(Circulation. 2000;102:1983.)
© 2000 American Heart Association, Inc.
Basic Science Reports |
Single-Beat Estimation of End-Systolic Elastance Using Bilinearly Approximated Time-Varying Elastance Curve
From the Department of Cardiovascular Dynamics, National Cardiovascular Center Research Institute, Osaka (T. Shishido, T. Sato, M.S., K. Sunagawa), and Department of Anesthesiology, Kyoto Prefectural University of Medicine, Kyoto (K.H., K. Shigemi), Japan.
Correspondence to Toshiaki Shishido, MD, PhD, Department of Cardiovascular Dynamics, National Cardiovascular Center Research Institute, 5-7-1 Fujishirodai, Suita, Osaka 565-8565, Japan. E-mail tosjoe{at}res.ncvc.go.jp
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Abstract |
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Background—Although left ventricular end-systolic elastance (Ees) has often been used as an index of contractility, technical difficulties in measuring volume and in changing loading conditions have made its clinical application somewhat limited. By approximating the time-varying elastance curve by 2 linear functions (isovolumic contraction phase and ejection phase) and estimating the slope ratio of these, we developed a method to estimate Ees on a single-beat basis from pressure values, systolic time intervals, and stroke volume.
Methods and Results—In 11 anesthetized dogs, we compared single-beat Ees with that obtained with caval occlusion. Although the decrease (but not the increase) in contractility (5.3 to 11.4 mm Hg/mL) and the change in loading conditions (3.7 to 34.0 mm Hg/mL) over wide ranges significantly altered the slope ratio, the estimation of Ees was reasonably accurate (y=0.97x+0.46, r=0.929, SEE=2.1 mm Hg/mL).
Conclusions—Ees can be estimated on a single-beat basis from easily obtainable variables by approximating the time-varying elastance curve by a bilinear function.
Key Words: contractility • elasticity • systole • ventricles • hemodynamics
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Introduction |
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TopAbstractIntroductionMethodsResultsDiscussionAppendix 1References |
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The end-systolic elastance (Ees), the slope of the end-systolic pressure-volume relationship (ESPVR), has been used as an index of cardiac contractility. Although recent studies challenged the initial concept1 2 of linear and load-insensitive ESPVR by demonstrating contractility-dependent curvilinearity3 4 and load-dependence,5 6 Ees is still a powerful index to assess the inotropic state in experimental as well as clinical settings.7 8 9 10 The technical difficulties in measuring this index, however, prevent its widespread clinical acceptance. Difficulties include the need for a precise high-fidelity left ventricular (LV) volume curve as well as the need for multiple pressure-volume (P-V) loops under various loading conditions. Introduction of the conductance catheter9 11 12 and of the concept of a hydromotive pressure source13 14 for single-beat Ees estimation has partly solved these difficulties. Mirsky et al15 16 developed a single-beat method to assess myocardial contractility by fitting a model to late systolic data and estimating the unstressed state. They reconstructed ESPVR from this myocardial contractility. With all their efforts, however, simple, less invasive, single-beat methods that allow a precise Ees estimation are still required.
Senzaki et al10 developed a framework for estimating Ees that assumes a load insensitivity of the time-varying elastance waveform, E(t). The method offers advantages in Ees estimation not only of not requiring high-fidelity volume measurement but also of being applicable on a single-beat basis. In a preliminary study, however, we found that the uniqueness of the elastance waveform could not be held when loading conditions or contractility was significantly changed. Such a limitation might be overcome if we could quantify the effects of contractility and loading conditions on the E(t) and incorporate them into the Ees estimation.
The purpose of this investigation, therefore, was to develop a framework for Ees estimation based on a characteristic E(t) while quantitatively incorporating its dependency on contractility and loading conditions. To this end, we approximated E(t) by 2 linear functions, one for the isovolumic contraction phase and the other for the ejection phase. We experimentally evaluated how changes in contractility and loading conditions affected the slope ratio of these 2 linear functions. The fact that the slope ratios were quantitatively correlated with contractility and loading conditions enabled us to estimate Ees over a wide range of contractility and loading conditions on a single-beat basis without instantaneous ventricular volume.
