(Circulation. 1999;99:2177-2184.)
© 1999 American Heart Association, Inc.
Basic Science Reports |
Hemodynamic Effects of Direct Biventricular Compression Studied in Isovolumic and Ejecting Isolated Canine Hearts
From the Department of Surgery, Division of Cardiothoracic Surgery (J.H.A.), and the Department of Medicine, Division of Circulatory Physiology (J.W., D.B.), College of Physicians and Surgeons, Columbia University, New York, NY, and Cardio Technologies, Inc, Pine Brook, NJ (A.R.L., H.R.L., J.E.T.). Dr Tsitlik is now at JVT Consultants, Cliffside Park, NJ.
Correspondence to John H. Artrip, MD, c/o Daniel Burkhoff, MD, PhD, Department of Medicine, Division of Circulatory Physiology, College of Physicians and Surgeons, Columbia University, MHB 5-435, 177 Fort Washington Ave, New York, NY 10032. E-mail ja276{at}columbia.edu
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Abstract |
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Background—Biventricular direct cardiac compression (DCC) can potentially support the failing heart without the complications associated with a blood/device interface. The effect of uniform DCC on left and right ventricular performance was evaluated in 7 isolated canine heart preparations.
Methods and Results—A computer-controlled afterload system either
constrained the isolated heart to contract isovolumically or simulated
hemodynamic properties of
physiological ejection. Biventricular
DCC was provided by a chamber surrounding the heart that allowed
adjustment of the compression pressure, onset time, and duration.
Through a series of ventricular preloads, the effect of DCC
on the end-systolic pressure-volume relationship (ESPVR) was
evaluated under isovolumic and ejecting conditions. Under both
conditions, DCC shifted the ESPVR of the left and right ventricles
upward by an amount approximately equal to the compression pressure.
The augmentation of end-systolic pressure for each initial
preload tested, however, was less under ejecting conditions, because
reductions in end-systolic and end-diastolic
volumes occurred with ejection. Nevertheless, the net effect was to
increase stroke volume. Measurement of
M
O2 demonstrated that at a given
ventricular volume, MO2 did
not change with DCC; however, peak ventricular pressure
increased substantially, so that the effective pressure-volume area
increased.
Conclusions—Biventricular DCC can augment
end-systolic pressure with no added costs of
MO2. Under ejecting conditions, this
augmentation of ventricular contracting ability manifests
as increases in stroke volume. Thus, DCC represents a feasible
alternative form of ventricular assist, and devices that
support the heart in this manner should be further explored.
Key Words: heart-assist device • heart failure • physiology • hemodynamics • ventricles
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Introduction |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Treatment of severe, acute cardiogenic shock remains a major clinical challenge. Regardless of whether it is due to an acute myocardial insult or the consequence of decompensation in the setting of long-standing heart failure, the repertoire of available medical and surgical therapies is somewhat limited and frequently ineffective. Although a variety of ventricular assist devices are available, most of these devices require direct contact with the patient's blood. Thus, thromboembolic events, the need for anticoagulation, hemolysis, and immune reactions are ever-present problems. There has been renewed interest in developing techniques to support the circulation by compressing the weakened heart from its external surface.
Some understanding of the impact of external cardiac compression on
ventricular performance has been obtained through
use of a conditioned muscle wrap, dynamic cardiomyoplasty. Despite
little improvement in cardiac output, this procedure has demonstrated
underlying physiological benefits of improved
myocardial contractility, reduced myocardial
O2 consumption
(MO2), and stabilization of
the remodeling process of heart failure.1 2 3 A significant
amount of experience has also been gained previously with the use of
pneumatic compression devices in the setting of complete cardiac
arrest.4 5 However, there has been little experience in
the use of such mechanical devices to augment contraction of a beating
but weakened heart.
