(Circulation. 1999;100:II-236.)
© 1999 American Heart Association, Inc.
Thoracic Transplantation and Ventricular Assist Devices |
Physiological and Hemodynamic Evaluation of Nonuniform Direct Cardiac Compression
Presented in part at the 71th Scientific Sessions of the American Heart Association, Dallas, Tex, November 8–11, 1998.
From the Department of Surgery, Division of Cardiothoracic Surgery (J.H.A.), and Department of Medicine, Division of Circulatory Physiology (G.-H.Y., D.B., J.W.), College of Physicians and Surgeons, Columbia University, New York, NY; and Cardio Technologies Inc (H.R.L.), Pine Brook, NJ.
Correspondence to Jie Wang, 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 jw147{at}columbia.edu
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Abstract |
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Background—Biventricular direct cardiac compression (DCC) has the potential to support the failing heart without the complications associated with a blood/device interface encountered with the use of current ventricular assist devices. A clinically designed DCC device that provides compression pressure around the base of the heart in synchrony with native ventricular contractions was evaluated with the use of an ex vivo and in vivo canine model of heart failure.
Methods and Results—The device was tested over a series of
ventricular preloads with the use of an ex vivo canine
heart preparation and computerized afterload system that mimicked the
conditions of heart failure. The end-systolic pressure-volume
relation of the left and right ventricles was shifted upward in
parallel by DCC, with the magnitude of the shift averaging 40% of the
device compression pressure. The device was tested in vivo with the use
of a canine model of acute ischemic heart failure in which
graded reductions in ventricular function were created
through serial coronary artery embolizations. Under the most
severe condition of heart failure, DCC improved cardiac output (CO) by
104% (0.80±0.33 to 1.63±0.40 L/min) and mean arterial
pressure by 95% (45.6±11 to 89.0±18.2 mm Hg). The CO was
typically restored to 
60% of the normal baseline value, despite
attempts to further increase CO by increasing the amount or duration of
compression pressure.
Conclusions—Nonuniform DCC significantly improves the left and right ventricular pressure-generating capability and, in the setting of acute heart failure, can increase CO and mean arterial pressure. Such DCC devices can potentially avoid the complications associated with currently available ventricular support devices that involve a blood/device interface.
Key Words: heart failure • hemodynamics • ischemia • physiology • cardiac assist devices
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Introduction |
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The effective treatment of acute cardiogenic shock often requires circulatory support with the use of mechanical left ventricular (LV) assist devices. However, these support devices require direct contact with the patient’s blood; thus, thromboembolic events, the need for anticoagulation, hemolysis, and immune reactions are frequently encountered problems. Ventricular assistance achieved through direct mechanical compression of the surface of the heart in synchrony with native ventricular contraction has the potential to support the failing heart without the complications associated with a blood/device interface.
The effects of synchronized direct cardiac compression (DCC) on ventricular mechanics have been previously studied with the use of isolated canine heart preparations.1 2 3 4 Results of those studies showed that for isovolumic contractions at a given volume, net ventricular pressure-generating ability for both ventricles could be augmented with external pressure and that the magnitude of this effect was similar for the LV and right ventricle (RV). Importantly, the increase in ventricular pressure-generating ability was achieved without an increase in myocardial oxygen demand.4 Under computer-simulated ejection conditions, such as those encountered in situ, the increase in ventricular function afforded with DCC manifested as significant increases in stroke volume (SV).4
In these earlier studies, the isolated heart was placed into a compression chamber, and uniform compression pressure was provided that could be varied in synchrony with native systole. Because of their physical size and configuration, these compression chambers cannot be used on a heart in vivo. Recently, DCC devices have been developed that have the potential to be used clinically to administer biventricular compression to a failing heart. These devices provide nonuniform compression to the heart such that the net forces form a circumference around the base of the heart, excluding the apex. The physiology and hemodynamic effects of nonuniform compression devices have not been studied systematically.
