
the pulmonary artery to measure continuous beat-tobeat cardiac output (CO). All signals were continuously
recorded on an eight-channel Gould chart recorder and
simultaneously sampled on line at 100 samples per
second with a Metrabyte analog-to-digital convertor
(Taunton, Mass) connected to a personal computer.
Experimental Protocol
All data were collected after a stabilization period of
15 to 30 minutes subsequent to completion of instrumentation and VAD implantation. The basic protocol
consisted of measurements in data groups that were 8
seconds in duration, with the respiration held at end
expiration. In each group, there were six normal cardiac
cycles followed by one experimental beat with rapid left
ventricular unloading. Unloading was achieved after the
R wave of the seventh beat by rapidly reducing the
pneumatic pressure of the VAD from 200 to -100
mm Hg, thus allowing the VAD to fill directly from the
left ventricle. The instantaneous changes produced by
this perturbation on the right ventricle were then
evaluated.
Data Analysis
Data were analyzed using a data acquisition and
analysis software package developed in our laboratory.
Data sets with evidence of arrhythmias or cycle-to-cycle
instability were discarded. Mean systolic pressures were
calculated by integration of LVP and RVP during
systole. Two measurements of systolic LV-to-RV interaction gains were determined: (1) mean ventricular
systolic pressure gain and (2) instantaneous systolic
gain. Mean ventricular pressure gain (mm Hg/mm Hg)
was defined as the ratio of changes in mean RV systolic
pressure divided by changes in mean LV systolic pressure for each of the six normal beats compared with the
unloaded beat. The instantaneous LV-to-RV pressure
gain at a given time (t) during systole was defined as the
ratio of the change in RVP to the change in LVP from
the control to the unloaded beat at time t. The systolic
period was normalized such that the time from end
diastole to end ejection ranged from 0.0 to 1.0. This
period was divided into 21 pressure points in 5%
increments of normalized systolic time. The pressure
values at these normalized times were determined by
linear interpolation of the sampled points. The instan-
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Circulation Vol 88, No 2 August 1993
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TABLE 1. Changes in Ventricular Pressures and Right
Ventricular Function Before and During the Unloaded Beat
Unloaded
Percent
Control
beat
beat
change
Parameter Group
11.2
-60.3+7.7§
30.0±6.8
LVMSP Normal 75.8+
63.7+10.9
22.5±8.9
-64.5±11.3§
(mm Hg) CHF
17.9+4.6
-9.7+4.0§
RVMSP Normal 19.7+4.3
26.3+6.7
22.1+6.6
-16.6±5.3t§
(mm Hg) CHF
2.9±2.3
10.6±4.0
LVEDP Normal 10.4+4.0
-8.7±12.6
17.0±10.0
14.8±7.2
(mm Hg) CHF
-2.5+4.2
3.8± 1.9
RVEDP Normal 3.9±2.0
-1.7±+1.8
7.3±2.6*
7.1±2.5*
(mm Hg) CHF
3.7±1.4
-2.3+18.2
Normal 3.8+1.1
CO
2.2+0.7*
1.5+0.6t
-28.5±24.8*
(L/min) CHF
29.4±8.9
-18.4±12.6§
Normal 35.5+7.6
RVSV
CHF
13.9+5.4t -36.5+16.1§
(mL)
21.9±7.6t
Normal 0.121+0.044 0.092±0.041 -26.5+13.1§
RVSW
CHF
0.073+0.032* 0.039+0.021* -46.7+15.2§
(J)
-5.7+6.3
Normal 0.283±0.032 0.268+0.042
Tej (s)
0.277+0.073 0.233+0.073 -16.5+7.4§
CHF
LV, left ventricular; RV, right ventricular; MSP, mean systolic
pressure; EDP, end-diastolic pressures; CO, cardiac output; SV,
stroke volume; SW, stroke work; Tej, duration of pulmonary artery
ejection; CHF, congestive heart failure. *P<.05, tP<.01 (CHF
compared with normal); 1P<.05, §P<.01 (unloaded beat compared with control beat).
taneous gains were determined for the last 70% of
systole, by which time there was a consistent reduction
in LVP during unloading.
RV stroke volume was computed by integration of
pulmonary artery flow for the whole cardiac cycle, and
RV stroke work was computed by the product of RV
developed pressure times stroke volume. Zero-flow
baseline was established as the average signal in the last
25% of the cycle before the beginning of systole. In each
group, the data from the control cycles (ie, not unloaded) were averaged to provide one value for each
parameter. Data sets were repeated 5 to 10 times for
each experiment and subsequently averaged for each
animal. Next, the data from all animals in each group
were pooled. All results shown are mean± 1 SD. Statistical comparisons between normal and CHF pigs were
performed with a nonpaired t test and between control
and unloaded beats with a paired t test. Statistical
significance of changes in instantaneous gains was determined by a two-way ANOVA (CHF versus normal
and time) with repeated measures on one factor (time).
