(Circulation. 1997;95:2423-2433.)
© 1997 American Heart Association, Inc.
Articles |
Quantitative Assessment of Alterations in Regional Left Ventricular Contractility With Color-Coded Tissue Doppler Echocardiography
Comparison With Sonomicrometry and Pressure-Volume Relations
From the Divisions of Cardiology (J.G., W.A.M., V.K.G.) and Anesthesiology and Critical Care Medicine (D.P.S., M.R.P.), University of Pittsburgh (Pa).
Correspondence to John Gorcsan III, MD, Division of Cardiology, University of Pittsburgh Medical Center, 200 Lothrop St, Pittsburgh, PA 15213-2582. E-mail gorcsan{at}a1.isd.upmc.edu
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Abstract |
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Background Tissue Doppler imaging (TDI) is a novel method of color-coding myocardial velocity on-line. The objective of the present study was to evaluate endocardial velocity with TDI as a method of objectively quantifying alterations in regional contractility over a wide range induced by inotropic modulation.
Methods and Results Myocardial length crystals were used to simultaneously assess regional left ventricular (LV) function, and high-fidelity pressure and conductance catheters were used to assess global LV contractility by pressure-volume relations in nine open-chest dogs. Mid-LV M-mode and two-dimensional color TDI images were recorded during control and inotropic modulation stages with dobutamine and esmolol. Predicted significant increases in TDI indices occurred with dobutamine: peak systolic velocity of 4.41±1.07 to 6.67±1.07 cm/s*, systolic time-velocity integral (TVI) of 0.43±0.12 to 0.62±0.10 cm*, and diastolic TVI of 0.49±0.11 to 0.71±0.17 cm*. Opposing significant decreases occurred with esmolol: peak systolic velocity of 4.46±0.94 to 2.31±0.81 cm/s*, systolic TVI of 0.47±0.12 to 0.19±0.11 cm*, and diastolic TVI of 0.55±0.11 to 0.33±0.11 cm* (*all P<.001 versus control). Changes in TDI peak systolic velocity were correlated with changes in fractional shortening (r=.88) and shortening velocity (r=.87) by sonomicrometry. Changes in TDI peak velocity from multiple mid-LV sites also correlated significantly with maximal elastance (r=.85±.04) from pressure-volume relations.
Conclusions TDI measures reflect directional and incremental alterations in regional and global LV contractility and have the potential to quantify regional LV function.
Key Words: dynamics • echocardiography • myocardium • mechanics • imaging
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Introduction |
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Echocardiography is an established clinical tool for the assessment of regional LV function in patients with cardiac disease. However, echocardiographic estimation of segmental LV contractility is routinely accomplished through visual interpretation of endocardial motion and myocardial thickening.1 This method is subjective, requires an experienced observer, and is at best only semiquantitative. TDI has been introduced recently as a modification of color flow Doppler instrumentation that allows analysis of high-amplitude, low-frequency Doppler shifts and the selective display of color-coded tissue velocities in real time.2 3 4 5 6 This technique has enabled the noninvasive determination of myocardial velocity in the human heart.5 6 7 8 9 10 Although shortening velocity is an established functional measure in isolated cardiac muscle preparations,11 the ability of endocardial velocity by TDI to quantify regional LV contractility over a wide range of values in the intact heart has not been evaluated rigorously. The objectives of this study in an open-chest canine model were to assess endocardial velocity with TDI as a method of quantifying LV contractility by (1) measuring alterations induced by positive and negative pharmacological inotropic modulation, (2) determining its relationship with regional function measured with implanted myocardial length crystals, and (3) determining its relationship with global LV contractility assessed with pressure-volume relations.