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Methods |
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TopAbstractIntroductionMethodsResultsDiscussionAppendix 1References |
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Theoretical Considerations: Single-Beat Estimation of Ees
To focus on the shape (but not amplitude) of the elastance curve, we normalized the elastance curve by both amplitude and time.1 2 As shown in Figure 1A
, we approximated the time-varying
elastance curve [E(t)] by a bilinear function: one for the isovolumic
contraction phase and the other for the ejection phase. We defined the
ratio of the slope in the ejection phase to that in the isovolumic
phase as 
. Note that is unaffected by both amplitude and time
normalization and can be graphically illustrated with normalized
elastance curves. By use of this approximation to the E(t) waveform,
Ees is expressed as
 | (1) |
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Combining Equation 1
with the concept of the P-V relation (Appendix)
yields
 | (2) |
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Preparation
The study conformed to the "Position of the American Heart
Association on Research Animal Use" adopted November 11, 1984, by the
American Heart Association. The study was performed in 11 mongrel dogs
(16 to 20 kg) anesthetized with pentobarbital sodium (30 mg/kg
IV) after premedication with ketamine hydrochloride (5
mg/kg IM). The dogs were ventilated with room air, and a 5F catheter
was placed in the right femoral vein for administration of fluids and
drugs. After a median sternotomy, the heart was suspended in a
pericardial cradle. A catheter with 2
micromanometers (SPC-751, Millar Instruments) was
introduced via the LV apex for simultaneous LV and aortic
(1 to 2 cm above the aortic valve) pressure recording. An
additional catheter was advanced to the main pulmonary artery
for hypertonic saline injection for volume signal calibration. Snares
made from capillary tubing were placed around the inferior
and superior venae cavae for caval occlusion. A 6F 12-electrode
conductance (volume) catheter (2-RH-216, Taisho Biomed Instruments) was
also introduced into the LV through a second stab wound at the apex.
This catheter was connected to a conductance volumetric system (Sigma 5
DF, Leycom). To minimize changes in parallel conductance deriving from
noncardiac volume changes, we placed an insulator sheet between the
heart and the lung. A pair of pacing electrodes was fixed at the right
atrial appendage for atrial pacing.
The ECG and instantaneous LV pressure and volume were digitized at 1000 Hz with 12-bit resolution [AD12-16D(98)H, Contec] and stored with a dedicated laboratory computer system (PC9821Ap, NEC) for subsequent analyses. During data acquisition, the action of the respirator was temporarily suspended at end expiration.
The volume signal was calibrated by use of the hypertonic saline technique as previously described in detail.11 12 In brief, saturated saline (1 to 2 mL) was rapidly injected into the main pulmonary artery to obtain the parallel conductance, the contribution of surrounding structures. The parallel conductance was repeatedly measured at the beginning of each protocol.
Experimental Protocols
Contractility Run (n=9)
After measurement of the baseline ESPVR, the bilateral cervical
vagi were cut, and the sympathetic nerves were transected at the level
of the stellate ganglia. A pair of electrodes was attached at the
distal end of one of the left cardiac sympathetic nerves. We
recorded ESPVR under enhanced contractility either
by 1- to 2-Hz left cardiac sympathetic nerve stimulation (n=6) or by
dobutamine administration (2 µg ·
kg-1 ·
min-1, n=3) and under
reduced contractility by propranolol
administration (0.2 mg/kg).
Afterload Run (n=9)
ESPVR was recorded after pharmacological alterations in
vascular resistance (afterload) with methoxamine (10 to 15
µg · kg-1
· min-1) or sodium
nitroprusside (3 to 10 µg ·
kg-1 ·
min-1) infusion. Animals
were pretreated with hexamethonium chloride (30 mg/kg)
and atropine (0.1 mg/kg) to completely block autonomic reflexes.