A P value of <.05 was considered significant.
All animals received humane care in compliance with
the "Principles of Laboratory Animal Care" formulated
by the National Society for Medical Research and the
"Guide for the Care and Use of Laboratory Animals"
prepared by the National Academy of Sciences and
published by the National Institutes of Health (NIH
Publication No 80-23, revised 1978).
Results
with
CHF
had
depressed CO, stroke volume, and
Pigs
stroke work and elevated RV end-diastolic pressures
compared with the normal pigs (Table 1). Although the
CHF animals had elevated heart rates during pacing,
there was no difference in resting heart rate between
CHF pigs (105 + 10 beats per minute) compared with
100
80
CHF
Normal
-Control beat
----Unloaded beat
60
LVP
(mmHg) 40
20
30r o
20
RVP
(mmHg)
10
15
0
10
PA FLOW
_5
-5
..
Time (O.1)
FIG 2. Waveforms: Instantaneous effects of reducing left
ventricular pressure (LVP) on right ventricular pressure
(RVP) and pulmonary artery (PA) flow are shown as typical
examples from one normal pig (left) and one pig in pacinginduced congestive heart failure (CHF, right). Data measured
in a single unloaded beat are shown superimposed on the
preceding (control) cardiac cycle in dashed lines.
normal pigs (102±21 beats per minute) during the
experimental measurements.
Data showing the effects of LV unloading on RV
pressure and pulmonary artery (PA) flow from a typical
normal pig and a pig with CHF are shown in Fig 2.
Pressure and flow waveforms from the acutely unloaded
beats are shown superimposed on the corresponding
waveforms from the previous cardiac cycle (a control
beat). The control beats demonstrate elevated end-diastolic pressures, decreased PA flow (CO), and decreased LV peak systolic pressure in the CHF animal
compared with normal. During the unloaded beat,
changes in systolic pressure were achieved without
changes in end-diastolic conditions. These reductions in
LV and RV systolic pressure did not change until after
the rapid upswing in LVP caused by pneumatic and
mechanical delays of approximately 60 milliseconds.
Once LVP began falling, there were instantaneous
corresponding reductions in RVP and PA flow. There
was a greater effect of LV unloading on RVP and PA
flow in the CHF pig than in the normal pig. In addition,
the duration of RV ejection was markedly shortened in
the CHF pig during the unloaded beat, with only slight
changes noted in the normal pig.
When pooling the data from all the pigs in each
group, the experimental change in LV mean systolic
pressure (LVMSP) was approximately the same in each
group (-40 to -45 mm Hg, or a -60% to -65%
reduction; see Table 1). However, the resultant decrease in RVMSP was >4 mm Hg for the CHF pigs
(- 16.6% reduction) compared with <2 mm Hg for the
normal pigs (-9.7% reduction). The mean systolic
LV-to-RV pressure gain, which is the ratio of these
Farrar et al Ventricular Interaction With Cardiomyopathy
TABLE 2. Summary of Systolic Ventricular Interaction Gains
for Normal Pigs and Pigs With Pacing-Induced Congestive
Heart Failure
Systolic gain
(mm Hg/mm Hg)
Mean gain
Time-varying
gains
Normal
0.040±0.011
CHF
0.103±0.018*
0.092±0.033 (NS)t
0.047±0.025
t=0.5
0.109±0.037*
0.027±0.026
t=0.75
0.030±0.026
0.231±0.087t
t=1.0
0.088±0.029*
0.027±0.026
Minimum
0.231±0.087*
0.095±0.038
Maximum
CHF, congestive heart failure. t=normalized time during systole. *P<.05; tP<.01; *P=.24.
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changes, was approximately 21/2 times greater in CHF
pigs (0.103±0.018 mm Hg/mm Hg) than in the normal
pigs (0.040±0.011 mm Hg/mm Hg) (Table 2). The experimental reduction in LVP during the unloaded beat
also resulted in significant reductions in RV stroke
volume (- 18.4% for the normal pigs, -36.5% for CHF)
and stroke work (-26.5% for normal pigs, -46.7% for
CHF) and duration of PA ejection (-16.5% for the
CHF group only), without changes in end-diastolic
pressure (Table 1).