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Methods |
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Preparation
Nine dogs, weighing 25.0±0.5 kg (range, 24.1 to 26.7 kg), were studied. The protocol was approved by the Institutional Animal Care and Use Committee and conformed to the position of the American Heart Association on research animal use. All dogs were anesthetized with sodium pentobarbital (30 mg/kg induction; 1.0 mg·kg-1·h-1 maintenance with intermittent boluses, if needed), endotracheally intubated, and mechanically ventilated. A 6F 11-pole multielectrode conductance catheter (Webster Laboratories) was inserted via the right internal carotid artery with its tip positioned in the LV apex through fluoroscopic guidance. An LV micromanometer catheter (MPC-500 Millar) was placed from the left common carotid artery. A 20-mm balloon catheter was inserted via the right femoral vein to the IVC. This balloon was partially filled with saline to intermittently occlude IVC flow and rapidly alter preload to determine sequential pressure-volume relations.12 13 14 15 A left lateral thoracotomy was performed through the fourth intercostal space, and the heart was suspended in a pericardial cradle. Pacemaker leads were attached to the right atrium to control heart rate by atrial pacing. A pair of piezoelectric length crystals to measure regional LV function were implanted
1 cm apart
to a depth of 1.0 to 1.5 mm in the lateral or free-wall surface of
the heart and aligned parallel with the longitudinal myocardial fibers.
This site was chosen because of its ease of access from the lateral
thoracotomy and to measure regional function in as close proximity to
the ultrasound transducer as possible without electrical or mechanical
interference. Crystal length data were processed with a
sonomicrometer (Model 120, Triton Technologies).
Echocardiography
Echocardiographic images were acquired using a
3.7-MHz transducer with a Toshiba SSA-380A ultrasound system (Toshiba
Medical Systems) with TDI capabilities. The
echocardiographic transducer was immersed in a saline
bath contacting the surface of the heart, placed within 2 cm of the
implanted piezoelectric crystals, and then aligned to the
midventricular short-axis plane and held stationary with a
mechanical support apparatus. The TDI system contained
modifications of conventional color flow Doppler instrumentation as
described previously in detail.4 5 7 10 Briefly, the
high-pass filter used to display blood flow was bypassed, and the
lower-frequency Doppler shifts of cardiac tissue motion were input
directly to the autocorrelator. High-frame-rate color Doppler
scanning was 30 Hz for a 90° two-dimensional sector at 12-cm depth
and 300 Hz for color M-mode scanning. Color-coded tissue velocity data
were superimposed onto conventional M-mode and two-dimensional images
on-line. Selected velocity ranges were ±9.49 cm/s for all M-mode
imaging and either ±7.11 cm/s or ±9.49 for two-dimensional imaging
with a pulse repetition frequency of 4.5 kHz. Tissue velocity values
were well below the Nyquist limits, and aliasing did not occur. Values
that exceeded the limits of the display range were saturated at the
highest color level. Ranges were selected to maximize sensitivity of
low velocity values while minimizing saturation of highest velocities
during systole. Images were recorded in duplicate for each stage of
the protocol using two separate postprocessing multicolored TDI
velocity maps. The first color map (Fig 1A
) contained
bidirectional data displayed as increasing velocities toward the
transducer in shades of red to orange to yellow, respectively, and
velocities increasing away from the transducer were displayed as shades
of blue to turquoise to green, respectively, and used to determine
velocity direction. A second map (Fig 1B) was unidirectional, but it
contained more colors to allow differentiation of increments of
velocity at 0.6 cm/s to improve the accuracy of subsequent visual
off-line analysis (Table 1). Color M-mode TDI
mid-LV images were recorded with a video color printer (UP-5000,
Sony Corp). Two-dimensional color TDI images were digitally acquired
using a frame grabber system (Imagevue, Nova Microsonics) in a
cine-loop format with an frame interval of 33 ms for 25 frames per
cardiac cycle gated from the ECG QRS complex.