The purpose of the study was 2-fold: (1) to study the effects of nonuniform DCC on ventricular physiology and 2) to test the hemodynamic effects of nonuniform DCC in the setting of acute heart failure. First, an ex vivo isolated canine heart preparation was used with which LV and RV pressure-volume relations could be controlled and accurately measured. DCC was tested over a series of ventricular preload volumes and under conditions mimicking heart failure. Next, the hemodynamic effects of DCC were tested in an in vivo canine model of ischemic heart failure in which graded reductions of cardiac function could be achieved. The DCC device was tested in the setting of 3 levels of reduced cardiac function to simulate various degrees of heart failure encountered clinically.
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Methods |
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General Surgical Preparation
A total of 23 adult male mongrel dogs (Team Associates) weighing between 34.8 and 22.0 kg (mean 26.7±4.2 kg) were used for the study. All animals 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). For all studies, dogs were anesthetized with pentobarbital sodium (30 mg/kg IV), intubated with an 8F endotracheal tube, and maintained with mechanical ventilation with humidified room air (Harvard Apparatus Inc).
DCC Device
Nonuniform DCC was provided by the CardioSupport System (Cardio
Technologies Inc). This device, which is illustrated in Figure 1
, consisted of an inflatable plastic
cuff, 2 air pumps, an epicardial ECG sensor, and a computer controller.
The cuff fits around the heart with an inflation bladder that
circumscribes both ventricular chambers and extends from
the midwall of the heart to the outflow tract. The cuff was held to the
heart with negative attachment pressure (200 mm Hg) applied to
the cardiac apex. Vertical ribbing extended from the apex of the cuff
to the inflation bladder and was used to prevent migration of the
inflation bladder. One pump was used to generate the attachment
pressure, and the other pump was used to generate the bladder inflation
pressure. A valved solenoid physically regulated the amount, onset, and
duration of cardiac compressions and was digitally controlled with the
computer console. A solid microtipped-catheter (Millar Instruments Inc)
placed in the driveline near the device was used to measure the
pressure inside the inflation bladder. The ECG sensor was connected to
pacing leads sewn in the heart, and the pneumatic pump was synchronized
to the native QRS complex with the computer controller. The device
could generate >200 mm Hg of compression pressure with inflation
periods varying between 10% and 50% of the cardiac cycle; however, an
inflation pressure of 100 mm Hg and a duration of 40% were
typically used throughout the experiment.
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Ex Vivo Canine Heart Study
Preparation
Six isolated cross-perfused canine hearts were studied according
to methods that were similar to those described
previously.5 Briefly, the femoral arteries and veins of a
dog ("support dog") were cannulated and connected to a perfusion
system that was used to supply oxygenated blood to the
isolated heart. The heart from the second dog ("heart donor dog")
was removed while metabolically supported with
arterial flow from the support dog. Two metal adapters were
sutured to atrioventricular valve rings and were used
to hold the isolated heart to individual ventricular volume
servopump systems. Water-filled balloons of the servopump systems were
then placed inside the ventricular cavities. A Millar
pressure transducer was placed inside each balloon to measure the
respective ventricular pressure. The
ventricular volume servopump systems were controlled with a
computer system that simulated hemodynamic properties
of the systemic and pulmonary circuits and allowed the
ventricles to eject against physiological
afterloads.6 7 A bipolar surface ECG was measured between
2 electrodes sutured to the surface of the heart.
Protocol
The ex vivo experimental protocol was designed to determine the
effects of nonuniform DCC on LV and RV systolic and
diastolic functions. The heart rate was set between 100 and
140 bpm with the use of atrial pacing, and the values of the simulated
vascular systems were adjusted to approximate the
hemodynamics of the heart failure state (RV
end-diastolic pressure 5 to 15 mm Hg, LV
end-diastolic pressure 15 to 20 mm Hg, SV 5 to 10 mL,
and peak arterial pressure 80 to 100 mm Hg). Under
these conditions, baseline LV and RV end-systolic and
end-diastolic pressure-volume (PV) relations (ESPVR and
EDPVR, respectively) were obtained through the recording of PV
data at 4 to 6 different filling volumes. The series of preloads was
obtained through simulation of increasingly severe degrees of
inferior vena caval occlusions in the computerized vascular
system. After the establishment of baseline steady-state conditions at
each preload setting, 5 s of data (ventricular pressures
and volumes) were recorded on the computer system. The DCC device
was then placed on the heart, and compressions were initiated.