The results of the ANOVA demonstrate that the
instantaneous gains vary significantly (P=.000) with
systolic time and that there is a significant (P=.034)
effect of CHF on these gains. The time-varying gains
became significantly greater (at P<.05) in CHF pigs
compared with normal pigs starting at a normalized
systolic time of 0.75 and remained elevated throughout
the last quarter of systole (Fig 3 and Table 2). The
interaction term was also highly significant (P=.000),
indicating that the pattern of instantaneous gains are
different in CHF animals and normal animals.
Discussion
The right heart and the left heart heart interact by
hemodynamic interactions (also referred to as indirect
interactions) and by mechanical interactions (also re0.20
._
0
0.15
> CHF
c:
A
0.10
S'U
1
0.05
Normal
Y
yA'?
0.00
0.0
0.2
0.4
0.6
0.8
1.0
Normalized systolic time
FIG 3. Graph: Instantaneous systolic left ventricular (LV)to-right ventricular (RV) interaction gain pooled for all
normal and congestive heart failure (CHF) pigs is shown as a
function of normalized systolic time, where 0.0 corresponds to
end diastole and 1.0 corresponds to end ejection.
723
ferred to as direct or anatomic interactions).19'21'31 Hemodynamic interactions occur because the right heart
and left heart are connected in series, and therefore the
output of one ventricle becomes the input of the other.
Mechanical interactions are due to the close anatomic
coupling between the right and left ventricles via the
shared interventricular septum, common muscle fibers
in the free walls, and the pericardium. It is useful to
further subdivide anatomic mechanical interactions into
those occurring during diastole and systole. Systolic
ventricular interaction is especially important as a determinant of right heart function since it is known that
a substantial portion of RV pressure generation is
contributed by the left ventricle.31'34'35
Ventricular interaction can be quantitated by interaction "gains," which are ratios of changes in pressure
in one ventricle produced by changes in the other
ventricle. Absolute values of interaction gains have been
shown to be substantially less during systole than diastole but important for both. For example, Slinker et a126
have measured diastolic interaction gains of 0.33 from
the right ventricle to the left ventricle, meaning that for
every 1 mm Hg change in end-diastolic pressure in the
right ventricle, there was a corresponding change in
end-diastolic pressure of 0.33 mm Hg in the left ventricle. In contrast, systolic pressure gains have been reported for LV-to-RV interaction to range in different
experimental preparations from 0.040 mm Hg/mm Hg
in intact dog hearts,34 0.054 mm Hg/mm Hg in the intact
porcine heart,35 0.08 in an isolated canine heart,22 and
0.086 calculated from data during a sudden increase in
aortic afterload in intact dog heart.9 Although an LVto-RV systolic gain of 0.05 to 0.10 appears small, it is
actually a significant determinant of RV systolic function.34'35 With an LV systolic pressure of 100 mm Hg,
this would correspond to a sizeable contribution of 5 to
10 mm Hg to RV systolic pressure, which is 20% to 40%
of RV peak systolic pressure34'35 and up to 43% of RV
stroke work.35 Maughan et a122 and Yamaguchi et a134
have demonstrated that the RV-to-LV systolic gain is
actually greater than from LV-to-RV, but the corresponding absolute magnitude of the contribution to LV
pressure is quite small. Therefore, the significance of
systolic ventricular interaction is greater for the right
ventricle than for the left ventricle.34
We recently presented our experimental method of
determining isolated systolic pressure interaction gain
in the intact heart using the same techniques as in the
present study.35 The rapid removal of blood from the
left ventricle after the R wave in a single systole assures
that end-diastolic conditions are unaltered and that the
resultant changes in RVP are due solely to isolated
systolic interactions. In the current series of normal
hearts, the mean systolic pressure gains averaged
0.040±0.011, identical to that of Yamaguchi et a134 and
not significantly different from the gain of 0.054±0.017
in our previous report.35
Furthermore, the current study shows that the pacing-induced model of dilated CHF increases the mean
systolic pressure gain almost 21/2 times that of the
normal pigs, to 0.103±0.018 mm Hg/mm Hg. The experimental reduction in mean systolic LVP produced
during rapid unloading was the same in both groups of
animals. However, the resultant change in mean systolic RV pressure was significantly greater in the CHF
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Circulation Vol 88, No 2 August 1993
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pigs than in the normal pigs, thus yielding the elevated
calculation of gain. We have shown previously that
rapid ventricular pacing in this model results in biventricular dilation with no change in wall thickness38 and
is a realistic model of dilated cardiomyopathy. Thus,
we can deduce that the contribution of the left ventricle to RV pressure increases significantly in dilated
cardiomyopathy.
