- Email: [email protected]
Quantitative Evaluation of the Segmental Left Ventricular Response to Dobutamine Stress by Tissue Doppler Echocardiography
Quantitative Evaluation of the Segmental Left Ventricular Response to Dobutamine Stress by Tissue Doppler Echocardiography William E. Katz,
MD,
Vijay K. Gulati, MD, Christine M. Mahler, and John Gorcsan III, MD
MS,
Tissue Doppler imaging displays color-coded myocardial velocity on-line and has potential to objectively quantify regional left ventricular function. Sixty patients, aged 56 {10 years, were studied to determine the normal and abnormal segmental endocardial velocity response to dobutamine stress, and the sensitivity, specificity, and accuracy of tissue Doppler imaging for detecting abnormal wall motion at peak stress as defined by routine visual interpretation. Separate 2-dimensional routine gray scale and color tissue Doppler image sets were acquired at rest and peak dobutamine stress in a digital cineloop format. Routine wall motion interpretation from gray scale images and color-coded peak systolic endocardial velocity from tissue Doppler images were determined independently. Twenty-two patients who reached their target heart rate and had normal wall motion at peak stress served as a control group. There were 19 patients who had wall motion abnormalities at
peak stress. Segmental peak endocardial velocities increased significantly in all segments in the control group. Endocardial velocity was significantly lower at peak stress in the pooled abnormal segments than in the pooled normal segments: 3.1 { 1.2 versus 7.2 { 1.9 cm/s, respectively (p õ0.05 vs normal control). However, the velocity response of abnormal apical segments could not be distinguished from normal controls by tissue Doppler imaging. Excluding apical segments, a peak velocity of °5.5 cm/s with peak stress had an average sensitivity of 96%, specificity of 81%, and accuracy of 86% for identifying abnormal segments at peak stress as defined by routine 2-dimensional criteria. Tissue Doppler imaging has the potential to quantify regional left ventricular function during dobutamine stress. Q1997 by Excerpta Medica, Inc. (Am J Cardiol 1997;79:1036–1042)
obutamine stress echocardiography has become established as a valuable diagnostic tool for the D evaluation of patients with coronary artery disease.
tively. The protocol was approved by the Institutional Review Board for Biomedical Research and all patients gave informed consent. Patients were aged 56 { 10 years (range 26 to 86), of which 17 were women. Indications for dobutamine stress echocardiography were preoperative evaluation in 34 patients and evaluation of chest pain in 26. Patients with abnormal wall motion at rest were not excluded. All patients were in normal sinus rhythm and none had bundle branch block.
1–6
Although clinically useful in its present form, a major limitation of echocardiographic study interpretation is the subjective visual interpretation of endocardial motion and wall thickening which is only semiquantitative.7 Tissue Doppler imaging is a novel echocardiographic technique that color codes myocardial velocity on-line and has the potential to objectively quantify regional left ventricular function.8–12 The objectives of this study were: (1) to evaluate the feasibility of applying tissue Doppler imaging to dobutamine stress echocardiography; (2) to determine the normal and abnormal quantitative regional endocardial velocity responses to dobutamine stress; and (3) to determine the sensitivity, specificity, and accuracy of tissue Doppler imaging for determining abnormal wall motion at peak stress compared with routine 2-dimensional echocardiographic visual interpretation.
METHODS Sixty consecutive patients referred for dobutamine stress echocardiography were studied prospecFrom the Division of Cardiology, University of Pittsburgh, Pittsburgh, Pennsylvania. Manuscript received August 28, 1996; revised manuscript received and accepted December 2, 1996. Address for reprints: John Gorcsan III, MD, Division of Cardiology, University of Pittsburgh Medical Center, 200 Lothrop Street, Pittsburgh, Pennsylvania 15213-2582.
