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1 Cardiovascular Imaging Center, Departments of Cardiology and 2 Cardiothoracic Sugery, Cleveland Clinic Foundation, Cleveland, Ohio 44195
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ABSTRACT |
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 TOP
 ABSTRACT
 INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Shortened early
transmitral deceleration times (EDT) have been
qualitatively associated with increased filling pressure and reduced
survival in patients with cardiac disease and increased left
ventricular operating stiffness (KLV). An
equation relating KLV quantitatively to
EDT has previously been described in a canine model but not in humans. During several varying hemodynamic
conditions, we studied 18 patients undergoing open-heart
surgery. Transesophageal echocardiographic two-dimensional
volumes and Doppler flows were combined with high-fidelity left atrial
(LA) and left ventricular (LV) pressures to determine
KLV. From digitized Doppler recordings, EDT was measured and compared against changes in
LV and LA diastolic volumes and pressures. EDT
(180 ± 39 ms) was inversely associated with LV end-diastolic
pressures (r = 
0.56, P = 0.004) and
net atrioventricular stiffness (r = 0.55,
P = 0.006) but had its strongest association with
KLV (r = 0.81,
P < 0.001). KLV was predicted
assuming a nonrestrictive orifice (Knonrest)
from EDT as Knonrest = (0.07/EDT)2 with
KLV = 1.01 Knonrest 0.02; r = 0.86, P < 0.001, 
K
(Knonrest KLV) = 0.02 ± 0.06 mmHg/ml. In adults
with cardiac disease, EDT provides an accurate
estimate of LV operating stiffness and supports its application as a
practical noninvasive index in the evaluation of diastolic function.
diastole; echocardiography; myocardial stiffness
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INTRODUCTION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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ABNORMALITIES of left ventricular (LV) diastolic function play an important role in the pathophysiology of myocardial and ischemic heart disease (17). Over the last two decades, Doppler echocardiography has emerged as the diagnostic modality of choice for the assessment of diastolic function. Several indexes derived from transmitral LV filling and pulmonary venous (PV) flow velocities are commonly used to estimate LV filling pressure, ventricular relaxation, and stiffness (2, 7, 8, 18, 23). LV operating stiffness (KLV), the slope of the ventricular pressure-volume curve (i.e., dP/dV during early and/or late LV filling), is one of the fundamental parameters of diastole. Increased KLV in patients with cardiac diseases causes increased end-diastolic pressure at rest and reduced cardiac output during exercise (13). LV stiffness is difficult to measure even with invasive techniques, requiring high-fidelity pressure measurements and synchronized volume assessment with high temporal resolution. A number of Doppler indexes have been associated with increased KLV, one of the most useful being the deceleration time of the early mitral filling wave (EDT). Although shortened EDT in patients with restrictive (14) and dilated cardiomyopathies has been associated with increased LV filling pressure, KLV (2, 25), and reduced survival (29), no human data exist that quantitatively relate EDT with KLV. Prior in vitro work has shown that the deceleration rate through a restrictive orifice is proportional to net ventriculoatrial stiffness (Kn) (5, 6) suggesting for the first time that stiffness might be measurable noninvasively. More recent experiments in an animal model of dilated cardiomyopathy have validated an analytic expression applicable to nonrestrictive orifices relating KLV to 1/EDT (16, 19). Whether similar relationships apply to humans with cardiac disease is unknown.
The aims of the following study were 1) to determine whether EDT might provide a quantitative estimate of KLV in humans; 2) to study the effect of varying preload in both EDT and KLV; and 3) to determine whether the relationship between EDT and KLV is better supported by physical principles of flow across a restrictive versus a nonrestrictive mitral orifice.
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METHODS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Patient population.
We studied 18 patients (age 62 ± 11 yr, 13 male)
undergoing elective open-heart surgery. Eleven patients had coronary
artery bypass surgery (CABG) only, two had mitral valve repair only, two had aortic valve replacement only, one had combined CABG and mitral
valve repair, one had combined CABG and mitral valve replacement, and
one had CABG and aneurysmectomy. Baseline clinical characteristics are
shown in Table 1. An institutional review
committee approved the study, and all patients provided informed
consent. All patients were hemodynamically stable and in regular sinus
rhythm at the time of the study.
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Intraoperative studies.