The instantaneous systolic gains are also significantly
increased in the CHF animals compared with normal
animals throughout the latter part of systole. These data
confirm our previous findings35 that systolic interaction
gains are time varying within systole. This may explain
some of the variability of measurements between researchers that used different techniques and made
measurements at different times within the cycle. The
data also show that the pattern of time-varying interaction gain is markedly different for CHF animals compared with normal animals. However, there are some
limitations to these methods that should be noted. First,
the experiment was designed to determine the response
throughout systole to LV unloading starting early in the
beat. The different responses in late systole between
CHF and normal animals could be due partially to RVP
changes not being made at the same RV volumes. A
different response may have resulted if single measurements were made after unloading at different times
during systole. Also, the fact that LV unloading reduces
the duration of PA ejection in the CHF animals also
would have some effect on the calculation of gains at
normalized systolic times.
It is well known that the principal cause of right heart
failure is left heart failure.39,40 Two known mechanisms
related to ventricular interaction are responsible for
depressed RV function during LV failure: pulmonary
hypertension and diastolic ventricular interaction. Pulmonary hypertension can occur when poor LV systolic
function results in increased left atrial pressure, increased pulmonary venous pressures, and a increase in
PA pressure and RV afterload (initially via indirect
hemodynamic interactions). Diastolic ventricular interactions can have a negative effect on RV function
during LV failure when the left ventricle dilates and the
septum shifts to the right, reducing diastolic RV compliance and impairing RV filling. Less is known about
the role of systolic ventricular interactions in heart
failure, but the results in the current study suggest that
systolic interactions become increasingly important and
may help the right ventricle compensate for any loss in
native contractility. However, during severe left heart
failure with reduced LV pressure, there would be a
corresponding reduction in the LV contribution to
systolic pressure generation of the right ventricle.
The results of the present experiment are also directly
relevant to right heart function in heart failure patients
who are supported with left VADs (LVADs). LVP can
be reduced significantly during normal operation of the
LVAD, which could thereby reduce the contribution of
LVP to RVP via systolic ventricular interaction.19,37 The
results from the present study provide an explanation
for the finding that there is no significant change in RV
function during LV unloading with an LVAD in normal
hearts,24'32'41'42 whereas significant impairment of RV
function has been reported during LV unloading in pigs
with pacing-induced CHF.37 The explanation is that
with increased systolic ventricular interaction in the
CHF pigs, the reduction in LVP resulted in a much
greater loss of LV systolic contribution to RVP generation than in the normal heart. The relative importance
of ventricular interaction in LVAD patients is unknown
but will probably be quite variable and could be more
than offset by other factors such as the reversal of
passive pulmonary hypertension and reduced rightheart afterload.19,43
Santamore and Burkhoff31 have developed a mathematical model of the effects of ventricular interaction on
the circulatory system. They incorporated the threecompartment model of Maughan et al,22 which describes systolic ventricular interaction as consisting of
three elastances representing the RV free wall, the
interventricular septum, and the LV free wall. In this
model, the pressure in the right ventricle is a function of
native Ema, contractility and volume plus the systolic
interaction gain times the LVP. Thus, they concluded
that the "effective" contractility of the right ventricle
can be greater than the native Ema. contractility because
of the presence of systolic interaction. LV-to-RV systolic ventricular interaction gain (G) in their model is
determined to be the parallel combination of the
elastances of the RV free wall (Erf) and the interventricular septum (Es):
G=Erf/(Ervf+Es)
If the interventricular septum is very stiff compared
with the RV free wall, then G approaches zero, and
there is no systolic interaction between the ventricles,
whereas if the septum is very compliant (such as a thin
rubber membrane), then ventricular interactions are
much larger, with G approaching one. If we use this
model to describe the 21/2-fold increase in systolic gain
during CHF observed in the present study, then we can
conclude that septal elastance has decreased significantly more than the RV free wall during CHF. In the
normal heart, a gain of 0.04 would indicate that E, is 24
times greater than Erv; in the CHF pigs, a gain of 0.10
would indicate that there has been a relative reduction
in Es to only nine times greater than Erv. This conclusion
is consistent with the findings by Little et a118 and
Slinker et al,23 who observed decreased ventricular
interaction during chronic pressure-overload hypertrophy, which was attributed to decreased septal compliance. Thus, systolic interaction is decreased during
conditions in which the septum is less compliant, such as
hypertrophy, and is increased during conditions in
which the septum is more compliant, such as dilated
cardiomyopathy.
Acknowledgments
This study was supported in part by grant R01-HL-45608
from the National Heart, Lung, and Blood Institute.
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Circulation. 1993;88:720-725
doi: 10.1161/01.CIR.88.2.720
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