Heart Rate Run (n=5)
We tested for the possible dependency of our estimation
technique on heart rate by crushing the sinus node region and
instituting atrial pacing to obtain ESPVR at different heart rates
(±25% of baseline heart rate).
ESPVR Determination From Multiple P-V Loops (True
Ees)
Conventional measurement ("gold standard") of
Ees was made from serial LV P-V loops obtained
during transient caval occlusions. The Ees and
V0 were calculated by an iterative linear
regression method.17 18 We excluded the first 5 beats to
avoid the possible effects of changes in parallel conductance
associated with alterations in right ventricular
volume.
Estimation of PEP and ET
In this study, the early isovolumic point
(ted) is defined as the moment when LV dP/dt
exceeds 30% of positive dP/dtmax to focus the
linear part of E(t) during the isovolumic contraction phase. The end of
the isovolumic contraction phase (tad) is defined
as the moment when the steep rise of the aortic pressure wave front
begins. End-systole (tes) is defined as the time
when dP/dt decreases to 20% of dP/dtmin. Thus,
PEP is obtained by subtracting ted from
tad; ET is obtained by subtracting
tad from tes.
Definition of Other Variables
We estimated effective arterial elastance
(Ea) as an index of afterload.
Ea was derived as the ratio of
Pes to SV.19 We also calculated
effective ejection fraction (EFe) as the ratio of
SV to stressed end-diastolic volume
[end-diastolic volume
(Ved)-V0] as a measure of
loading conditions. According to the framework of
ventricular-arterial coupling,
EFe approximates the ratio of
Ees to
Ees+Ea (Appendix).
Data Analysis
Estimated Ees(SB) and
V0(SB) were both compared with their respective
gold standards derived from multiple P-V loops. We also compared
estimated Ees(SB) with the estimation obtained by
the methods by Senzaki et al.10 We used the same
normalized elastance curve as appears in their report. Agreement of
ESPVR lines (SEE of ESPVR) was quantified by the root mean square of
the Pes difference over the
physiological volume range.
Data are presented as mean±SD. One-way repeated-measures ANOVA
with the Newman-Keuls test was applied for multiple comparison under
each run. Estimated and true Ees and
V0 were compared by linear regression
analysis. Multiple regression analysis was used to
determine the dependency of on various indexes of
contractility and loading conditions.
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Results |
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TopAbstractIntroductionMethodsResultsDiscussionAppendix 1References |
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Effect of Various Interventions on Ees and Ea
The Table
summarizes the
effects of various interventions on Ees as
estimated by the standard method and on Ea.
Ees and Ea values ranged
between 5.3 and 28.8 mm Hg/mL and between 3.7 and 34.0
mm Hg/mL, respectively, for all interventions (total of 69 beats).
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Contractility Run
Ees increased with enhanced
contractility (13.2±3.3 to 22.3±5.9 mm Hg/mL,
P<0.05) and decreased with reduced
contractility (8.8±2.4 mm Hg/mL,
P<0.05). Ea increased with both
enhanced (9.1±2.5 to 12.3±4.0 mm Hg/mL, P<0.05) and
reduced (15.5±3.6 mm Hg/mL, P<0.05)
contractility.
Afterload Run
Ea decreased from 14.6±6.3 to 9.0±3.6
mm Hg/mL (P<0.05) with vasodilation and increased with
vasoconstriction (21.8±7.2 mm Hg/mL, P<0.05). These
interventions did not significantly alter
Ees.
Heart Rate Run
Bradycardia decreased Ees nonsignificantly
(11.1 to 9.7 mm Hg/mL, P=NS) with no sizable changes
in Ea, suggesting concomitant alterations in
arterial resistance. Vasoconstriction in response to
decreased cardiac output might have counterbalanced the decrease in
Ea. Tachycardia nonsignificantly
increased Ees (17.4 mm Hg/mL,
P=NS) and Ea (11.4 to 14.1
mm Hg/mL, P=NS). Ees was different
between bradycardic and tachycardic conditions
(P<0.05).