To begin exploring the effects of external cardiac compression on ventricular performance, Kawaguchi et al6 7 8 studied left ventricular (LV) mechanics of isolated canine hearts placed inside a chamber whose pressure could be varied in synchrony with cardiac contraction. Results of those studies showed that at a given volume, net ventricular pressure-generating capabilities could be augmented by external pressure without increasing myocardial oxygen demand. However, many fundamental questions remain. It has not been determined how external compression affects LV pressure generation at different volumes (ie, on the end-systolic and end-diastolic pressure-volume relationships [ESPVR and EDPVR, respectively]), how right ventricular (RV) mechanics are affected, or how LV and RV filling volumes and stroke volumes (SVs) would be affected under conditions of physiological preloading and afterloading.
The purpose of this study was to evaluate the effects of uniform,
biventricular direct cardiac compression (DCC) on LV and RV
performance and overall hemodynamics under both
isovolumic and ejecting conditions. We used an isolated canine heart
preparation in which physiological afterload
conditions were imposed on the heart to permit a study of the effects
of DCC on preload volumes and cardiac output under conditions that
mimic those encountered in situ. Finally,
MO2 was measured to assess the
relationship between changes in overall hemodynamic
performance and energy demands of the heart.
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Methods |
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Surgical Preparation
A total of 14 adult male mongrel dogs weighing between 22.0 and 24.0 kg were used for the study. All animals involved in the study received humane care in compliance with the Guide for the Care and Use of Laboratory Animals published by the National Institutes of Health (NIH publication No. 85-23, revised 1985).
Seven isolated canine hearts were studied by methods that were similar
to those described previously9 and are shown schematically
in Figure 1
. In brief, 2 mongrel dogs
were anesthetized with pentobarbital sodium 30 mg/kg IV. The
femoral arteries and veins of 1 dog ("support dog") were cannulated
and connected to a perfusion system used to supply
oxygenated blood to the isolated heart. The second dog
("heart donor dog") was mechanically ventilated, a midline
sternotomy was performed, and the heart was removed while being
metabolically supported by arterial flow from
the support dog. The left and right atria were opened, and all the
chordae tendineae were freed from the leaflets of both mitral and
tricuspid valves. Two metal adapters were sutured to the mitral and
tricuspid rings. These adapters hold the isolated heart to individual
ventricular volume servopump systems. A cannula was placed
into the mouth of the coronary sinus to permit collection of
coronary venous blood. When the surgical preparation was
complete, water-filled balloons of the servo systems were placed inside
the LV and RV cavities. A solid-state pressure transducer (Millar
Instruments) was placed inside each balloon to measure the respective
ventricular pressure.
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Coronary arterial pressure was set to 
100
mm Hg and held constant by a servo system that regulates blood flow
rate out of the support dog. The temperature of the perfusate
was maintained at 35°C with a heat exchanger. The coronary
sinus venous blood flow was measured continuously by a transit-time
flow probe (Transonic) positioned at the outlet of the coronary
sinus drain. The difference in oxygen content between
arterial and coronary venous blood
(SavO2) was measured
continuously by absorption spectrophotometer (A-VOX
Systems).10 The arterial pH,
PO2, and
PCO2 were measured periodically
during each experiment to ensure nearly 100%
SaO2 during periods of data
collection. LV O2 consumption was calculated from
the measurements of coronary blood flow and
SavO2 as described below.
Pacing electrodes were sutured to the atrial tissue, and the heart was paced at a rate 10 to 15 bpm greater than the spontaneous rate (mean paced rate, 104±4 bpm). A bipolar surface ECG was measured between 2 electrodes sutured to the surface of the heart.
Impedance Loading System
The ventricular volume servo systems were controlled
by a computer system that either constrained the hearts to contract
isovolumically or simulated hemodynamic properties of
the systemic and pulmonic circuits to allow
physiological ejection patterns. A digital computer
was programmed with the differential equations representing
the closed-loop system of systemic and pulmonary
circulations.11 This model provides a reasonable
representation of vascular pressure-flow relations of the real
circulation for simulating many aspects of coupling of ventricles and
their respective vascular loads.12 The
parameter values of each of the resistive and capacitive
elements in the model could be specified from the computer keyboard. To
implement the loading of ventricles by this model, the computer
digitizes the instantaneous LV and RV pressures and calculates the
appropriate instantaneous flow into or out of each ventricle. The flow
signals are integrated digitally and converted to an analog signal,
which is used as the command signal for the respective volume servo
system.