Hemodynamic data were recorded after a new
hemodynamic steady state was established.
In Vivo Canine Heart Study
Preparation
For each in vivo experiment (n=11), the right carotid artery was
cannulated with a Millar pressure transducer that was introduced into
the LV for the measurement of LV pressure. The right internal jugular
vein was similarly cannulated with a Millar pressure transducer that
was introduced into the RV for the measurement of RV pressure. The left
carotid artery was cannulated with a Tygon catheter pressure transducer
(Statham P32, Gould) to measure arterial pressure. The
animal was placed in the left lateral decubitus position, and a
standard lateral thoracotomy was performed through the 5th intercostal
space. The incision remained open for the duration of the experiment. A
flow probe (Transonic Systems Inc) was placed around the ascending
thoracic aorta to measure cardiac output (CO). Temporary cardiac pacing
leads were sewn into the LV apex and right atrial appendage to
record the epicardial ECG. A custom-made silicon catheter was then
introduced into the dominant coronary artery (left anterior
descending or left circumflex) and was used for coronary
microembolizations to gradually induce more severe levels of heart
failure.
Coronary Microembolization
As described previously,8 9 aliquots of 90-µm
glass beads (25 000) were injected into the coronary artery
every 3 to 5 minutes until the desired level of acute heart failure was
achieved. Three levels of heart failure were attempted in each animal,
with the degree of failure based on the approximate percent reduction
in CO. Mild heart failure was defined as a 30% reduction in CO from
baseline, moderate heart failure was defined as a 30% to 60%
reduction in CO, and severe heart failure was defined as a >60%
reduction in CO. Ventricular ectopy was treated with
intravenous lidocaine (20 mg/kg loading dose followed by a
constant infusion of 1 mg · kg-1 ·
min-1). Ventricular fibrillation was
treated with cardioversion with internal paddles set at 10 to 50 J.
Protocol
A total of 8 dogs were used to test the effects of nonuniform
DCC in vivo. The experimental protocol was designed to address (1) the
impact of the placement of the device on baseline
hemodynamic function and (2) the ability of the device
to augment blood pressure and CO in an acutely failing heart.
Impact of Placement of DCC Device on Baseline Hemodynamic
Parameters
Hemodynamic data (pressure and flow) were
obtained at the baseline condition; an appropriately sized device was
then placed on the heart and fixed with negative attachment pressure.
Without turning on the device, hemodynamic data were
recorded after a stable state was reached. To test whether cuff
placement had any impact on baseline hemodynamics,
these data were compared with the data obtained before the placement of
the cuff on the heart.
Ability of Nonuniform DCC to Augment an Acutely Failing
Heart
Once the appropriate level of heart failure was achieved and
baseline data were obtained, the DCC device was placed on the heart,
and synchronized ventricular compressions were initiated.
DCC was sustained until hemodynamic signals attained a
stable state. After the completion of data acquisition, the device was
removed from the heart and additional embolizations were performed to
create the next desired level of failure. This cycle was repeated so
that data were obtained in states of mild, moderate, and severe heart
failure.
To exclude the possibility of any observed beneficial effect of DCC being attributed to spontaneous ventricular recovery, 3 dogs served as internal controls. They underwent the placement of hemodynamic monitors and coronary microembolization as described above, but DCC was not performed.
Data Collection and Statistical Analysis
All monitored signals were calibrated and zeroed before each
experiment. Data were recorded on an 8-channel charted recorder
(30-V8808-10; Gould electronics equipped with a National Instruments
Analog-In-Digital Conversion System), and periods of interest were
digitally sampled (1000 Hz) and analyzed offline with the use
of a data analysis program written in Microsoft BASIC.
Measurements were averaged over 3 to 5 beats.
For the ex vivo heart study, the end-systolic pressure
(Pes) and volume (Ves) of
each ventricular beat were determined through
identification of the top left corner of each PV loop, whereas the
end-diastolic pressure (Ped) and
volume (Ved) points were determined through
identification of the bottom right corner. The ESPVR was determined
through linear regression analysis with the formula
Pes=Ees(Ves-Vo).