Effect of Interventions on Time-Varying Elastance Curve
Figure 2 shows examples of
normalized E(t) curves (normalized by both amplitude and time) obtained
in the same dog under baseline conditions and after administration of
methoxamine under complete blockade of autonomic systems to
increase afterload and reduce contractility,
respectively. was reduced from 0.6 under baseline conditions to 0.3
with depressed contractility and increased afterload.
Similar differences in the E(t) curve were observed in all animals. As
summarized in the Table, was 0.61±0.11 under baseline
conditions, reaching values as low as 0.43±0.13 (P<0.05)
with reduced contractility. Enhancing
contractility did not change significantly.
Vasodilation increased from 0.43±0.10 under baseline conditions to
0.56±0.14 (P<0.05), and vasoconstriction decreased to
0.33±0.04 (P<0.05). Heart rate did not alter
significantly.
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Determinants of
We examined the dependence of on various
parameters, such as EF, EFe,
Ees, Ea, and PEP/(PEP+ET),
by linear regression analysis. We selected these variables
because is likely to be sensitive to changes in
contractility, loading conditions, and coupling between
them. As shown in Figures 3A and 3B,
was tightly positively correlated with EFe
(r=0.900) and EF (r=0.858). also correlated
positively with Ees (r=0.657, Figure 3C) and negatively with Ea
(r=-0.572, Figure 3D) and with PEP/(PEP+ET)
(r=-0.393, Figure 3E). Correlations between and
vascular resistance, heart rate, Ved, and
Ped were all poor (data not shown).
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Estimation of
As we show in Equation 2, our method requires the precise
value of . Although EFe and
Ees itself are good predictors of , these
values are unavailable beforehand. Instead, we used conventional EF to
predict (univariate model, =0.022+1.171EF,
r=0.858). was also correlated with PEP/(PEP+ET), an
index based on systolic time intervals. This index is directly
coupled with an index of ventricular
contractility (PEP/ET) that was used previously but is
rarely used now. We also used both EF and PEP/(PEP+ET) to improve the
accuracy of prediction of [bivariate model,
=-0.210+1.348EF+0.682PEP/(PEP+ET), r=0.875]. Although
both models predicted reasonably well, the SEE was smaller in the
latter model.
True Versus Estimated Ees and V0
Figures 4A and 4B show scatterplots
comparing Ees(SB) with true
Ees. Both models estimated
Ees reasonably well. The slope and intercept were
not significantly different from unity and zero, respectively, with
either model for . However, SEE was less with the bivariate model
than with the univariate model (2.1 versus 2.4
mm Hg/mL).
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Figures 4C and 4D show the scatterplots for the estimated versus
true V0. The accuracy of prediction of
V0 was much less than that of
Ees with either model for .
Figure 5 shows the scatterplots for
Ees and V0 estimated by the
method of Senzaki et al10 but with our data. The method of
Senzaki et al produced a lower correlation between estimated and true
values of Ees and V0
(r=0.420 and 0.404, respectively) as well as a larger SEE
(5.6 mm Hg/mL and 5.5 mL, respectively) than Figure 4.
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On average, the SEE of ESPVR was 6.9, 6.8, and 10.1 mm Hg for our method with the univariate and bivariate models and the method of Senzaki et al, respectively.
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionAppendix 1References |
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We found that the E(t) curve could be approximated by a bilinear function up to end systole, although the precise waveform of the E(t) was dependent on contractilities and loading conditions. The results indicated that Ees estimated by our method correlated well with conventional estimation over a wide range of cardiac contractilities and loading conditions.