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Conductance Catheter
A 20-kHz constant-amplitude current of 0.03 mA RMS between
proximal distal electrode pairs was used with a data processor as
described previously (Leycom Sigma 5DF).12 13 14 15 Briefly, an
electrical field is generated in equipotential planes between each of
the intervening electrodes, and blood volume between any two sensing
electrodes is considered to be a disc. Changes in volume are sensed as
a change in resistance in the cross-sectional area of each disc, with
the sum of all segments reflecting the total volume. The volume offset
caused by parallel conductance was calculated according to the
hypertonic saline method and subtracted from total conductance to
measure LV volume.15 All physiological
signals were digitized at 150 Hz for display and storage on a computer
workstation (Apollo Computer Model DN3550). All variables,
including TDI endocardial time-velocity plots described subsequently,
sonomicrometry length, and pressure-volume data, were transferred to a
customized program on ASYST software as described previously (ASYST
Software Technologies, Inc).15 16 17
Protocol
Physiological data were recorded during
periods of end-expiratory apnea to minimize cardiopulmonary
interactions.18 Echocardiographic and
sonomicrometry data were simultaneously recorded at
steady state conditions, and pressure-volume data were recorded
during IVC occlusion for each stage of the experiment. The study
consisted of two portions: positive inotropic modulation with
dobutamine and negative inotropic modulation with esmolol.
Each pharmacological infusion was preceded by a control period of data
collection to ensure a stable baseline for reference. Data sets were
collected in triplicate for each control run. Eight dogs received
dobutamine infused at 4
µg·kg-1·min-1
for 5 to 10 minutes. Esmolol was infused at 500
µg·kg-1·min-1
in 2 dogs and 750
µg·kg-1·min-1
in 7 dogs for 5 to 10 minutes. Dogs were randomly assigned to receive
dobutamine or esmolol first, and infusion of the second
drug was separated by a 15-minute wash-out period during which
physiological variables returned to baseline
values. Right atrial pacing was performed during esmolol infusion to
maintain the heart rate similar to that of the control run preceding
esmolol for each animal. Pacing was not used during
dobutamine infusion, and the control data set with the
highest spontaneous heart rate preceding the dobutamine
challenge were selected for comparison with the dobutamine
data.
Echocardiographic Analysis
TDI color M-mode prints obtained with the use of both
bidirectional and unidirectional color maps (Fig 2A and 2B) were analyzed to construct endocardial
time-velocity plots of the lateral wall and septum. These plots were
made through conversion of the endocardial color pixels to numerical
values with the use of visual analysis and the data in Table 1
.
Our group has shown interobserver and intraobserver variabilities to be
6±9% and 7±8%, respectively, with the use of this
method.10 A minimum of 2 consecutive beats were
analyzed, or 120 data points for each stage of the protocol in
each animal. A brief, relatively high-velocity shift toward the center
of the LV cavity consistently occurred after the onset of
systole identified by the onset of the QRS complex that corresponded to
isovolumic contraction on the LV pressure signal.19 The
following calculations were performed on each of the time-velocity
plots (Fig 3): peak isovolumic contraction velocity,
peak systolic velocity, systolic time-velocity
integral, and time to peak systolic velocity.
Diastolic function was assessed by determining peak
diastolic velocity, diastolic time-velocity
integral, and time to peak diastolic velocity. The early
and late portions of the diastolic velocity profile
described previously in humans merged with the heart rates encountered
in this canine model, and E and A components could not be assessed
separately.7
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Digitally acquired two-dimensional TDI images were analyzed for
peak systolic velocity in the following standard six segmental
sites for the midventricular level1 :
anteroseptal, anterior, anterolateral, inferolateral,
inferior, and inferoseptal. Color-coded peak
systolic velocities were selected individually for each segment
for each stage of the protocol from frame-by-frame analysis
from the onset of systole, excluding early rapid shifts from isovolumic
contraction and conversion of colors to numerical values (see Table 1).
Temporal heterogeneity of segmental velocities was
observed with peak systolic velocity occurring comparatively
earlier in septal segments.7 20 Accordingly,
analysis of multiple frames was necessary because peak
systolic velocity did not occur at the same time in all
segments.