The EDPVR was analyzed with nonlinear regression
analysis according to the equation
Ped=Po+
Vedß.
Statistical comparisons of the ESPVR and EDPVR between control and
active compression states were accomplished with the use of ANCOVA. For
the nonlinear EDPVR, the data relation was first linearized by plotting
ln(Pes-Po) versus
ln(Ved) before the application of ANCOVA.
For the in vivo studies, ANOVA was performed to detect statistically significant differences between groups, and paired t tests with Bonferroni’s corrections were performed to detect statistical differences between control and test conditions.
All statistical analyses were performed with commercially available software (SYSTAT). In all cases, a P value of <0.05 was considered statistically significant.
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Results |
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Ex Vivo Studies
Effects of DCC on Ventricular ESPVRs and EDPVRs
The effects of DCC on the PV relations of a representative experiment are shown in Figure 2
. The average ESPVR and EDPVR
parameter values obtained from the 6 experiments are
summarized in Table 1.
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As determined with ANCOVA, DCC with the device shifted the ESPVR of
both the LV and RV upward in a parallel manner; there was no
statistically significant effect on the slope
(Ees), but there was a large decrease in the
extrapolated volume-axis intercept (Vo). The
magnitude of the upward shift of the ESPVR, which indexes the amount of
pressure support provided with the DCC device, averaged 39.8±16.4
mm Hg for the LV and 40.3±12.9 mm Hg for the RV. Thus, 40%
of the 100 mm Hg of DCC pressure applied with the device was
transmitted to the heart. The effect of DCC on the EDPVR varied
somewhat among hearts and between the LV and RV. The
representative PV loops plotted in Figure 2
show
that although LV EDPVR is little affected, there is a leftward shift in
the RV EDPVR. Data pooled from all hearts analyzed with ANCOVA
demonstrated statistically significant differences between the
parameter values and ß for the EDPVR of both
ventricles, suggesting, on average, small leftward shifts in both RV
and LV curves.
Effects of DCC on Steady-State Hemodynamics
To investigate the effects of DCC on steady-state
hemodynamics, baseline ventricular
pressures and volumes were determined with LV filling pressure adjusted
to 15 to 20 mm Hg. DCC was then initiated, and
hemodynamic parameters were reassessed
after the achievement of steady-state conditions. The results are
summarized in Table 2 and demonstrate
significant improvements in RV and LV pressures and volumes that amount
to an average 26.7±18.6% increase in SV.
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In Vivo Studies
Impact of Placement of DCC Device on Baseline Hemodynamic
Function
The potentially adverse effects of simply placing the DCC
device on heart function were studied in 7 dogs, as outlined in
"Methods." Data summarized in Table 3
indicate that placement of the cuff on the heart caused a slight but
statistically significant reduction in both peak aortic flow and CO.
The reduction in CO was 10% and was not influenced by the amount of
attachment pressure (data not shown), nor was this consistently
observed in the 3 levels of heart failure. No other
hemodynamic parameter was influenced by
placement of the device.
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Effect of DCC in Acute Ischemic Heart Failure
The effects of nonuniform DCC in mild, moderate, and severe
acute ischemic heart failure were tested in 8 adult male
mongrel dogs. Due to interanimal variability and instabilities, not all
animals achieved each level of heart failure. Mild and moderate heart
failure was attained in 5 dogs, whereas severe heart failure was
attained in all 8 dogs. Baseline data obtained at each level of heart
failure and under normal conditions are shown in Table 4. ANOVA demonstrated significant
differences between these groups for all of the
hemodynamic parameters tested. This model
provided no evidence for spontaneous ventricular recovery
after microembolization. In fact, the 3 dogs that underwent
coronary embolization without the subsequent benefit of
ventricular assist demonstrated progressive deterioration
in ventricular function, resulting in cardiac arrest within
21±13 minutes of completion of embolization.