Load Dependence of the Time-Varying Elastance Curve
A number of reports indicate that there are both positive and
negative effects of ejection on
Ees.20 Length-dependent changes in
the affinity of contractile proteins for calcium ions21 or
in the amount of calcium release22 have a positive
inotropic effect, whereas the uncoupling effects of shortening,
viscoelastic properties, or length-dependent changes in
transsarcolemmal kinetics of calcium have a negative inotropic
effect.23 24 25 26 Thus, the time course of the elastance curve
could also be modulated when the loading condition is altered over a
wide range.
Sagawa et al25 showed in excised, cross-circulated, blood-perfused canine hearts that the instantaneous E(t) curve depended on loading conditions and thus on the methods of defining E(t). Other investigators also reported differences between isovolumic and ejecting contractions on the shape of E(t),6 indicating that afterload significantly influenced the time course of contraction and relaxation of the LV. Our data further demonstrated that the shape of the E(t) curve was dependent on loading conditions even in in situ hearts. Senzaki et al10 assumed constancy in the shape of the E(t) curve in examining data recorded from humans. Although they include data from patients with various diseases, we speculate that a lack of data obtained under pharmacological interventions on their part is what prevented them from observing significant variability in the shape of the E(t) curve.
Technical Advantages of Our Method
Although the Ees provides a load-insensitive
index of contractile state, its clinical application has been limited
for various reasons. Our method has the advantage of removing 2 major
hindrances to clinical application of the Ees
concept. First, our method needs only Ved and
Ves but not "instantaneous" LV volume. We
have shown that with Ved and
Ves obtained by conductance catheter, our method
is capable of estimating Ees and
V0 with an accuracy similar to that of the
multiple-loop method. Second, one need not alter loading conditions.
This is of tremendous benefit because changing loading conditions could
lead to reflex-mediated change in hemodynamics. Our
method, moreover, can be applied to studying rapid changes in
contractility, such as occur with
arrhythmias.
Comparison With Other Methods
Both our method and that of Senzaki et al10 have the
advantage that neither instantaneous LV volume measurements nor
manipulation of loading conditions is needed. They are different in
that we have introduced the load dependence of the E(t) curve. We
tested whether this load dependence would improve the accuracy of
Ees and V0 estimation by
examining the wider range of coupling conditions. We have demonstrated
that at least in normal dogs, we successfully improved the accuracy of
Ees and V0 estimation. This
advantage becomes evident only if we study the ranges of coupling
conditions wider than the physiological range.
Although we studied a wider range of coupling conditions, our study has
the limitation that we did not study normal or diseased human
hearts.
Applications of This Method
As already stated, we believe that this method greatly enhances
the use of Ees in the clinical as well as in the
experimental setting. Clinically, in the
catheterization laboratory, it is relatively easy to
register high-fidelity pressures as well as Ved
and Ves for estimating the single-beat
Ees. In the experimental setting, there has been
a growing need for methods to estimate a load-independent index of
contractility in small animals (rats and mice), because
these species are especially useful in genetic engineering to produce
cardiovascular disease models. Because of the
advantages stated in the previous section, our method is especially
suited for the estimation of contractility in small
animals.
Limitations
Some investigators have observed in dogs that ESPVR is not
necessarily linear but rather shows a curvilinearity that is dependent
on contractility.3 4 We found, in the
present data, that ESPVR was predominantly linear and that
nonlinearity accounted for only 2% of the variance (data not shown).
Because of this apparent linearity, we reasoned that curvilinearity was
not a factor compromising our estimation accuracy. Our method thus
seems to be able to estimate the apparent linear slope of ESPVR
determined between Ved and
Ves. However, interpretations of the estimated
V0 should be made with caution, because the
V0 values were obtained by a linear extrapolation
outside of the operating volume.
We imposed a wide range of contractilities and loading conditions. The
dynamic afterload properties, arterial compliance, and
characteristic impedance were not explicitly altered. Indeed, when
characteristic impedance is effectively increased, as in aortic
stenosis or hypertrophic obstructive
cardiomyopathy, it is known that the shape of the
E(t) curve changes.25 Obviously, we need to further
investigate whether E(t) can be approximated by a bilinear function and
whether the estimation of holds even in such conditions.