Sonomicrometry and Pressure-Volume Relations
Sonomicrometry data during each of the steady state periods
described above were analyzed for fractional shortening,
shortening velocity, and regional stroke work. Fractional shortening
was defined as the ratio of the difference between
end-diastolic length and end-systolic length to
end-diastolic length. Shortening velocity was calculated as
the first derivative of the sonomicrometry length signal, with peak
shortening velocity being its maximal absolute value in systole.
Regional stroke work was the integral of pressure with respect to
length from pressure-length loops.
Global LV performance was evaluated by calculating the following relatively load-independent measures of contractility from pressure-volume loops during IVC occlusion: Emax, Ees, and PRSW.17 21 22 23 24 Briefly, time-varying elastance was derived every 7 ms from linear regression of the isochronous pressure-volume points of differently loaded beats beginning with end diastole and continuing past end systole with the maximal value defined as Emax. Ees was the slope of end-systolic points (maximum pressure/volume) from each loop on the basis of an automated iterative linear regression technique. PRSW was the slope of the stroke work ( pressure d volume) versus end-diastolic volume relationship.
Statistical Analysis
All data are presented as mean±SD. Changes in measures
of contractility induced by inotropic modulation were
compared with the use of an ANOVA for repeated measures for all
physiological variables. To account for the
possible influence of changes in heart rate, a
multivariate analysis of variance was also
performed using heart rate as the changing covariate. The degree of
change from control values by the above respective methods was
comparatively evaluated with the use of least-squares linear regression
analysis. Significance corresponded to a value of
P<.05.
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Results |
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Endocardial Velocity-Time Data
TDI data from the first and second control periods were similar. Consistent significant increases in systolic and diastolic endocardial velocities occurred with dobutamine infusion in both lateral and septal segments on the basis of TDI color M-mode analysis (Fig 4A
),
although heart rate was not significantly changed from 140±18 to
146±15 bpm. Pooled results of peak systolic velocity,
systolic time-velocity integral, and diastolic
time-velocity integral are shown in Fig 5. In addition,
isovolumic contraction velocity increased from 6.80±1.76 to 7.60±1.70
cm/s, diastolic peak velocity increased from 7.33±1.67 to
8.90±0.97 cm/s, time to peak systolic velocity decreased from
121±50 to 98±49 ms, and time to peak diastolic velocity
decreased from 372±35 to 331±38 ms (P<.005 for all). Peak
diastolic velocity was often saturated at the highest
velocity within the range selected and likely represents an
underestimate of its true value with dobutamine. These
findings are consistent with the positive inotropic properties
of the selective ß1-agonist dobutamine in
inducing an increase in contractility. Opposing
predicted decreases in TDI endocardial velocity variables occurred
with decreasing contractility by infusion with the
ß-blocker esmolol (Figs 4B and 5). In addition, peak isovolumic
contraction velocity decreased from 6.26±1.78 to 3.92±1.69 cm/s, and
peak diastolic velocity decreased from 8.06±1.75 to
5.98±2.23 cm/s (P<.005 for both). Times to peak
systolic and diastolic velocities were unchanged.
These changes occurred while heart rate was nearly identical to that of
the control period matched for this portion of the experiment (132±11
versus 132±10 bpm). The significance of all of the above changes
remained unaltered when multivariate analysis
was performed with heart rate as the changing covariate, reflecting
true changes in contractility.
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Peak Endocardial Velocity From Multiple Segmental Sites
Two-dimensional TDI endocardial velocity data were
consistently available from all six regional sites in all 9 of
these dogs with minimal TDI endocardial color dropout in our open-chest
preparation, as shown in Fig 1. As expected on the basis of the
Doppler equation, the calculated velocities were lower in the
segments in which endocardial movement was less parallel to the
ultrasound beam than the lateral and septal segments from our lateral
thoracotomy transducer location, and these represent an
underestimation of their true values.25 However,
consistent significant changes in relative segmental velocity
occurred in all sites with alterations in
contractility induced with dobutamine
and esmolol (Table 2).