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In the 8 dogs undergoing the experimental protocol, DCC was performed
at each level of ischemic heart failure that was created, and
all hemodynamic parameters were compared
with values obtained before ventricular assist with the
device removed from the heart. Chart recordings from a
representative experiment are shown in Figure 3. The average effects of DCC on all
hearts studied are summarized in Table 4 and demonstrate
significant improvements in all hemodynamic
parameters tested with the moderate and severe conditions
of heart failure. Plotting of the degree of heart failure (indexed
according to the percent reduction in CO from normal) versus the change
in SV contributed by DCC (Figure 4a) or
versus the change in LV systolic pressure contributed by DCC
(Figure 4b) illustrates the direct correlation between
hemodynamic benefit provided by DCC and the degree of
ventricular dysfunction.
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Although DCC demonstrated significant hemodynamic
improvement in the more severe conditions of heart failure, DCC did not
restore CO to the baseline control value of 2.90 L/min. This is more
clearly illustrated in Figure 5, which
shows a plot of the CO during active DCC as a function of unassisted
CO. With the line of regression for the data and the line of identity
(x=y) drawn on the same axis, an approximate
upper range of CO obtained with DCC is established (between 1.3 and 2.0
L/min). In addition, the intersection between these 2 lines establishes
a point of marginal benefit; at unassisted CO values below this point,
DCC improves ventricular function, and at unassisted CO
values above this point, DCC reduces ventricular
function.
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Effect of DCC on Right and Left Heart Function
To investigate the differential effects of DCC on the LV and RV in
vivo, in 5 open-chest canine experiments, both the LV and RV were
instrumented with pressure transducers, and data from the most severe
condition of heart failure were analyzed. RV systolic
pressure increased by 132% (28.0±6.3 to 65.0±22.2 mm Hg), and
LV systolic pressure increased by 58% (66.6±26.3 to
105.2±16.9 mm Hg). Despite the markedly increased relative
pressure changes for the RV, the absolute changes in systolic
pressure were similar for both ventricles. The RV
end-diastolic pressure decreased by 29% (16.0±7.0 to
11.4±8.1 mm Hg), and the LV end-diastolic pressure
decreased by 32% (17.0±8.0 to 11.4±6.8 mm Hg).
Effect of Compression Pressure on CO
To investigate whether additional compression pressure could
further augment CO, DCC was performed first with a pressure of 100 and
then 150 mm Hg in 6 of the in vivo experiments with animals with
severe heart failure. The additional 50 mm Hg of compression
pressure increased LV systolic pressure by 11% (from
99.7±26.7 to 110.3±39.2 mm Hg) and peak aortic flow by 20%
(from 6.03±3.01 to 7.23±3.24 L/min) and reduced LV
end-diastolic pressure by 26% (from 15.3±9.3 to
11.3±7.3 mm Hg). However, CO was further increased by only 4%
(from 1.57±0.46 to 1.63±0.50 L/min), and mean arterial
pressure was increased by only 5% (from 92.0±20.6 to 96.5±23.3
mm Hg).
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Discussion |
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Initial investigations into the effects of DCC on ventricular physiology involved the use of a similar ex vivo canine heart preparation but included a compression chamber to administer pressure evenly over the surface of both ventricles. Those studies demonstrated that uniform DCC shifts the LV and RV ESPVRs upward in a parallel manner by an amount approximately equal to the compression pressure (PDCC).4 In the current set of ex vivo experiments, DCC applied with the nonuniform compression device demonstrated similar effects on the ESPVR of both the LV and RV; however, the magnitude of the upward shift in ESPVR (as determined by
Vo ·
Ees) was 40% of PDCC.
The difference between PDCC and
Vo · Ees reflects
the incomplete transmission of the device compression pressure to the
ventricular chambers.
The increase in systolic function afforded by nonuniform DCC
was accomplished with a small but significant effect on both LV and RV
diastolic function. Statistically significant changes in
the parameters of the EDPVR ( and ß) were observed for
both ventricles and likely represent changes in wall
characteristics due to physical attachment of the cuff to the heart.
These findings are in contrast to the findings from earlier studies in
which the idealized compression chamber had little affect on
diastolic function.4 In terms of impact on
overall pump function, this effect on diastolic function
will slightly counteract the effects on the systolic
properties.