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TABLE I Color-Coded Tissue Doppler Velocity Values Velocity (cm/s) Color White/yellow Light yellow Yellow/yellow orange Orange/yellow Light orange Orange Red/orange Red Black Dark blue Blue Blue/turquoise Dark turquoise Turquoise Blue/green Green/green turquoise Green
9.5 Scale
11.5 Scale
9.5 8.3 7.1 5.9 4.7 3.6 2.4 1.2 0.0 01.2 02.4 03.6 04.7 05.9 07.1 08.3 09.5
11.5 10.0 8.6 7.2 5.8 4.3 2.9 1.4 0.0 01.4 02.9 04.3 05.8 07.2 08.6 010.0 011.5
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apical windows in all patients in this study. Tissue velocity values were well below the Nyquist limits of the selected velocity ranges and aliasing did not occur. Tissue Doppler images were recorded using a multicolored postprocessing velocity map that displayed increasing velocity values toward the transducer in shades of red to orange to yellow, respectively, and increasing velocities away from the transducer in shades of blue to turquoise to green, respectively (Table I). Protocol: Dobutamine was infused by a standard protocol in 3-minute stages in rates of 5, 10, 20, 30, 40, and up to 50 mg/kg/min to achieve a heart rate ¢85% of the patient’s maximum agepredicted rate (220 0 age). The infusion was discontinued if new severe wall motion abnormalities, ischemic electrocardiographic changes, or limiting side effects occurred. Atropine up to 1.0 mg was also given to a subset of patients in an attempt to achieve ¢85% of the target heart rate.1 – 6 The tissue Doppler velocity range was selected at the time of baseline data acquisition to display peak systolic velocity in the low to midportion of the color display range to allow for detection of increases in systolic velocity at peak dobutamine stress within the same velocity range (Table I). Proper selection of the velocity range was important because velocity values that exceeded the limits of the selected range were displayed as saturated at the highest color-coded value, and could therefore be underestimated. Separate sets of black and white 2-dimensional and tissue Doppler images were acquired at baseline and peak stress from FIGURE 1. Tissue Doppler images at rest and peak dobutamine stress of a northe standard 4 views: parasternal long mal control patient showing the maximal systolic endocardial velocities. A, paraxis, parasternal short axis, apical 4asternal long-axis view; B, parasternal short-axis view; C, apical 4-chamber chamber, and apical 2-chamber. Data view; D, apical 2-chamber view. were acquired using a digital acquisition system (Nova Microsonics, Imagevue, Echocardiography: Echocardiographic data were Allendale, New Jersey) in a cineloop format with a acquired with a 2.5- or 3.75-MHz transducer and an frame interval of 16 ms for 25 frames per cardiac ultrasound system with tissue Doppler capabilities cycle gated from the electrocardiographic QRS com(SSA-380A, Toshiba Corp., Tochigi, Japan), de- plex and stored digitally on a 4.5-inch optical disk. scribed elsewhere in detail.10 – 13 Briefly, tissue Black and white and color tissue Doppler image sets Doppler imaging is a modification of routine color from each patient were subsequently separated, ranflow Doppler signal processing, bypassing the high- domly assigned an alphanumeric code to conceal the pass filter and inputting the comparatively lower fre- patient’s identity, and reviewed in a random order to quency Doppler data from myocardial motion di- investigators blinded to the alternate data set. rectly into the autocorrelator. Calculated velocity Data analysis: All analyses were identically perdata are color-coded and superimposed on the con- formed for baseline and peak stress images. Routine ventional 2-dimensional images. Frame rates were images were analyzed using the standard 20-segment approximately 40 Hz for a 607 sector with a 15.4 cm model of the American Society of Echocardiogradepth using a 3.75-MHz transducer and a pulse rep- phy.7 Routine wall motion assessment was peretition frequency of 4.5 KHz. The left ventricle could formed as a consensus between 2 independent be imaged within this depth from the parasternal and observers blinded to all tissue Doppler and clinical CORONARY ARTERY DISEASE/DOBUTAMINE STRESS TISSUE DOPPLER ECHOCARDIOGRAPHY
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tively high-velocity shifts of brief duration due to conformational changes occurred during isovolumic contraction, peak systolic velocity was measured ú50 ms from the onset of the electrocardiographic QRS complex to correspond to systolic ejection.11 – 14 Peak systolic velocity for individual segments was selected from individual frames because of the temporal heterogeneity of normal electrical activation, with peak velocity characteristically occurring in septal segments before free wall segments.11 Intra- and interobserver variability in visual interpretation of tissue Doppler color-coded velocity data was analyzed for 10 randomly selected studies and expressed as the difference divided by their mean values.15,16 Statistical analysis: Differences in variables from baseline to peak stress were analyzed using analysis of variance for repeated measures. Potential differences in regional endocardial velocity responses to peak dobutamine stress in normal and abnormal segments compared with routine 2-dimensional criteria were analyzed using an unpaired t test. Post hoc sensitivity, specificity, and accuracy analyses were performed to select tissue Doppler velocity criteria to identify an abnormal segmental response at peak stress defined by routine 2-dimensional criteria. Significance was determined as p õ0.05.