External Compression Device
As shown in Figure 1
, the heart was placed inside a
Lucite compression chamber. A nylon lining inside the chamber contacted
the heart and ensured that any blood draining from the heart did not
enter the compression tubing but rather drained out the bottom chamber
to return to the isolated heart. Cardiac compression pressure
(PDCC) was provided to the chamber from a valved
compressed-air cell that was regulated by a computer and allowed for
adjustment of PDCC, onset, and duration. The
amount of pressure was measured by a Millar microtip catheter placed in
the driveline near the chamber. The onset of PDCC
was synchronized with the QRS complex of the explanted heart.
Experimental Protocol
Four different protocols were performed.
Protocol 1 was designed to determine the effects of external compression on the ESPVR and EDPVR in isovolumically contracting LVs and RVs. To obviate potential confounding effects of interventricular interaction on the results, ESPVR and EDPVR of each ventricle were measured separately with the contralateral ventricle emptied of volume so that there was no developed pressure. Also, coronary blood flow and SavO2 were measured during the LV ESPVR/EDPVR run. These parameters, along with ventricular pressures, were measured with and without active compression at several volumes. The compressions were performed with a pressure of 50 mm Hg and a duration of 40% of the cardiac cycle.
In protocol 2, the effects of the timing of the onset of compression, the duration of compression, and the amount (pressure) of compression were then studied individually under isovolumic conditions at a single setting of LV and RV volumes.
In protocol 3, the effects of external compression under ejecting
conditions were investigated. Parameter values for the
simulated vascular systems were set to approximate heart failure
conditions: LV and RV end-diastolic pressures of 20 and
10 mm Hg, respectively; LV and RV ejection fractions of 20%;
peak LV pressure less than 90 mm Hg; and peak RV pressure
greater than 35 mm Hg. Because it is not possible to adjust
each of these variables (because these variables are
interdependent, with a relationship that is heavily dependent on the
contractile state of each ventricle), these set points served as
guidelines for adjusting parameter variables, not
strict criteria. After a group of parameter values had been
decided on and hemodynamic conditions had been
stabilized, data were recorded. The device was then turned on at a
PDCC of 50 mm Hg and a duration of 40% of
the cardiac cycle. Once conditions had stabilized with the device on
(5 minutes), data were recorded.
Finally, in protocol 4, the effects of compression on ESPVR and EDPVR during ejecting conditions were achieved by simulation of a vena caval occlusion, which resulted in a gradual reduction in ventricular end-diastolic volumes (EDVs). This was performed both with and without active compression at a pressure of 50 mm Hg and a duration of 40% of the cardiac cycle.
Data Analysis
All data were digitally sampled at a rate of 1000 Hz for 5
seconds and analyzed with a data analysis program
written in Microsoft BASIC. Measurements were averaged over 3 to 5
beats and analyzed offline.
End-systolic pressure (ESP, Pes) was
defined as peak pressure for isovolumic contractions. For ejecting
beats, end-systolic volumes (ESVs, Ves)
and ESPs were defined by the point in the cardiac cycle at which the
instantaneous ratio between pressure and volume attained a maximal
value. ESPVRs were analyzed by linear regression
analysis applied to data from the different volume beats
according to the formula
Pes=Ees(Ves-Vo),
and EDPVRs were analyzed by nonlinear regression
analysis according to the equation
Ped=Po+ßVed
,
where Ees is end-systolic elastance,
Vo is volume axis intercept,
Ped is EDP, Po is pressure
when ventricular volume is zero, Ved is EDV, and
ß and are constants. The effects on metabolic
parameters were assessed by determining the relation
between MO2 and total
mechanical energy indexed by pressure-volume area (PVA).