All patients underwent a complete transesophageal echocardiographic
(TEE) study using a Hewlett-Packard Sonos 1500 or 2500 (Andover, MA),
equipped with a multiplane transesophageal probe. These
echocardiographs were chosen in part because they lacked any
significant intrinsic temporal delay in the audio Doppler signal output
that would effect comparison with the hemodynamic data. After the
pericardium was opened and major cardiac vessels were cannulated, a
calibrated dual-sensor, high-fidelity pressure transducer catheter
(model SPC-751, Millar) was introduced through the right upper
pulmonary vein and advanced under TEE guidance until the distal
transducer was in the LV cavity and the proximal in the left atrium
(LA). Two-dimensional images of the LA and LV were acquired and stored
in 0.5 in. videotape and digital media. Pulsed Doppler velocities were
obtained sequentially at the levels of the left upper pulmonary vein
(PV), mitral annulus, and mitral leaflet tips. These were recorded at a
speed of 100 mm/s on 0.5 in. super VHS videotape. A timing signal
marker was coupled to the echocardiographic system and to the data
acquisition board to match pressure and Doppler signals for each
corresponding heartbeat (Fig. 1). LA and
LV pressures, electrocardiograms, and timing marker signals were
digitally acquired with 1-ms resolution using a multifunction I/O board
(AT-MIO-16, National Instruments, Austin, TX) interfaced with a
computer workstation (Pentium 200 MHz PC) using customized software
developed using LabVIEW v.5.0 (National Instruments, Austin, TX). In
addition, the audio Doppler signals (forward and reverse flow) were
directly acquired at 20 kHz using a second multifunction I/O board
(National Instruments). These were processed using a short-time Fourier
transform to reconstruct spectral Doppler images with <5-ms resolution
(Fig. 2). Extracted Doppler velocity
profiles were resampled to allow precise temporal alignment with LV and
LA pressure data. Color Doppler assessment of mitral regurgitant (MR)
volume using the proximal isovelocity surface area method (PISA) was
performed when MR was present (22).
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Hemodynamic conditions. Three complete sets of data including LA and LV pressures, echocardiographic chamber volumes, and pulsed Doppler velocities at the pulmonary vein, mitral annulus, and leaflet tips were acquired during suspended ventilation before cardiopulmonary bypass, during partial (1.5-2 l/min) cardiopulmonary bypass, and after surgery. Ventilation was suspended for at most 20-30 s at a time during which time data collection was performed. All patients had continuous routine oxygen saturation monitoring, and at no time did the value decrease below 95%. The use of intravenous inotropes and vasoactive drugs was maintained steady throughout each phase of data collection. Intravenous neosynephrine was administered at the discretion of the anesthesiologist to increase mean blood pressure by 15% in the postpump study compared with the prepump study if the patient was clinically stable.
Data measurements and analysis.
From each data set, LA and LV end-systolic (ESV) and end-diastolic
volumes (EDV) were measured using Simpson's biplane disk method, and
ejection fraction was determined. Consistent with clinical practice,
EDT was calculated as the time from the peak of
the E wave to the zero-velocity intercept of the regression line of the
E wave velocity deceleration profile (2). From the LA
pressure tracings, peak pressure during atrial contraction (PLA-A), ventricular systole (PLA-V), and
lowest pressure during atrial (PLA-X) and
ventricular relaxation (PLA-Y) were measured.
From the LV pressure waveform, we measured minimum LV pressure
(PLV-Min), LV pressure before LA contraction
(PLV-A) and LV end-diastolic pressure (PLV-ED).
From the LV pressure waveform, the time constant of isovolumic
relaxation (
) was determined using Weiss' monoexponential equation
(28), after curve fitting by use of the
Levenberg-Marquardt nonlinear least-squares parameter estimation
technique (21). To be consistent with previous work by
Yellin et al. (30), a zero asymptote (b = 0) was used.
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Hypothesis testing. To establish which physiological parameters influence EDT, we compared EDT with LA and LV ESV and EDV, stroke volume, MR volume, LA and LV pressures, the LV pressure rise (dPeLV) and the LA pressure decay (dPeLA) during early filling, and LA and LV stiffness (KLA, KLV-E, KLV-A, and KLV) by using 1) Pearson's correlation with Bonferroni's adjustment for multiple comparisons and 2) single and multiple linear regression analysis.