RESULTS Five patients were excluded from analysis because of suboptimal echocardiographic windows, with complete data sets available in 55 patients or 92% of attempted studies (Figures 1 and 2). Of these, 36 patients had normal dobutamine stress studies by routine visual wall motion assessment1 – 6 and 22 who reached ¢85% of their age-predicted heart FIGURE 2. Tissue Doppler images from patients with abnormal segments rate were selected as a control group. Nineby routine echocardiography and abnormal velocity responses at peak dobutamine stress. A and B, parasternal long- and short-axis views from a teen patients had an abnormal dobutamine patient with an abnormally low anteroseptal velocity response (arrowstress study defined as having at least 2 hyheads) color-coded as dark blue rather than turquoise or green. This papokinetic or akinetic segments at peak stress tient had an akinetic anteroseptum at peak dobutamine stress by routine by routine 2-dimensional criteria, and all 19 imaging. C, apical 4-chamber view of a patient with a hypokinetic inferior reached ¢85% of their predicted heart rate. septum at peak stress and an abnormally low peak velocity at peak stress (arrowheads) color-coded as orange rather than yellow. D, apical 2-chamClinical variables between abnormal and ber view of a patient with an abnormally low peak velocity response occontrol groups were similar except for gencurring diffusely at peak stress (arrowheads) color-coded as orange rather der (Table II). The availability of segmental than yellow. This patient had diffuse hypokinesia at peak stress. tissue Doppler imaging data for analysis is shown in Table III. Despite the suboptimal data with segments scored as follows: 1 Å normal, incidence angle of the ultrasound beam for Doppler 2 Å hypokinetic, 3 Å akinetic, or 4 Å dyskinetic. calculations of lateral segmental velocity, data were Digitized tissue Doppler image sets were indepen- available from a high proportion of all segments with dently analyzed by investigators blinded to the re- the exception of the apical segments from the apical sults of routine 2-dimensional analysis and all other views. The interobserver variability of tissue Doppclinical data. Peak endocardial velocity was deter- ler color-coded velocity analysis was 3.8 { 16.5% mined for each of the 20 segments converting color- and intraobserver variability was 04.8 { 8.2%, recoded pixels to velocity values using Table I. Frame- taining the sign to show bias. There were a total of by-frame analysis of the digitized cineloops was 229 segments interpreted to be hypokinetic or akiused to select peak systolic velocity. Because rela- netic at peak stress by routine visual assessment. In1038
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TABLE II Clinical and Dobutamine Protocol Data
Number Ages (yr) Men/women Maximum heart rate (min01) Maximum dobutamine (mg/kg/min) Atropine (mg)
Normal Control Group
Abnormal Group
22 58 { 12 11/11 144 { 10 46 { 5 0.2 { 0.2
19 62 { 12 13/6 137 { 15 42 { 8 0.5 { 0.3
TABLE III Tissue Doppler Data Availability (41 patients; 44 total segments/patient) Number of Segments (%) Parasternal long axis Basal anteroseptum Midanteroseptum Basal posterior Midposterior
Number of Segments (%) Apical 4 chamber Basal septum Midseptum Apical septum Basal lateral Midlateral Apical lateral Apical 2-chamber Basal inferior Midinferior Apical inferior Basal anterior Midanterior Apical anterior
pared with the normal segmental response in parasternal views and for basal and midsegments from apical views. In contrast, tissue Doppler measures were unable to distinguish between abnormal and normal apical segments at peak stress from apical views. Sensitivity, specificity, and accuracy for a peak velocity of °5.5 cm/s to identify an abnormal segment at maximal stress appear in Figures 6 and 7, excluding apical segments. Velocities ú5.5 cm/s with the most commonly used velocity range of { 9.5 cm/s corresponded to a peak velocity coded as yellow or turquoise-green. In apical segments, the accuracy for a peak velocity of 5.5 cm/s to identify an abnormal segment at maximal stress was lower at 59%, with a sensitivity of 34% and a specificity of 95%.
DISCUSSION This study demonstrates that quantitative evaluation of the segmental left ventricular response to dobutamine stress can be accomplished by on-line color-coded tissue Doppler measures of endocardial velocity. Tissue Doppler data were available from a Parasternal short axis relatively large series of consecutive patients and a Anteroseptum 73 (89) 73 (89) Anterior 75 (91) 72 (89) high proportion of segmental sites. Alterations in enLateral 73 (89) 62 (76) docardial velocity induced by dobutamine stress Posterior 76 (93) 62 (76) from multiple segmental sites could be serially asInferior 76 (93) 60 (73) sessed to quantify segmental function. With the exInferoseptum 73 (89) 44 (54) ception of apical segments, the endocardial velocity response to peak stress was significantly blunted in abnormal hypokinetic or akinetic segments, although significant increases in endocardial velocity occurred in both normal and abnormal segments. A peak systolic velocity response of °5.5 cm/s at peak stress was useful in identifying abnormal segments in all but apical segments. Tissue Doppler imaging can quantify left ventricular function by color-coding myocardial velocities. Recent studies have documented the accuracy of tissue Doppler imaging in measuring endocardial velocity by showing a close correlation with more traditional hand-traced M-mode FIGURE 3. Bar graphs of pooled peak systolic endocardial tissue Doppler velocities for techniques.10,11,17,18 This method the parasternal long- and short-axis views of the normal and abnormal segments at baseline and peak dobutamine stress. has also been shown to quantify segmental regional dysfunction dividual tissue Doppler segmental results are listed in patients with coronary artery disease or cardioin Table IV and pooled results by view in Figures 3 myopathy.10,11,19 Other investigators have shown the to 5. Consistent significant increases in segmental utility of tissue Doppler measures of mitral annular responses were seen with peak dobutamine stress in velocity to differentiate constrictive pericarditis from the normal control group. The endocardial velocity restrictive cardiomyopathy.20 This present study exalso significantly increased with peak stress in most tends the utility of quantitative tissue Doppler segabnormal segments. However, the peak velocity in mental analysis to the clinically relevant dobutamine abnormal segments was significantly blunted com- stress echocardiography examination. 73 79 79 79
(89) (86) (96) (96)
78 71 68 77 76 65
(95) (87) (83) (94) (93) (79)
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TABLE IV Segmental Peak Systolic Velocity Data at Maximal Stress Segments Normal Velocity (cm/s)
Segments Normal
Abnormal Velocity (cm/s)
Velocity (cm/s)
No.