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Relationship of TDI Velocity with Measures of Regional Function
by Sonomicrometry
Similar significant changes in regional LV function were
demonstrated with the use of implanted piezoelectric crystals. Group
mean fractional shortening increased with dobutamine from
11±5% to 15±3% and decreased with esmolol from 11±3% to 7±3%
(P<.01 versus control for both). Highly significant changes
in regional stroke work also occurred: from 1.42±0.71 to 2.18±0.72
mJ/cm2 with dobutamine and from 1.57±0.72 to
0.62±0.45 mJ/cm2 with esmolol (P<.0001 versus
control for both). Peak shortening velocity significantly increased
with dobutamine from 1.0±0.3 to 1.4±0.4 cm/s and
decreased with esmolol from 0.9±0.2 to 0.6±0.2 cm/s
(P<.01 versus control for both). Changes in fractional
shortening and regional stroke work with inotropic modulation were
significantly correlated with changes in peak systolic TDI
velocity (Fig 6). Although absolute values of shortening
velocity with sonomicrometry were less than endocardial velocity with
TDI as expected because these methods measure nearly perpendicular
vectors of contraction, changes in shortening velocity were correlated
with changes in peak systolic TDI velocity induced by inotropic
modulation (r=.88, y=0.82x-12.8).
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Relationship of TDI Velocity With Pressure-Volume
Relations
Pressure-volume loop data were unavailable with IVC occlusion in 1
dog each during dobutamine and esmolol infusion because of
conductance catheter artifacts. In the remaining animals, significant
alterations in global LV contractility with
dobutamine were demonstrated by an increase in group mean
Emax from 2.38±0.50 to 3.99±1.75 mm Hg/mL and in
Ees from 1.88±0.56 to 2.86±1.2 mm Hg/mL ( both
P<.05 versus control) (Fig 7). Catheter
artifact occurred selectively during diastole with
dobutamine in 2 of these dogs, which interfered with the
calculation of PRSW. There was a trend for this index to increase from
61±18 to 83±31 mm Hg (P=.09) with 7 dogs. Decreases
in contractility with esmolol were reflected by a
significant decrease in group mean PRSW from 70±24 to 38±15
mm Hg (P<.05) and nearly significant decreases in
Emax from 3.08±1.64 to 1.32±0.65 mm Hg/mL
(P=.06) and in Ees from 1.86±0.55 to
1.32±0.65 mm Hg/mL (P=.08). Alterations in peak
lateral and septal endocardial velocities by TDI M-mode were
significantly correlated with changes in Emax,
Ees, and PRSW (Fig 8).
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To assess the ability of endocardial velocity to reflect changes in
regional contractility from multiple segmental sites
using two-dimensional TDI, anteroseptal, anterior, anterolateral,
inferolateral, inferior, and inferoseptal sites were
individually correlated with changes in Emax and
Ees. Changes in peak endocardial velocity from all sites
were significantly associated with changes in Emax
(r=.85±.4, SEE=39±6%) and Ees
(r=.74±.9, SEE=39±9%). Correlations of individual sites
with Emax are shown as examples (Fig 9).