To determine whether EDT and KLV respond in a similar manner to preload alterations, we compared PLV-ED, KLV, and EDT before and after preload reduction using paired Student's t-tests. We also tested whether the relationship between KLV and EDT was similar during low and normal preload by linear regression. In an early attempt at predicting ventricular stiffness from transmitral flow, we showed that passive flow through a restrictive orifice between chambers of constant compliance should have a linear velocity decay (dV/dt = AoKn/
)(5),
where Ao is orifice area, and is density.
Because blood exiting the LA during early LV filling tends to be
replaced by blood entering through the pulmonary veins, one can
reasonably assume that KLA remains relatively constant and that Kn directly reflects
KLV. Thus, according to this analytic
expression, the deceleration rate of the early mitral filling wave
(EDecel = dV/dt = E/EDT) is linearly related to KLV. One limitation of this approach is that it
neglects the effect of inertial forces, which significantly prolong
flow across nonrestrictive orifices (6). Little et al.
(16) more recently proposed a formula for nonrestrictive
valves based on a simplified model of transmitral flow as a harmonic
oscillator
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(1) |
)1/2 and
Lml is mitral leaflet length. Applying typical
values of Amv (4 cm2) and
Lma (3 cm) yields Lma 
9.8 cm. Substituting this back into Eq. 1 and converting
from centimeter-gram-second units to conventional ones (1 mmHg = 1,333 dyn/cm2) yields
Knonrest = (0.07/EDT)2. This equation
was used to generate Knonrest for all
hemodynamic data sets in all patients, which were then compared with
measured KLV by linear regression and analysis
of agreement.
To determine whether the relationship between
EDT and KLV is better
supported by physical principles of flow across a restrictive (Krest) versus nonrestrictive
(Knonrest) mitral orifices, we compared the
differences between measured and predicted KLV
by both methods using paired Student's t-tests. The mean
difference (K) between the predicted and the actual LV
stiffness was determined as: Krest = Krest KLV and
Knonrest = Knonrest KLV.
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RESULTS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Hemodynamic measurements were obtained in 18 patients. In each patient, recording of measurements from three different conditions were attempted. Fifteen patients had all three measurements recorded. One patient undergoing mitral valve replacement had two data sets recorded but did not have invasive data following valve replacement. One patient only had two conditions collected because of hemodynamic instability and, in one patient, two data sets were rejected because of technical problems during acquisition. Overall, 50 of the 52 available data sets were analyzed. No complications related to the experimental protocol occurred.
Two-dimensional and Doppler echocardiographic variables and hemodynamic characteristic for the group are shown in Table 1. LV EDV ranged from 31 to 158 ml (92 ± 36 ml), ejection fraction from 0.20 to 0.74 (0.54 ± 0.13), PLV-ED from 6 to 40 mmHg (16 ± 9 mmHg), and KLV from 0.02 to 0.51 mmHg/ml (0.16 ± 0.11 mmHg/ml), indicating significant heterogeneity in the study group.
The correlation between EDT and hemodynamic
parameters is shown in Table 2.
By univariate analysis, a shorter EDT (180 ± 39 ms) was associated with higher LV PLVED
(r = 0.56, P < 0.005), higher LV
dPLV (r = 0.67, P < 0.001), higher LV KLV-A (r = 0.73, P < 0.001), and higher LV operating stiffness during
the total filling period (KLV, r = 0.81, P < 0.001). In addition, higher PLA-Y (r = 0.49, P = 0.04) was also associated with a shorter EDT.
There was an inverse relationship between the
EDT and MR volume as determined by PISA
(r = 0.49, P = 0.05). The magnitude of dPeLA during early LV filling was significant (12 ± 10 mmHg) and also correlated significantly with
EDT (r = 0.54,
P = 0.008). This LA pressure drop was significantly
higher than the LV pressure rise during early filling
(LVdPE = 1.3 ± 1.6 mmHg, P < 0.001). Neither LVdPE nor KLV-E had
a significant association with EDT. Figure
3A illustrates an example of the simultaneous pulsed
Doppler, LV and LA pressure, and pressure-volume curve (Fig.