MO2 was defined as the
product of SavO2 and
coronary blood flow. PVA was determined, as detailed
previously, as the area contained within the ESPVR and the EDPVR up to
the volume of the isovolumic beat.13
Statistical comparisons of the linear ESPVRs and
MO2-PVA relationships between
control and active compression states were done by ANCOVA. The
nonlinear EDPVRs were linearized
[ln(Ped-Po)=lnß+
· lnVed] and then compared statistically by
ANCOVA. Other parameters were expressed as mean±SD and
were compared by paired t tests. All statistical
analyses were performed with commercially available software
(SYSTAT). In all cases, a value of P<0.05 was considered
statistically significant.
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Results |
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Effects of DCC on Isovolumic ESPVR and EDPVR
Results from a representative experiment are shown in Figure 2
; a summary of the average
results and statistical comparisons obtained from 7 hearts is provided
in Table 1. DCC shifted the ESPVR
of both the LV and RV upward in a parallel manner by an amount
approximately equal to the PDCC. In terms of the
parameter values, there was little effect on the
Ees values, but Vo values
were decreased. ANCOVA revealed highly significant decreases in
Vo for both ventricles (P<0.001),
with slight increases in Ees only for the RV that
were statistically (P=0.03) but not
physiologically significant. The EDPVRs were
not affected for either ventricle.
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Effect of DCC on MO2-PVA
Relationship
At a given ventricular volume,
MO2 did not change
significantly during active compression. Peak total
ventricular chamber pressure was increased substantially,
so that the effective PVA also increased significantly. Accordingly,
there was a large effect on the
MO2-PVA relationship, with a
significant decrease in slope (A) but with little influence on the
y intercept (B): A relates to the oxygen consumption per
PVA, whereas B is the oxygen consumption for no external work (ie,
PVA=0). These findings were confirmed in the 5 animals in which these
measurements were made. The values for A and B, as well as the
probability value obtained from the ANCOVA comparing control and DCC
values, are summarized in Table 2.
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Effect of PDCC, Compression Onset Time, and
Compression Duration
Representative pressure waveforms for the LV, RV,
and compression device with PDCCs of 0, 25,
50, and 100 mm Hg are illustrated in Figure 3a. Peak LV and RV pressures increased
linearly as PDCC was increased, with the
relationship between PDCC and change in peak
pressure being statistically indistinguishable from the line of
identity. These findings were confirmed in the 4 animals in which these
measurements were made systematically, as shown in Figure 4 (y=x,
r2=0.999, P=NS compared
with line of identity).
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Figure 3b and 3c illustrates representative
pressure-time waveforms for the LV, RV, and device obtained with
different compression onset times (ranging between 0 and 150 ms from
the QRS spike) and with different compression durations (ranging
between 20% and 60% of the cardiac cycle). Although peak pressures
did not vary significantly for either ventricle with the different
compression onset times or durations, there was consistent
influence on the shape of the pressure waves.
Effect of DCC on Hemodynamics During
Ejection
The effects of DCC on hemodynamic
parameters during ejecting conditions are summarized in
Figure 5. As summarized in the figure,
for both the LV and RV, ESPs increased significantly, whereas EDPs
decreased (Figure 5a and 5c). In contrast to the isovolumic data, the
increase in peak ventricular pressures were substantially
less than the PDCC. As will be detailed below
(see Discussion), this is because DCC also created significant
reductions in LV and RV ESVs (Figure 5b and 5d). Although EDVs were
also decreased, there was a significant 60% increase in SV (Figure 5b).
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Effect of DCC on ESPVR and EDPVR During Ejection
The effects of DCC on ESPVR and EDPVR during ejecting
conditions are shown in the representative results of
Figure 6. Similar to the findings with
isovolumic conditions, the ESPVRs of both the LV and RV were shifted
upward in a parallel manner by an amount approximately equal to the
PDCC.