Parasternal long axis Basal anteroseptum Midanteroseptum Basal posterior Midposterior
7.08 8.49 7.50 7.05
{ 2.46 { 1.57 { 1.59 { 1.45
3.12 3.21 4.15 3.46
{ 1.67* { 1.79* { 1.95* { 1.20*
(13) (16) (5) (12)
Parasternal short axis Anteroseptum Anterior Lateral Posterior Inferior Inferoseptum
8.74 6.25 5.74 6.83 7.11 6.77
{ 1.14 { 1.60 { 1.26 { 1.85 { 1.60 { 1.91
2.60 2.10 3.00 3.04 4.05 3.20
{ 1.42* { 1.01* { 0.57* { 0.66* { 1.67* { 1.75*
(14) (13) (2) (8) (16) (17)
Abnormal Velocity (cm/s)
No.
Apical 4 chamber Basal septum Midseptum Apical septum Basal lateral Midlateral Apical lateral
7.71 7.78 3.77 7.33 5.70 3.30
{ 1.83 { 1.93 { 3.10 { 1.96 { 1.96 { 2.90
2.93 2.99 2.66 3.80 4.05 3.28
{ 1.18* { 1.16* { 1.12 { 0.30* { 0.62 { 1.82
(15) (16) (13) (4) (5) (13)
Apical 2 chamber Basal inferior Midinferior Apical inferior Basal anterior Midanterior Apical anterior
7.96 6.77 5.19 7.17 5.38 4.20
{ 1.68 { 1.69 { 1.87 { 2.11 { 1.74 { 2.92
4.24 3.51 2.81 5.25 4.24 2.97
{ 1.69* { 1.72* { 1.94* { 0.27 { 0.71 { 1.63
(12) (14) (8) (2) (3) (8)
*p õ0.05 versus normal. No. Å number of abnormal segments by routine 2-dimensional criteria.
phy has become widely utilized, variability in the visual interpretation of wall motion assessment has been demonstrated in a recent multicenter study with interinstitutional agreement of only 73%.22 Quantitative standardization of echocardiographic data interpretation, such as establishing velocity thresholds by tissue Doppler imaging for an abnormal segmental response to stress, has the potential to decrease the interobserver variability and increase interinstitutional agreement. Study limitations: An alternative diagnostic evaluation for coronary artery disease, such as coronary angiography, radionuclide perfusion imaging, myocarFIGURE 4. Bar graphs of pooled peak systolic endocardial tissue Doppler velocities for the apical 4-chamber view at basal, midventricular, and apical levels of the normal and dial contrast echocardiography, abnormal segments at baseline and at peak stress. or positron emission tomography was not part of this study. AcThe ischemic cascade is a pathophysiologic con- cordingly, an evaluation of the comparative accuracy tinuum with segmental dysfunction due to myocar- of routine visual wall motion assessment versus tisdial ischemia occurring before either electrocardio- sue Doppler endocardial velocity in the same patient graphic changes or angina pectoris is manifest.21 could not be a part of this study without a third stanThis concept has served as the clinically useful basis dard of reference. Because visual wall motion asof stress echocardiography to detect early signs of sessment has been widely established to identify abischemia.1 – 6 In a recent review of 568 patients who normal segmental left ventricular function with underwent stress echocardiography using routine vi- stress, it represents an acceptable reference standard sual assessment of wall motion, sensitivity was 89%, to evaluate the tissue Doppler technique.1 – 7 It is thespecificity 80%, and overall accuracy 87% for de- oretically possible that tissue Doppler measures of tecting angiographically significant coronary artery endocardial velocity may be superior to visual asdisease.4 In addition, a positive dobutamine-atropine sessment because of its quantitative basis; however, stress echocardiographic study has been shown to be this study is unable to draw this conclusion. A lima very powerful predictor of perioperative cardiac itation of this technique is that the incidence angle events in patients undergoing major vascular sur- of the ultrasound beam affects Doppler velocity gery.5 Although dobutamine stress echocardiogra- calculations.23 Accordingly, endocardial movement 1040
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FIGURE 5. Bar graphs of pooled peak systolic endocardial tissue Doppler velocities for the apical 2-chamber view at basal, midventricular, and apical levels of the normal and abnormal segments at baseline and at peak stress.