3B). As demonstrated in this case, LV filling starts before
the nadir of LV pressure, and LV pressure crossover occurs before a
significant LV pressure rise, indicating a negative value for LV
operating stiffness during early filling, a phenomenon that could be
explained by the effect of active relaxation (12).
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By multiple linear regression, both LV ejection fraction and deceleration time were independent determinants of KLV, with no additional significant independent contribution from any other physiological variable.
Effect of preload reduction in EDT and KLV.
LV EDV decreased from 102 ± 36 ml before cardiopulmonary bypass
to 87 ± 38 ml during partial cardiopulmonary bypass
(P = 0.009). As expected, KLV
decreased during preload reduction from 0.20 ± 0.12 mmHg/ml at
PLVED = 19 ± 10 mmHg to
KLV = 0.11 ± 0.07 mmHg/ml at
PLVED = 14 ± 7 mmHg, P = 0.0008, Fig. 4A. In a similar manner, EDT increased from 166 ± 37 to 196 ± 35 ms, P = 0.0006 (Fig. 4B). The
relationship between observed (KLV) and
predicted stiffness assuming nonrestrictive orifice
(Knonrest) was similar during normal
(r = 0.83, KLV = 1.08Knonrest 0.01 mmHg/ml,
P < 0.01) and low preload (r = 0.91, KLV = 0.87Knonrest 0.01 mmHg/ml, P < 0.001, Fig. 5).
There was no significant change in LV relaxation ( = 57 ± 15 ms before vs. 53 ± 10 ms during partial bypass,
P = 0.22).
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Quantitative prediction of KLV using EDT.
Using the simplified equation for restrictive orifices, we found a
modest correlation between observed and predicted
(Krest) stiffness (r = 0.71, P < 0.001, Fig. 6) but a
significant underestimation [KLV = 2.56 Krest + 0.01 mmHg, K
(Krest KLV) = 0.10 ± 0.09 mmHg/ml], which could be attributed to
significant unaccounted effects of inertial forces. On the other hand,
applying Little's equation for nonrestrictive orifices to the 50 hemodynamic states yielded Knonrest ranging from
0.07 to 0.52 mmHg/ml (0.18 ± 0.10 mmHg/ml). There was a
significantly closer agreement between Knonrest and KLV: KLV = 1.01Knonrest 0.02, r = 0.86, P < 0.001, K = 0.02 ± 0.06 mmHg/ml (Fig. 7, A and
B). These differences between observed and predicted LV
stiffness using both methods [(Krest KLV) vs. (Knonrest KLV)] were highly significant
(P < 0.0001).
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DISCUSSION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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The results of the present study indicate that in adults with cardiac disease, early LV EDT provides a good estimate of KLV and thus may be used as a practical noninvasive clinical index in the evaluation of diastolic function. In addition, our findings suggest that changes in measurements of EDT in individual patients or study populations over time may be caused by changes in preload.
KLV is governed by a complex interplay of myocardial stiffness (largely related to the tissue collagen content) (10), ventricular geometry (hypertrophy) (9), and myocardial relaxation (26). In a "compliant" LV (low KLV) increasing filling volumes result in proportionally smaller increments in end-diastolic pressure than in a "stiffer" ventricle. Increased stiffness may occur as a result of LV remodeling in hypertensive cardiac disease and infiltrative hypertrophic and dilated cardiomyopathies, part of the normal aging process, and is often responsible for reduced cardiac output during exercise. Unfortunately, KLV is difficult to measure in clinical practice even with invasive techniques, which require simultaneous high-fidelity pressure measurements and volume assessment with high temporal resolution. Several Doppler echocardiographic indexes of LV filling have been proposed as qualitative estimates of KLV, including deceleration time of the early mitral filling wave (EDT) (2, 24). Shortened deceleration times have been associated with reduced ventricular compliance in patients with restrictive cardiomyopathy (14) and poor survival in congestive heart failure (29). Whereas these observations have been of great value in identifying patients with reduced ventricular compliance, the lack of quantitative rigor in relating EDT to compliance has limited the utility of this index in serial followup of patients undergoing pharmacological therapy.