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Discussion |
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Several non–blood-contact devices that assist the heart by directly compressing the external surface are currently under development. The methods for achieving DCC use a pneumatic driver to provide an equally distributed pressure over the epicardial surface of the LV and RV. Unlike cardiac compression with a skeletal muscle wrap (cardiomyoplasty), in which the compression forces vary with ventricular volume,1 7 cardiac compression with the present pneumatic system is independent of such factors, and we therefore refer to it as a constant-pressure DCC device. The isolated canine heart preparation offers a unique opportunity to study the effects of constant-pressure DCC under a variety of hemodynamic loading conditions while being able to characterize ventricular effects with accurate measurements of ventricular volume.
Under isovolumic conditions, the total pressure measured inside
the LV cavity equals the sum of the pressure generated because of
systolic and diastolic myocardial properties
(normally referred to as the transmural pressure) plus the pressure
applied by the device to the heart surface. Accordingly, the isovolumic
ESPVR was shifted upward by an amount approximately equal to the
PDCC for both ventricles. In other words, there
was no change in the Ees but a substantial
decrease in the Vo. The reduction in
Vo was predictably related to the
PDCC and the baseline value of
Ees
(
Vo=-PDCC/Ees),
with the extrapolated Vo values typically
assuming negative values. Negative extrapolated
Vo values have been observed previously in the
setting of increased contractility, where ESPVRs are
curvilinear.14 Fitting a linear equation to these
curvilinear relations frequently resulted in negative values of
extrapolated Vo. However, the negative
Vo values observed with DCC reflect the
extrapolations from the upwardly shifted ESPVRs rather than erroneous
linear extrapolations of nonlinear relationships. In summary, despite
the constancy of Ees, DCC results in an increased
overall pump strength by an amount related to
PDCC.
Importantly, the benefits for systolic function are
achieved with no apparent effect on ventricular
diastolic function or on intrinsic myocardial properties.
The EDPVRs were not affected for either ventricle: and ß did not
change. In addition, the increase in overall pump strength is achieved
without added metabolic cost to the myocardium.
The slope changes of the
MO2-PVA relationship observed
with DCC in the present study do not reflect effects on myocardial
properties, but rather the enhanced net pressure-generating capacity in
the absence of an increase in oxygen consumption.
The effects of DCC on hemodynamic
performance under ejecting conditions are more complicated. As
under isovolumic conditions, the ESPVRs of both ventricles were shifted
upward, with the change in Vo being related to
Ees and PDCC as described
above for isovolumic conditions (Figure 2 versus Figure 6). Unlike isovolumic conditions, however, peak
ventricular pressure during DCC was not simply the sum of
PDCC and unassisted peak LV pressure. This is
because application of DCC under ejecting conditions influences ESV and
EDV, as shown in Figure 5. Importantly, the shift in EDV is not
related to an effect on diastolic properties (demonstrated
by an absence of effect on the EDPVRs, shown in Figures 2 and 6); rather, it reflects changes due to the increased
ventricular pumping capacity (demonstrated by a decrease in
ESV). In other words, preload decreases when pump strength
increases.
These effects are explainable within the context of current
theories of ventricular-vascular coupling,15
in which ventricular contractile state is quantified by
Ees and Vo, afterload by
the effective arterial elastance
(Ea), and preload by EDV.