FIGURE 6. Sensitivity, specificity, and accuracy for an endocardial velocity of °5.5 cm/s for identifying an abnormal segment at peak stress for parasternal long- and short-axis views.
that is not parallel to the ultrasound beam will have an underestimation of its true velocity, and segments where movement is nearly perpendicular to the angle of imaging can have dropout where the resultant calculation of velocity is zero. Because myocardial contraction includes longitudinal shortening and rotation in addition to circumferential shortening, we observed endocardial excursion to be truly perpendicular to the ultrasound beam only a few times. In addition, the high signal-to-noise ratio from the tissue Doppler shifts results in enhanced sensitivity to detect tissue motion, even in these nearly perpendicular segments. Furthermore, a threshold velocity of °5.5 cm/s at peak stress appeared to distinguish between normal and abnormal segments regardless of segmental site. However, tissue Doppler measures were unable to reliably
FIGURE 7. Sensitivity, specificity, and accuracy for an endocardial velocity of °5.5 cm/s for identifying an abnormal segment at peak stress for the basal and midventricular segments from the apical views.
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identify an abnormal segmental response in the apical segments, which remains a limitation of this technique. Other influences on the Doppler segmental velocities are whole heart translation motion, right ventricular volume overload and abnormal electrical activation, which can be easily recognized by routine imaging.24,25 The translational motion from exaggerated respirations with exercise may likely represent a limitation, although this study did not attempt to evaluate tissue Doppler imaging with exercise stress. Furthermore, the possibility of an increase in translational motion with inotropic stimulation was a potential limitation of this study. A method to correct for Doppler angle, translational motion, and ventricular interaction is use of the transmural myocardial velocity gradient.19 This prototype analysis system can mathematically correct for Doppler angle and can subtract whole heart motion from transmural thickening velocity, but was not available for this study. Another limitation of myocardial velocity to quantify regional function is the effect of heart rate. Although heart rate correction algorithms may be developed in the future to overcome this limitation, this is yet to be tested.26 Despite these limitations, tissue Doppler imaging has potential to enhance the quantitative approach to interpretation of dobutamine stress echocardiograms. 1. Sawada SG, Segar DS, Ryan T, Brown SE, Dohan AM, Williams R, Fineberg NS, Armstrong WF, Feigenbaum H. Echocardiographic detection of coronary artery disease during dobutamine infusion. Circulation 1991;83:1605–1614. 2. Marcovitz PA, Armstrong WF. Accuracy of dobutamine stress echocardiography in detecting coronary artery disease. Am J Cardiol 1992;69:1269– 1272. 3. Segar DS, Brown SE, Sawada SG, Ryan T, Feigenbaum H. Dobutamine stress echocardiography correlation with coronary artery lesion severity as determined by quantitative angiography. J Am Coll Cardiol 1992;19:1197–1202. 4. Pellikka PA, Roger VL, Oh JK, Miller FA, Seward JB, Tajik J. Stress echocadiography. Part II. Dobutamine stress echocardiography: techniques, implementation, clinical applications, and correlations. Mayo Clin Proc 1995;70:16– 27. 5. Poldermans D, Arnese M, Fioretti P, Salustri A, Boersma E, Thomson IR, Roelandt JRTC, van Urk H. Improved cardiac risk stratification in major vascular surgery with dobutamine-atropine stress echocardiography. J Am Coll Cardiol 1995;26:648–653. 6. Poldermans D, Fioretti PM, Forster T, Thomson IR, Boersma E, El-said EM, du Bois NAJJ, Roelandt JRTC, van Urk H. Dobutamine stress echocardiography for assessment of perioperative cardiac risk in patients undergoing major vascular surgery. Circulation 1993;87:1506–1512. 7. Schiller NB, Shah PM, Crawford M, DeMaria A, Devereux R, Feigenbaum H, Gutgesell H, Reichek N, Sahn D, Schnittger I, Silverman NH, Tajik AJ. Recommendations for quantitation of the left ventricle by two-dimensional echocardiography. J Am Soc Echocardiogr 1989;2:358–367.