Prior in vitro work has suggested that the deceleration rate through a
restrictive orifice is proportional to Kn
(5). In this early attempt, we showed that passive flow
through a restrictive orifice between chambers of constant stiffness
should have a linear velocity decay (dV/dt = AoKn/), with
convincing in vitro proof (6), suggesting for the first
time that KLV be measurable noninvasively. This
observation neglects Newton's second law, assuming that blood velocity
across the mitral valve is given instantaneously by the simplified
(noninertial) Bernoulli equation: P = 1/2v2. Net stiffness is by
definition dp/dV, where dV reflects the movement of blood from the LA to the LV. By the derivative
chain rule, because p and V are unique functions of time,
dp/dV can be written as
(dp/dt)/(dV/dt). From the Bernoulli
equation, dp/dt is
v(dV/dt), and
dV/dt is given from the mitral valve area
(Amv) and instantaneous velocity (v)
as Amvv. Thus
Kn = (dv/dt)/Amv.
This equation was implicitly validated in humans with mitral stenosis
when we showed that the mitral pressure half-time was directly related
to net atrioventricular compliance and the square root of the initial
pressure gradient and inversely related to valve area
(27). However, for patients with normal mitral valve area,
inertia keeps blood moving forward, even after the atrioventricular gradient has fallen to zero, significantly prolonging deceleration time
(relative to what would be expected without inertia) and thus
underestimating true stiffness. Thus it is not surprising that applying
this principle to the current data set yielded a predicted
KLV based on assumption of a
Krest of 0.06 ± 0.03 mmHg/ml, correlating
with true KLV (r = 0.71), but
with significant underestimation: KLV = 2.56Krest + 0.01, r = 0.71, P < 0.001, K
(Krest KLV) = 0.10 ± 0.09 mmHg/ml.
To avoid this restrictive orifice requirement, Little's group has
modeled the atrium, ventricle, and valvular apparatus as a simple
harmonic oscillator, a purely inertial system, with validation in a
canine model (16, 19). With this inertial paradigm, they showed that EDT is inversely proportional to the
square root of ventricular stiffness KLV, or
EDT 
1/
. With the
development of congestive heart failure over a 4-wk period of rapid
atrial pacing (with LV end-diastolic pressure rising from 9.8 to 34.3 mmHg), deceleration time fell from 88 to 51 ms with close correlation
to 1/ (r = 0.94). Although encouraging, extrapolating their results to humans with various cardiac diseases needs to be done cautiously because the number
of animals was small and constituted a homogeneous group, all with
dilated cardiomyopathy. One of the assumptions that Little made is that
the effect of LA stiffness is negligible, because during early LV
filling the LA behaves mostly as a conduit, maintaining relatively
constant volume and pressure as the volume of blood that moves to the
LV is replaced by incoming flow from the pulmonary veins. Although our
results indicate that this assumption may not be entirely correct in
humans, where a significant LA pressure drop occurred during early LV
filling, it is gratifying that direct application of Little's formula
to the current data suggests that KLV can indeed
be predicted quantitatively from EDT in patients with cardiac disease.
It should be recognized that the concept of LV "compliance" during early diastole is complicated because of the competing effects of ongoing ventricular relaxation and filling. The relatively low rise in LV pressure during early filling (which even falls early after mitral valve opening) can be explained by ongoing active LV relaxation reducing early LV operating stiffness, explaining the prolonged EDT in patients with delayed LV relaxation. In contrast, the presence of a rapid isovolumic descent toward the concave-downward portion of the LV pressure-volume curve at low ESV in vigorous ventricles with rapid active relaxation may explain the apparent paradox of the "pseudorestrictive filling pattern" seen in healthy children and athletes: below the equilibrium volume, the diastolic pressure-volume curve actually is stiffer than at the equilibrium volume, thus producing shorter deceleration times. For purposes of this study, we used a simple but clinically appealing definition of stiffness, the change in pressure during diastole divided by the change in volume, which showed the strongest (inverse) correlation with EDT. Other authors have sought indexes of end-diastolic LV stiffness, because it best reflects the passive properties of the fully relaxed LV chamber. Rossvoll and Hatle (24) have shown that the duration of the pulmonary venous A wave was prolonged when LV end-diastolic pressure was elevated, whereas the transmitral A wave was shortened by the rapid rise in pressure in the ventricle. A pulmonary A wave longer in duration than the mitral A wave predicted patients with LV end-diastolic pressure >15 mmHg with a sensitivity of 85% and a specificity of 79%. Furthermore, the difference in flow duration was correlated with end-diastolic pressure (r = 0.68) and the rise in LV pressure with atrial contraction (r = 0.70). Appleton et al.(1) noted a similar value to the mitral and pulmonary venous A wave duration in estimating LV end-diastolic pressure, as well as the importance of LA size in identifying patients with diastolic dysfunction when the transmitral flow profile is equivocal (1). These observations, although clinically helpful, have been so far empirical and have certain limitations. The latter method requires the presence of regular sinus rhythm and stable heart rates because both mitral inflow and PV flow cannot be recorded simultaneously. Furthermore, the duration of the mitral A wave, but not the AR, may be shortened by the onset of ventricular systole, therefore changes in heart rate or P-R interval will alter their relationship. Pulmonary venous AR waves are often difficult to record by transthoracic Doppler. In addition, patients with restricted LV filling have small or absent atrial reversal waves possibly due to either atrial mechanical failure (20) or increased stiffness in the pulmonary venous vasculature.