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,
dobutamine runs; 
, esmolol runs. |
Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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This study demonstrates that color-coded endocardial velocity data obtained from TDI M-mode and two-dimensional recordings predicted alterations in regional LV contractility induced by pharmacological inotropic modulation and compared favorably with indices of regional myocardial function assessed with sonomicrometry and global contractility measured with pressure-volume relations. Significant alterations in systolic and diastolic regional function induced by dobutamine and esmolol infusion were detected with TDI measures. These findings are consistent with the known pharmacological effects of dobutamine and high-dose ß-blockers on systolic and early diastolic LV function.24
These findings are of potential clinical importance because the most commonly used routine echocardiographic technique to assess regional LV function is subjective visual assessment of wall motion using descriptors such as hyperdynamic, hypokinesis, akinesis, or dyskinesis to identify abnormal function.1 These descriptors may be numerically scored and represent a semiquantitative approach.26 However, there is a wide range of degrees of abnormality in wall motion, and numerical scoring likely represents an oversimplification of an objective means to quantify regional function.7 Other quantitative echocardiographic methods have been described previously using M-mode tracings and two-dimensional images to assess regional LV function, including radial shortening or the centerline method.27 28 29 Although accurate, these methods require tedious hand-tracing of endocardial and epicardial borders from digitized images, and the time-consuming nature of these methods has limited widespread clinical use. An alternative automated echocardiographic method to detect blood-tissue borders by using integrated backscatter signal analysis has been validated to quantify global ventricular function online.15 16 17 30 This technique has been modified more recently by color-coding endocardial excursion, known as color kinesis, and it also has potential to quantify regional function.31 The principal difference between color kinesis and TDI is that the former uses ultrasonic backscatter information to display the endocardial distance traveled in sequential 33-ms frames, whereas TDI uses multigated Doppler with autocorrelator instrumentation to calculate and display myocardial velocity. The comparatively higher-amplitude TDI signals have the advantage of enhanced sensitivity, although color kinesis does not appear to be affected by the angle of incidence that affects Doppler calculations. Both methods of assessing regional function are affected by whole heart motion, although the calculation of velocity gradient by TDI has potential to overcome this limitation.6
TDI described in this present study uses Doppler shifts to quantify myocardial motion on line by rapidly calculating and displaying color-encoded velocity data. An advantage of TDI compared with hand-tracing of endocardial borders is that Doppler shifts created by tissue motion are of high amplitude with a favorable signal-to-noise ratio compared with routine color flow Doppler mapping, B-mode scanning, or backscatter analysis.4 5 6 This enhances the ability of TDI to be applied to large proportion of consecutive patients.10 Although time-consuming off-line analysis was also required to generate endocardial time-velocity plots from the TDI M-mode images in this present study, color-coded peak systolic velocity values may be rapidly assessed visually from online images. In addition, the variability of TDI analysis has been suggested to be less than that of routine quantitative echocardiographic methods.32 33 Furthermore, a prototype semiautomated TDI analysis system has been developed recently to convert calibrated color-coded velocity pixels to a digital velocity matrix.6 This system has promise to speed TDI analysis and further enhance objectivity of data interpretation.
The velocity of myofiber shortening has been widely used as a standard of regional contractility in isolated papillary muscle preparation11 but only recently has been applied to assess LV function in the intact heart. Other investigators have demonstrated the ability of pulsed Doppler echocardiography to determine posterior wall or mitral annular velocities within a sample volume.34 35 Sutherland, Yamazaki, and colleagues recently introduced the use of autocorrelator technique, which was used previously for color-coded blood flow mapping, to measure cardiac tissue velocity with enhanced spatial resolution.2 3 4 5 36 The TDI system used in the present study has enhanced temporal resolution compared with previous prototype systems to detect rapid physiological events not previously measured. In addition to quantifying resting wall motion abnormalities, TDI appears to be well suited as a means to assess relative changes in regional LV contractility in serial studies. Potential clinical applications include serial assessment of ischemic regional dysfunction in dobutamine stress and viability echocardiographic studies.37
Study Limitations
An important limitation of endocardial velocity by TDI to
quantify regional function is that these data may be affected by
variables other than regional contractility.
Cardiac rotation or conditions that result in whole heart motion, such
as right ventricular volume overload or paradoxical septal
motion after cardiac surgery, may affect regional endocardial velocity
values independent of regional function.38 39 However,
endocardial velocity is representative of thickening
velocity in the vast majority of clinical situations, and translational
motion did not occur in our preparation, in which the heart was
supported with a pericardial cradle. Another limitation is that
alterations in segmental function induced by regional ischemia
were not specifically evaluated in this study. It is possible that
asynchronous LV movement may make this approach less robust. Additional
studies are necessary to define the sensitivity of endocardial velocity
by TDI to quantify regional dysfunction induced by ischemia. It
is promising that these potential limitations may be overcome by
determination of transmural thickening velocity and mathematically
subtracting translational motion as a result of calculating myocardial
velocity gradient by a more recently described prototype TDI
analysis system.6 A limitation of data
analysis used in this present study is the tedious and
time-consuming visual conversion of color pixels to velocity values
only every 16 ms. Although the semiautomated TDI analysis
system could not be retrospectively applied to the data set from this
experiment, it has potential to greatly improve temporal resolution and
the quantitative accuracy of subsequent studies. Another limitation of
using TDI as a means to assess regional LV function is that endocardial
velocity will be significantly affected by changes in heart rate.