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8. Sutherland GR, Stewart MJ, Groundstroem KWE, Moran CM, Fleming A, Guell-Peris FJ, Reimersma RA, Fenn LN, Fox KAA, McDicken WN. Color Doppler myocardial imaging: a new technique for assessment of myocardial function. J Am Soc Echocardiogr 1994;7:441–458. 9. Yamazaki N, Mine Y, Sano A, Hirama M, Miyatake K, Yamagishi M, Tanaka N. Analysis of ventricular wall motion using color-coded tissue Doppler imaging system. Jpn J Appl Phys 1994;33:3141–3146. 10. Miyatake K, Yamagishi M, Tanaka N, Uematsu M, Yamazaki N, Mine Y, Sano A, Hirama M. New method of evaluating left ventricular wall motion by color-coded tissue Doppler imaging: in vitro and in vivo studies. J Am Coll Cardiol 1995;25:717–724. 11. Gorcsan J, Gulati, VK, Mandarino WA, Katz WE. Color-coded measures of myocardial velocity throughout the cardiac cycle by tissue Doppler imaging to quantify regional left ventricular function. Am Heart J 1996;131:1203–1213. 12. Gorcsan J, Strum DP, Mandarino WA, Gulati VK, Pinsky MR. Quantitative assessment of alterations in regional left ventricular contractility by color-coded tissue Doppler echocardiography: comparison with sonomicrometry and pressure-volume relations. Circulation 1997; in press. 13. Gulati VK, Katz WE, Follansbee WP, Gorcsan J. Mitral annular descent velocity by tissue Doppler echocardiography as an index of global left ventricular function. Am J Cardiol 1996;77:979–984. 14. Olsen CO, Rankin JS, Arentzen CE, Ring WS, McHale PA, Anderson RW. The deformational characteristics of the left ventricle in the conscious dog. Circ Res 1981;49:843–855. 15. Wallerson DC, Devereux RB. Reproducibility of quantitative echocardiography: factors affecting variability of imaging and Doppler measurements. Echocardiography 1986;3:219–235. 16. Hinelman RB, Cassidy MM, Landzberg JS, Schiller NB. Reproducibility of quantitative two-dimensional echocardiography. Am Heart J 1988;115:425– 431. 17. Palka P, Lange A, Fleming AD, Sutherland GR, Fenn LN, McDicken WN. Doppler tissue imaging: myocardial wall motion velocities in normal subjects. J Am Soc Echocardiogr 1995;8:659–668. 18. Donovan LD, Armstrong WF, Bach DS. Quantitative Doppler tissue imaging of the left ventricular myocardium: validation in normal subjects. Am Heart J 1995;130:100–104. 19. 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. 20. Garcia MJ, Rodriguez L, Ares M, Griffin BP, Thomas JD, Klein AL. Differentiation of constrictive pericarditis from restrictive cardiomyopathy: assessment of left ventrcicular diastolic velocities in longitudinal axis by Doppler tissue imaging. J Am Coll Cardiol 1996;27:108–114. 21. Nesto RW, Kowalchuk GJ. The ischemic cascade: temporal sequence of hemodynamic, electrocardiographic and symptomatic expressions of ischemia. Am J Cardiol 1987;57:23C–30C. 22. Hoffmann R, Lethen H, Marwick T, Arnese M, Fioretti P, Pingitore A, Picano E, Buck T, Erbel R, Flachskampf FA, Hanrath P. Analysis of interinstitutional observer agreement in interpretation of dobutamine stress echocardiograms. J Am Coll Cardiol 1996;27:330–336. 23. Sahn DJ. Instrumentation and physical factors related to visualization of stenotic and regurgitant jets by Doppler color flow mapping. J Am Coll Cardiol 1988;12:1354–1365. 24. Ryan T, Petrovic O, Dillon JC, Feigenbaum H, Conley MJ, Armstong WF. An echocardiographic index for separation of right ventricular volume and pressure overload. J Am Coll Cardiol l985;59:l8–24. 25. Schnittger I, Keren A, Yock PG, Allen MD, Modry DL, Zusman DR, Mitchell RS, Miller DC, Popp RL. Timing of abnormal septal motion after cardiopulmonary bypass operations. J Thorac Cardiovasc Surg 1986;91:619–623. 26. Colan S, Borow K, Neumann A. The left ventricular systolic stress-velocity of fiber shortening relation: a load independent index of myocardial contractility. J Am Coll Cardiol 1984;4:715–724.
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MD,
Vijay K. Gulati, MD, Christine M. Mahler, and John Gorcsan III, MD
MS,
Tissue Doppler imaging displays color-coded myocardial velocity on-line and has potential to objectively quantify regional left ventricular function. Sixty patients, aged 56 {10 years, were studied to determine the normal and abnormal segmental endocardial velocity response to dobutamine stress, and the sensitivity, specificity, and accuracy of tissue Doppler imaging for detecting abnormal wall motion at peak stress as defined by routine visual interpretation. Separate 2-dimensional routine gray scale and color tissue Doppler image sets were acquired at rest and peak dobutamine stress in a digital cineloop format. Routine wall motion interpretation from gray scale images and color-coded peak systolic endocardial velocity from tissue Doppler images were determined independently. Twenty-two patients who reached their target heart rate and had normal wall motion at peak stress served as a control group. There were 19 patients who had wall motion abnormalities at
peak stress. Segmental peak endocardial velocities increased significantly in all segments in the control group. Endocardial velocity was significantly lower at peak stress in the pooled abnormal segments than in the pooled normal segments: 3.1 { 1.2 versus 7.2 { 1.9 cm/s, respectively (p õ0.05 vs normal control). However, the velocity response of abnormal apical segments could not be distinguished from normal controls by tissue Doppler imaging. Excluding apical segments, a peak velocity of °5.5 cm/s with peak stress had an average sensitivity of 96%, specificity of 81%, and accuracy of 86% for identifying abnormal segments at peak stress as defined by routine 2-dimensional criteria. Tissue Doppler imaging has the potential to quantify regional left ventricular function during dobutamine stress. Q1997 by Excerpta Medica, Inc. (Am J Cardiol 1997;79:1036–1042)
obutamine stress echocardiography has become established as a valuable diagnostic tool for the D evaluation of patients with coronary artery disease.
tively. The protocol was approved by the Institutional Review Board for Biomedical Research and all patients gave informed consent. Patients were aged 56 { 10 years (range 26 to 86), of which 17 were women. Indications for dobutamine stress echocardiography were preoperative evaluation in 34 patients and evaluation of chest pain in 26. Patients with abnormal wall motion at rest were not excluded. All patients were in normal sinus rhythm and none had bundle branch block.