Limitations. Our study was performed in the operating room on patients with an open chest and pericardium. The pericardial influence on diastolic filling has been investigated using animal models and in patients undergoing cardiac surgery (15). The end-diastolic pressure-volume relationship may be shifted downward slightly after pericardiectomy (3, 11). Whereas removing the pericardium alters the interventricular and the atrioventricular interdependence, these effects tend to be very small and should not alter significantly the overall relationship of intracardiac hemodynamic parameters.
The effects of positive pressure ventilation are to reverse the usual respirophasic changes in left- and right-sided flows, with right-sided flow decreasing rather than increasing with inspiration, partially blunted when the thorax is open. However, these effects were minimized by collecting the data during apnea at atmospheric pressure. We have used TEE measurements of LV volumes and added mitral annular flow calculation of flow rates (dV/dt) to derive LV stiffness. Volume measurements derived by TEE may be less accurate than those provided by transthoracic or epicardial echo but are more practical for application in our experimental setting. In addition, there are inherent and often operator-dependent errors in measuring LV and LA volumes using the Simpson's biplane disk method. To minimize these errors, all TEE studies were performed by a single physician with advanced training and expertise in echocardiography (M. J. Garcia). Particular attention was placed on careful manipulation of the TEE probe to minimize LV foreshortening. However, despite careful attention to technique and analysis methods, these inherent limitations in assessing volumes may, in part, account for the observed scattering of the data. Measurements of EDT may be difficult to obtain in patients with tachycardia and shortened A-V intervals because of E and A fusion. Fortunately, in our study population, a clear separation between the E and A waves was observed in all patients under all conditions. The association between EDT and Kn and the importance of KLA may be underestimated due to greater inaccuracy of the method that we employed for LA volume calculations, because we used the ratios of systolic over total pulmonary venous flow derived from a single pulmonary vein sample and adjusted for mitral regurgitant volumes. Although our study demonstrates a strong correlation between EDT derived Knonrest and KLV, there was significant scattering of the data. Therefore, this quantitative index may be most useful in interpreting changes that occur within an individual over time. In conclusion, this study demonstrated that EDT, an easily obtained Doppler filling parameter, may not only provide qualitative and prognostic information in patients with diastolic dysfunction, but it can also provide a quantitative estimate of KLV. Because KLV may vary with preload alterations, this index may also be utilized to evaluate the effect of therapeutic interventions in patients with congestive heart failure.| |
ACKNOWLEDGEMENTS |
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This study was supported in part by Grant-in-Aid NEO-97-225-BGIA from the American Heart Association, North-East Ohio Affiliate (M. J. Garcia), National Aeronautics Space Administration Grant NCC9-60, Houston, TX (J. D. Thomas, M. J. Garcia, N. L. Greenberg), and National Heart, Lung, and Blood Institute Grant ROI HL-56688-01A1, (J. D. Thomas).
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FOOTNOTES |
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Address for reprint requests and other correspondence: M. J. Garcia, Dept. of Cardiology, Desk F-15, The Cleveland Clinic Foundation, 9500 Euclid Ave., Cleveland, OH 44195 (E-mail: garciam{at}ccf.org).
The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
Received 5 April 2000; accepted in final form 25 August 2000.
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REFERENCES |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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