Accordingly, heart rates were controlled by an electronic pacemaker in
this experimental model. This may be a practical limitation because
heart rates cannot be easily controlled in clinical settings. However,
it is possible that heart rate correction algorithms may be developed
for endocardial velocity values similar to other functional
measures,40 although this has yet to be tested.
Another limitation of the present TDI system is that true values of endocardial velocity are underestimated from segmental sites in which movement is not parallel to the Doppler beam, in particular, where motion is perpendicular to the beam at which the measured component is zero. Although no angle of incidence correction was performed in this experiment, significant changes in relative velocity occurred in all segments from the midventricular short-axis plane. Although myocardial fiber orientation is complex and velocity shifts may occur in the long axis dimension and in a rotary fashion, the principal vector is endocardial motion toward the LV center from the short-axis plane.10 28 Changes in relative velocity from nonparallel sites were also significantly associated with alterations in global contractility determined by pressure-volume relations. In addition, an off-line TDI angle correction algorithm has been described by other investigators that has the potential to overcome this limitation.5 6 TDI measures of myocardial velocity have clinical potential to assess alterations in regional LV function in particular as refinements in this technology continue to occur.
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Selected Abbreviations and Acronyms |
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Acknowledgments |
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This study was supported in part by a grant from Toshiba America Medical Systems. The authors are grateful to Nobuo Yamazaki for his technical expertise and guidance.
Received August 5, 1996; revision received November 29, 1996; accepted December 9, 1996.
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A. J. Sinusas, X. Papademetris, R. T. Constable, D. P. Dione, M. D. Slade, P. Shi, and J. S. Duncan Quantification of 3-D regional myocardial deformation: shape-based analysis of magnetic resonance images Am J Physiol Heart Circ Physiol, August 1, 2001; 281(2): H698 - H714. [Abstract] [Full Text] [PDF]
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 A. A. IONESCU, A.-A. IONESCU, N. PAYNE, I. OBIETA-FRESNEDO, A. G. FRASER, and D. J. SHALE Subclinical Right Ventricular Dysfunction in Cystic Fibrosis . A Study Using Tissue Doppler Echocardiography Am. J. Respir. Crit. Care Med., April 1, 2001; 163(5): 1212 - 1218. [Abstract] [Full Text]
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T. Edvardsen, H. Skulstad, S. Aakhus, S. Urheim, and H. Ihlen Regional myocardial systolic function during acute myocardial ischemia assessed by strain Doppler echocardiography J. Am. Coll. Cardiol., March 1, 2001; 37(3): 726 - 730. [Abstract] [Full Text] [PDF]
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G. Derumeaux, J. Loufoua, G. Pontier, A. Cribier, and M. Ovize Tissue Doppler Imaging Differentiates Transmural From Nontransmural Acute Myocardial Infarction After Reperfusion Therapy Circulation, January 30, 2001; 103(4): 589 - 596. [Abstract] [Full Text] [PDF]
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 E. Vermes, R. Houel, M. Simon, P. Le Besnerais, and D. Loisance Doppler tissue imaging to predict myocardial recovery during mechanical circulatory support Ann. Thorac. Surg., December 1, 2000; 70(6): 2149 - 2151. [Abstract] [Full Text] [PDF]
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S. Urheim, T. Edvardsen, H. Torp, B. Angelsen, and O. A. Smiseth Myocardial Strain by Doppler Echocardiography : Validation of a New Method to Quantify Regional Myocardial Function Circulation, September 5, 2000; 102(10): 1158 - 1164. [Abstract] [Full Text] [PDF]