1–6
Although clinically useful in its present form, a major limitation of echocardiographic study interpretation is the subjective visual interpretation of endocardial motion and wall thickening which is only semiquantitative.7 Tissue Doppler imaging is a novel echocardiographic technique that color codes myocardial velocity on-line and has the potential to objectively quantify regional left ventricular function.8–12 The objectives of this study were: (1) to evaluate the feasibility of applying tissue Doppler imaging to dobutamine stress echocardiography; (2) to determine the normal and abnormal quantitative regional endocardial velocity responses to dobutamine stress; and (3) to determine the sensitivity, specificity, and accuracy of tissue Doppler imaging for determining abnormal wall motion at peak stress compared with routine 2-dimensional echocardiographic visual interpretation.
METHODS Sixty consecutive patients referred for dobutamine stress echocardiography were studied prospecFrom the Division of Cardiology, University of Pittsburgh, Pittsburgh, Pennsylvania. Manuscript received August 28, 1996; revised manuscript received and accepted December 2, 1996. Address for reprints: John Gorcsan III, MD, Division of Cardiology, University of Pittsburgh Medical Center, 200 Lothrop Street, Pittsburgh, Pennsylvania 15213-2582.
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TABLE I Color-Coded Tissue Doppler Velocity Values Velocity (cm/s) Color White/yellow Light yellow Yellow/yellow orange Orange/yellow Light orange Orange Red/orange Red Black Dark blue Blue Blue/turquoise Dark turquoise Turquoise Blue/green Green/green turquoise Green
9.5 Scale
11.5 Scale
9.5 8.3 7.1 5.9 4.7 3.6 2.4 1.2 0.0 01.2 02.4 03.6 04.7 05.9 07.1 08.3 09.5
11.5 10.0 8.6 7.2 5.8 4.3 2.9 1.4 0.0 01.4 02.9 04.3 05.8 07.2 08.6 010.0 011.5
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apical windows in all patients in this study. Tissue velocity values were well below the Nyquist limits of the selected velocity ranges and aliasing did not occur. Tissue Doppler images were recorded using a multicolored postprocessing velocity map that displayed increasing velocity values toward the transducer in shades of red to orange to yellow, respectively, and increasing velocities away from the transducer in shades of blue to turquoise to green, respectively (Table I). Protocol: Dobutamine was infused by a standard protocol in 3-minute stages in rates of 5, 10, 20, 30, 40, and up to 50 mg/kg/min to achieve a heart rate ¢85% of the patient’s maximum agepredicted rate (220 0 age). The infusion was discontinued if new severe wall motion abnormalities, ischemic electrocardiographic changes, or limiting side effects occurred. Atropine up to 1.0 mg was also given to a subset of patients in an attempt to achieve ¢85% of the target heart rate.1 – 6 The tissue Doppler velocity range was selected at the time of baseline data acquisition to display peak systolic velocity in the low to midportion of the color display range to allow for detection of increases in systolic velocity at peak dobutamine stress within the same velocity range (Table I). Proper selection of the velocity range was important because velocity values that exceeded the limits of the selected range were displayed as saturated at the highest color-coded value, and could therefore be underestimated. Separate sets of black and white 2-dimensional and tissue Doppler images were acquired at baseline and peak stress from FIGURE 1. Tissue Doppler images at rest and peak dobutamine stress of a northe standard 4 views: parasternal long mal control patient showing the maximal systolic endocardial velocities. A, paraxis, parasternal short axis, apical 4asternal long-axis view; B, parasternal short-axis view; C, apical 4-chamber chamber, and apical 2-chamber. Data view; D, apical 2-chamber view. were acquired using a digital acquisition system (Nova Microsonics, Imagevue, Echocardiography: Echocardiographic data were Allendale, New Jersey) in a cineloop format with a acquired with a 2.5- or 3.75-MHz transducer and an frame interval of 16 ms for 25 frames per cardiac ultrasound system with tissue Doppler capabilities cycle gated from the electrocardiographic QRS com(SSA-380A, Toshiba Corp., Tochigi, Japan), de- plex and stored digitally on a 4.5-inch optical disk. scribed elsewhere in detail.10 – 13 Briefly, tissue Black and white and color tissue Doppler image sets Doppler imaging is a modification of routine color from each patient were subsequently separated, ranflow Doppler signal processing, bypassing the high- domly assigned an alphanumeric code to conceal the pass filter and inputting the comparatively lower fre- patient’s identity, and reviewed in a random order to quency Doppler data from myocardial motion di- investigators blinded to the alternate data set. rectly into the autocorrelator. Calculated velocity Data analysis: All analyses were identically perdata are color-coded and superimposed on the con- formed for baseline and peak stress images. Routine ventional 2-dimensional images. Frame rates were images were analyzed using the standard 20-segment approximately 40 Hz for a 607 sector with a 15.4 cm model of the American Society of Echocardiogradepth using a 3.75-MHz transducer and a pulse rep- phy.7 Routine wall motion assessment was peretition frequency of 4.5 KHz. The left ventricle could formed as a consensus between 2 independent be imaged within this depth from the parasternal and observers blinded to all tissue Doppler and clinical CORONARY ARTERY DISEASE/DOBUTAMINE STRESS TISSUE DOPPLER ECHOCARDIOGRAPHY
