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Circulation. 1997;95:2423-2433

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(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

John Gorcsan, III, MD; David P. Strum, MD; William A. Mandarino, MS; Vijay K. Gulati, MD; Michael R. Pinsky, MD

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


*    Abstract
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*Abstract
down arrowIntroduction
down arrowMethods
down arrowResults
down arrowDiscussion
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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


*    Introduction
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*Introduction
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down arrowDiscussion
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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.


*    Methods
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up arrowAbstract
up arrowIntroduction
*Methods
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down arrowDiscussion
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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 {approx}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 {approx}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 1ADown) 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 1BDown) was unidirectional, but it contained more colors to allow differentiation of increments of velocity at {approx}0.6 cm/s to improve the accuracy of subsequent visual off-line analysis (Table 1Down). 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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Figure 1. Tissue Doppler images of the midventricular short-axis plane from a dog with a lateral thoracotomy with color-coded velocities in midsystole. The lateral wall is closest to the transducer. Left, An example of the bidirectional color map. Right, Same frame with a different unidirectional postprocessing map.


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Table 1. Tissue Doppler Color-Coded Velocity Values

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 2ADown and 2BDown) 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 1Up. 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 3Down): 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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Figure 2. Examples of TDI color M-mode images obtained during control and inotropic modulation phases with alterations in color-coded velocity. The M-mode scan line was placed through the midventricular short-axis image obtained from a lateral thoracotomy shown in Fig 1Up with the lateral wall (LAT) appearing above the septum (SEPT). Composite A demonstrates the bidirectional color map, and composite B demonstrates the identical frames with the unidirectional color map. RV indicates right ventricle.



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Figure 3. Examples of data analysis of septal and lateral wall time-velocity plots constructed from TDI M-mode images. Velocity data sets acquired from the lateral thoracotomy images were inverted (multiplied by -1) to correspond to the standard orientation of the human transthoracic parasternal view with the septum above. I indicates isovolumic contraction; D, diastolic; S, systolic; and TVI, time-velocity integral.

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 1Up). 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.


*    Results
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*Results
down arrowDiscussion
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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 4ADown), 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 5Down. 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 4BDown and 5Down). 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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Figure 4. Examples of simultaneous waveform data of septal and lateral wall time-velocity plots by TDI (tissue Doppler imaging) and shortening velocity by implanted crystals with alterations induced by dobutamine (A) and esmolol (B), respectively. Velocity data sets acquired from the lateral thoracotomy images were inverted (multiplied by -1) to correspond to the standard orientation of the human transthoracic parasternal view.



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Figure 5. Pooled lateral wall and septal endocardial velocity data from TDI color M-mode time-velocity plots during control and inotropic modulation. Predicted significant increases in TDI indices of systolic and diastolic function occur with dobutamine and decreases with esmolol infusions. TVI indicates time-velocity integral.

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 1Up. 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 2Down).


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Table 2. Alterations in Peak Systolic Velocity by Two-Dimensional TDI Induced by Dobutamine and Esmolol

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 6Down). 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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Figure 6. Relationships of changes in peak systolic velocity by TDI with changes in fractional shortening and regional stroke work by sonomicrometry during alterations in contractility induced by inotropic modulation.

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 7Down). 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 8Down).



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Figure 7. Examples of pressure-volume loops with Ees demonstrating alterations in LV contractility.



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Figure 8. Relationships of changes in peak systolic velocity by TDI with changes in indices of contractility by pressure-volume relations during inotropic modulation.

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 9Down).



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Figure 9. Relationships of changes in peak endocardial systolic velocity by TDI from multiple midventricular segmental sites with changes in Emax induced by inotropic modulation. {bullet}, dobutamine runs; {blacktriangleup}, esmolol runs.


*    Discussion
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up arrowAbstract
up arrowIntroduction
up arrowMethods
up arrowResults
*Discussion
down arrowReferences
 
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.


*    Selected Abbreviations and Acronyms
 
Ees = end-systolic elastance
Emax = maximal elastance
IVC = inferior vena cava
LV = left ventricular
ms = millisecond(s)
PRSW = preload recruitable stroke work
TDI = tissue Doppler imaging


*    Acknowledgments
 
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.


*    References
up arrowTop
up arrowAbstract
up arrowIntroduction
up arrowMethods
up arrowResults
up arrowDiscussion
*References
 

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  6. Uematsu M, Miyatake K, Tanaka N, Matsuda H, Sano A, Yamazaki N, Hirama M, Yamagishi M. Myocardial velocity gradient as a new indicator of regional left ventricular contraction: detection by two-dimensional tissue Doppler imaging technique. J Am Coll Cardiol. 1995;26:217-223.[Abstract]
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