Finally, our way of defining early isovolumic point and end systole from the pressure wave was somewhat arbitrary. We distinguished end systole (time with maximal elastance) from end ejection. Indeed, end systole is earlier than the end of ejection.17 Kono et al17 observed that Ees would be overestimated if end-ejection criteria were used, although the difference was small. We purposely defined early isovolumic point at the moment when dP/dt reached 30% of its maximum rather than 10%. This effectively extracted the linear part of the elastance curve during the isovolumic contraction phase and thereby improved the accuracy of bilinear approximation of E(t) curves. To apply this method to noninvasively obtained data, further investigation is needed on how the definitions of early isovolumic point and end systole affect the accuracy.
Summary
Identifying the load dependence of the waveform of E(t) and using
its approximation by a bilinear function, we developed a method for
estimating Ees and V0 on a
single-beat basis without need for instantaneous LV volume or changes
in loading conditions. This method proved itself capable of estimating
Ees and V0 with reasonable
accuracy over a wide range of contractilities and loading conditions.
We conclude that this technique is useful in the quantitative
assessment of LV contractility in experimental studies
and is worth studying further in the clinical setting.
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Acknowledgments |
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This study was supported by a grant from the Science and Technology Agency, Encourage System of the Center of Excellence, by a Health Sciences Research Grant on Advanced Medical Technology (FY1997), and in part by a Ground Research Announcement for Space Utilization promoted by NASDA and Japan Space Forum.
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Appendix 1 |
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TopAbstractIntroductionMethodsResultsDiscussionAppendix 1References |
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As shown in Figure 1B
, Ead,
Eed, and Ees will be
approximated by Pad, Ped,
and putative peak pressure when there is no ejection
(Pmax) according to the relations
 | (3) |
 |
 |
on both sides by
(Ved-V0) and substituting
Equation 3 into the result yields
 | (4) |
Ees can be estimated from
Pmax, Pes, and
SV13 14 as
 | (5) |
Substituting Pmax in Equation 5 with Equation 4
yields Equation 2.
According to the framework of
ventricular-arterial coupling using the
ESPVR,19 SV is derived as
 |
Dividing SV by Ved-V0
yields
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Received March 23, 2000; revision received May 17, 2000; accepted May 19, 2000.
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References |
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TopAbstractIntroductionMethodsResultsDiscussionAppendix 1References |
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S. Klotz, I. Hay, M. L. Dickstein, G.-H. Yi, J. Wang, M. S. Maurer, D. A. Kass, and D. Burkhoff Single-beat estimation of end-diastolic pressure-volume relationship: a novel method with potential for noninvasive application Am J Physiol Heart Circ Physiol, July 1, 2006; 291(1): H403 - H412. [Abstract] [Full Text] [PDF]
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K. Uemura, T. Kawada, M. Sugimachi, C. Zheng, K. Kashihara, T. Sato, and K. Sunagawa A self-calibrating telemetry system for measurement of ventricular pressure-volume relations in conscious, freely moving rats Am J Physiol Heart Circ Physiol, December 1, 2004; 287(6): H2906 - H2913. [Abstract] [Full Text] [PDF]
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P. Segers, V. Tchana-Sato, H. A. Leather, B. Lambermont, A. Ghuysen, J.-M. Dogne, P. Benoit, P. Morimont, P. F. Wouters, P. Verdonck, et al. Determinants of left ventricular preload-adjusted maximal power Am J Physiol Heart Circ Physiol, June 1, 2003; 284(6): H2295 - H2301. [Abstract] [Full Text] [PDF]
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K. E. Kjorstad, C. Korvald, and T. Myrmel Pressure-volume-based single-beat estimations cannot predict left ventricular contractility in vivo Am J Physiol Heart Circ Physiol, May 1, 2002; 282(5): H1739 - H1750. [Abstract] [Full Text] [PDF]
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