Ea is proportional to total
peripheral resistance (TPR) and inversely proportional to
the cardiac cycle duration (T): Ea
TPR/T. The
Ea line is a line drawn on the pressure-volume
plane starting on the volume axis at the EDV whose slope equals
-Ea. The Ea line therefore
provides a means of graphically depicting afterload on the same axes as
the ventricular pressure-volume relations and loops. The
intersection of the Ea line and the ESPVR
provides an estimate of the end-systolic pressure-volume point
for the specified Ees, Vo,
EDV, and Ea. As illustrated in Figure 7, if baseline ESPVR is shown by the
solid blue line and baseline Ea and EDV are shown
by the solid red line, then the baseline pressure-volume loop would be
approximated by the thick solid black line. If DCC is applied, the
ESPVR would be shifted upward by an amount equal to
PDCC (dashed-dotted blue line). Under conditions
in which neither preload volume nor afterload resistance would change,
the new pressure-volume loop would be approximated by the thin solid
black line. Peak pressure of this loop is increased compared with
baseline by only 50% of PDCC; SV is increased
by 40%. In practice, however, preload is also reduced during DCC,
so the Ea line shifts leftward (dashed-dotted red
line), which has the effect of diminishing both the pressure- and
SV-augmenting effects of DCC, as shown by the green pressure-volume
loop. Thus, the amount of pressure and SV augmentation will be
dependent on the baseline contractile state, the baseline afterload
resistance, and the amount of EDV shift caused by DCC.
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These interrelationships are further summarized in Figure 8. The dashed line in panel a shows how
SV varies as a function of contractile state at a fixed EDV (50 mL) and
a fixed afterload (Ea=5 mm Hg/mL). The
solid line at the top depicts how DCC with a PDCC
of 50 mm Hg would affect this relationship, assuming that there
were no change in EDV. As EDV decreases, however, this curve shifts
downward, as shown by the middle and lower solid lines. Graphs
depicting the amount of SV augmentation (expressed in absolute and
relative terms, panels b and c, respectively) formally illustrate 2
fundamental aspects of the physiology of constant-pressure DCC. First,
the amount of augmentation is a function of baseline contractile state.
Substantial SV augmentation is achieved only in a weak heart
(Ees<3 mm Hg/mL, which is 40% of
normal Ees of a 20-kg dog). Second, the reduction
in EDV will blunt SV augmentations and can even result in a diminution
at higher baseline levels of contractile state.
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A full explanation of the effects of DCC, however, is more
complicated. DCC affects both ventricles, and only a single-ventricle
analysis has been presented above. Because the
intrinsic contractile strength, measured in terms of
Ees, of the RV is much less than that of the LV,
the effects of DCC on the RV are significantly greater under every
condition. As Figure 5 shows, reductions in RV EDV are
substantially greater than in the LV, with the RV being nearly emptied
during active DCC. The amount of preload shifts and ultimate degree of
pressure and flow augmentation will therefore depend on the complex
effects of the unequally altered pumping capacity of the LV and RV.
Although there is no analytical solution to this problem, numerical
solutions could be used to understand the relationship between baseline
cardiovascular parameter values, shifts of
LV and RV EDVs, and pressure and flow augmentation by DCC.
Effects of DCC have been studied previously in isolated hearts.6 7 8 In those studies, however, ESPVRs and EDPVRs were not directly investigated, single-ventricle preparations were used, and predetermined LV volume changes were imposed on the LV. With regard to the last point, EDVs, ESVs, and SVs were specified in the previous studies, and effects of DCC on LV pressure generation were measured. In contrast, in our physiological afterloading system, volumes were allowed to shift in response to changes in effective LV and RV pumping strengths as they would in vivo. Although different volume settings were studied in the previous investigations, Vo values were assumed to be constant, and changes in performance were interpreted as reflecting changes in Ees. In our study, ESPVRs were directly measured to reveal that with a device that delivers a constant PDCC, Ees does not shift, but rather Vo is decreased. Accordingly, insights into the in vivo effects of DCC could be obtained.
With the increased use of mechanical assist devices and the complications associated with a blood/device interface, there has been a renewed interest in supporting the failing but still beating heart with external mechanical compression. The present study in isolated hearts demonstrates the feasibility of mechanical DCC as an alternative form of ventricular assist and provides the foundation for understanding the physiological effects of such a device in vivo.
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Acknowledgments |
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This research was sponsored in part by funding provided by Cardio Technologies, Inc, Pine Brook, NJ.
Received May 28, 1998; revision received November 17, 1998; accepted December 15, 1998.
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