The ESPVR and EDPVR data presented above provide
load-independent characterizations of how DCC influences intrinsic
ventricular pump function. These data do not, however,
reveal the effects of DCC on ventricular pressure and
volumes in the physiological setting, where preload
volumes vary as a consequence of altered pump function. Earlier
studies4 and the ex vivo data presented in Table 2 demonstrate that DCC increased LV Pes;
however, with the increased ventricular pumping capacity,
there was a corresponding decrease in Ves and
Ved. Consequently, the DCC-assisted ventricle is
functioning at lower preload volumes, and the increase in
Pes observed under steady-state conditions is
significantly less than the transmitted compression pressure (ie,
magnitude of the upward shift in the ESPVR). These findings are
predictable on the basis of our previous ex vivo studies and
explainable within the context of current theories of
ventricular/vascular coupling.10 This theory
predicts that the amount of Pes and SV
augmentation from DCC is dependent on the baseline contractile state,
the baseline afterload resistance, and the amount of
Vo and Ved
shift.4 In turn, the shifts in Vo
and Ved both depend on the transmission of
PDCC to the ventricular chambers.
As predicted on the basis of the ex vivo studies, the increased
ventricular pumping capacity with DCC manifested as
significant increases in LV systolic pressure
(Ps), significant decreases in LV
Ped, and significant increases in SV with the in
vivo heart failure model that was used. Also predicted from the ex vivo
studies was that these hemodynamic benefits were
related to the underlying ventricular contractile state and
were most apparent with the weakest hearts. Figure 4 illustrates
the change in SV and LV Ps as a function of
ventricular contractile state and demonstrates that
ventricular function had to deteriorate by 30% before
DCC actually improved these parameters.
Although DCC was able to significantly improve ventricular
pumping capacity under the more severe conditions of heart failure, DCC
did not restore CO to the normal baseline value. This is clearly
illustrated in Figure 5, which provides a plot of the CO during
active DCC as a function of unassisted CO and demonstrates an
approximate upper limit to the level of assisted CO. Attempts to
increase the inflation pressure by an additional 50 mm Hg only
marginally improved CO despite relatively pronounced changes in LV
Ps and peak aortic flow. Thus, the inability to
normalize CO is not likely to be due to a deficiency in contractile
assistance but rather to a limit on ventricular filling.
The reduction in CO observed with simple placement of the cuff on the
heart (Table 3) and the leftward shift of the EDPVR observed
with the ex vivo studies support this concept.
Data from the ex vivo and in vivo studies suggest that DCC pressure is equally distributed across both ventricles; however, the LV and RV function at different levels of contractility and pump into vascular systems with different arterial impedances. Based on the single ventricular analysis presented here, the effects of DCC on the RV will be proportionally greater than the effects on the LV. Under steady-state conditions, however, the SV must be approximately the same for both ventricles, so the proportionally greater effect of DCC on the RV cannot translate into a larger SV for the RV than for the LV. In other words, the amount of ventricular preload shifts and the degree of SV augmentation will depend on the effects of DCC on the unequal pumping capacity and vascular resistance of the LV and RV. Because the RV functions at lower levels of contractility and pumps into vascular beds with lower resistances, the ultimate degree of PDCC to be used will be critically dependent on the effect of DCC on the RV; that is, an increase in PDCC to values above those required to completely empty the RV will fail to further increase LV outputs.
In summary, the present study provides basic information concerning the physiological effects of a novel biventricular support device and demonstrates the effectiveness of this device in vivo. Nonuniform DCC with a new assist device that delivers compression forces around the circumference of the heart can increase LV and RV pressure-generating capability and, in the setting of acute ischemic heart failure, can significantly improve systemic hemodynamics and CO. This device has the potential to avoid many of the complications associated with currently available ventricular support devices that involve the use of a blood/device interface. However, future studies will have to address the effects of cardiac compression on underlying ventricular function and the potential damaging effects of compression forces on the myocardium. These studies must be performed over longer periods and use chronic models of heart failure to appropriately address these limitations.
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Acknowledgments |
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This work was supported in part by a grant from Cardio Technologies Inc. Dr Wang was supported in part by an Investigatorship Award from the American Heart Association, New York City Affiliate, and a Grant-in-Aid from the American Heart Association (National Center).
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