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K. Shan, R. J. Bick, B. J. Poindexter, S. Shimoni, G. V. Letsou, M. J. Reardon, J. F. Howell, W. A. Zoghbi, and S. F. Nagueh Relation of tissue Doppler derived myocardial velocities to myocardial structure and beta-adrenergic receptor density in humans J. Am. Coll. Cardiol., September 1, 2000; 36(3): 891 - 896. [Abstract] [Full Text] [PDF]
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P. Palka, A. Lange, J. E. Donnelly, and P. Nihoyannopoulos Differentiation Between Restrictive Cardiomyopathy and Constrictive Pericarditis by Early Diastolic Doppler Myocardial Velocity Gradient at the Posterior Wall Circulation, August 8, 2000; 102(6): 655 - 662. [Abstract] [Full Text] [PDF]
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L. Hatle and G. R. Sutherland Regional myocardial function--a new approach. Eur. Heart J., August 1, 2000; 21(16): 1337 - 1357. [PDF]
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C. Jarnert, M. Mejhert, M. Ring, H. Persson, and M. Edner Doppler tissue imaging in congestive heart failure patients due to diastolic or systolic dysfunction: a comparison with Doppler echocardiography and the atrio-ventricular plane displacement technique Eur J Heart Fail, June 1, 2000; 2(2): 151 - 160. [Abstract] [Full Text] [PDF]
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G. Derumeaux, M. Ovize, J. Loufoua, G. Pontier, X. Andre-Fouet, and A. Cribier Assessment of Nonuniformity of Transmural Myocardial Velocities by Color-Coded Tissue Doppler Imaging : Characterization of Normal, Ischemic, and Stunned Myocardium Circulation, March 28, 2000; 101(12): 1390 - 1395. [Abstract] [Full Text] [PDF]
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D. P. Strum and M. R. Pinsky Modeling of Asynchronous Myocardial Contraction by Effective Stroke Volume Analysis Anesth. Analg., February 1, 2000; 90(2): 243 - 243. [Abstract] [Full Text] [PDF]
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D. P. Strum and M. R. Pinsky Esmolol-Induced Regional Wall Motion Abnormalities Do Not Affect Regional Ventricular Elastances Anesth. Analg., February 1, 2000; 90(2): 252 - 252. [Abstract] [Full Text] [PDF]
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F Larrazet, D Pellerin, D Daou, S Witchitz, C Fournier, A Prigent, and C Veyrat Concordance between dobutamine Doppler tissue imaging echocardiography and rest reinjection thallium-201 tomography in dysfunctional hypoperfused myocardium Heart, October 1, 1999; 82(4): 432 - 437. [Abstract] [Full Text] [PDF]
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G. Geskin, C. M. Kramer, W. J. Rogers, T. M. Theobald, D. Pakstis, Y.-L. Hu, and N. Reichek Quantitative Assessment of Myocardial Viability After Infarction by Dobutamine Magnetic Resonance Tagging Circulation, July 21, 1998; 98(3): 217 - 223. [Abstract] [Full Text] [PDF]
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G. Derumeaux, P. Mulder, V. Richard, A. Chagraoui, C. Nafeh, F. Bauer, J.-P. Henry, and C. Thuillez Tissue Doppler Imaging Differentiates Physiological From Pathological Pressure-Overload Left Ventricular Hypertrophy in Rats Circulation, April 2, 2002; 105(13): 1602 - 1608. [Abstract] [Full Text] [PDF]
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T. Edvardsen, S. Urheim, H. Skulstad, K. Steine, H. Ihlen, and O. A. Smiseth Quantification of Left Ventricular Systolic Function by Tissue Doppler Echocardiography: Added Value of Measuring Pre- and Postejection Velocities in Ischemic Myocardium Circulation, April 30, 2002; 105(17): 2071 - 2077. [Abstract] [Full Text] [PDF]
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