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tively high-velocity shifts of brief duration due to conformational changes occurred during isovolumic contraction, peak systolic velocity was measured ú50 ms from the onset of the electrocardiographic QRS complex to correspond to systolic ejection.11 – 14 Peak systolic velocity for individual segments was selected from individual frames because of the temporal heterogeneity of normal electrical activation, with peak velocity characteristically occurring in septal segments before free wall segments.11 Intra- and interobserver variability in visual interpretation of tissue Doppler color-coded velocity data was analyzed for 10 randomly selected studies and expressed as the difference divided by their mean values.15,16 Statistical analysis: Differences in variables from baseline to peak stress were analyzed using analysis of variance for repeated measures. Potential differences in regional endocardial velocity responses to peak dobutamine stress in normal and abnormal segments compared with routine 2-dimensional criteria were analyzed using an unpaired t test. Post hoc sensitivity, specificity, and accuracy analyses were performed to select tissue Doppler velocity criteria to identify an abnormal segmental response at peak stress defined by routine 2-dimensional criteria. Significance was determined as p õ0.05.
RESULTS Five patients were excluded from analysis because of suboptimal echocardiographic windows, with complete data sets available in 55 patients or 92% of attempted studies (Figures 1 and 2). Of these, 36 patients had normal dobutamine stress studies by routine visual wall motion assessment1 – 6 and 22 who reached ¢85% of their age-predicted heart FIGURE 2. Tissue Doppler images from patients with abnormal segments rate were selected as a control group. Nineby routine echocardiography and abnormal velocity responses at peak dobutamine stress. A and B, parasternal long- and short-axis views from a teen patients had an abnormal dobutamine patient with an abnormally low anteroseptal velocity response (arrowstress study defined as having at least 2 hyheads) color-coded as dark blue rather than turquoise or green. This papokinetic or akinetic segments at peak stress tient had an akinetic anteroseptum at peak dobutamine stress by routine by routine 2-dimensional criteria, and all 19 imaging. C, apical 4-chamber view of a patient with a hypokinetic inferior reached ¢85% of their predicted heart rate. septum at peak stress and an abnormally low peak velocity at peak stress (arrowheads) color-coded as orange rather than yellow. D, apical 2-chamClinical variables between abnormal and ber view of a patient with an abnormally low peak velocity response occontrol groups were similar except for gencurring diffusely at peak stress (arrowheads) color-coded as orange rather der (Table II). The availability of segmental than yellow. This patient had diffuse hypokinesia at peak stress. tissue Doppler imaging data for analysis is shown in Table III. Despite the suboptimal data with segments scored as follows: 1 Å normal, incidence angle of the ultrasound beam for Doppler 2 Å hypokinetic, 3 Å akinetic, or 4 Å dyskinetic. calculations of lateral segmental velocity, data were Digitized tissue Doppler image sets were indepen- available from a high proportion of all segments with dently analyzed by investigators blinded to the re- the exception of the apical segments from the apical sults of routine 2-dimensional analysis and all other views. The interobserver variability of tissue Doppclinical data. Peak endocardial velocity was deter- ler color-coded velocity analysis was 3.8 { 16.5% mined for each of the 20 segments converting color- and intraobserver variability was 04.8 { 8.2%, recoded pixels to velocity values using Table I. Frame- taining the sign to show bias. There were a total of by-frame analysis of the digitized cineloops was 229 segments interpreted to be hypokinetic or akiused to select peak systolic velocity. Because rela- netic at peak stress by routine visual assessment. In1038
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TABLE II Clinical and Dobutamine Protocol Data
Number Ages (yr) Men/women Maximum heart rate (min01) Maximum dobutamine (mg/kg/min) Atropine (mg)
Normal Control Group
Abnormal Group
22 58 { 12 11/11 144 { 10 46 { 5 0.2 { 0.2
19 62 { 12 13/6 137 { 15 42 { 8 0.5 { 0.3
TABLE III Tissue Doppler Data Availability (41 patients; 44 total segments/patient) Number of Segments (%) Parasternal long axis Basal anteroseptum Midanteroseptum Basal posterior Midposterior
Number of Segments (%) Apical 4 chamber Basal septum Midseptum Apical septum Basal lateral Midlateral Apical lateral Apical 2-chamber Basal inferior Midinferior Apical inferior Basal anterior Midanterior Apical anterior
pared with the normal segmental response in parasternal views and for basal and midsegments from apical views. In contrast, tissue Doppler measures were unable to distinguish between abnormal and normal apical segments at peak stress from apical views. Sensitivity, specificity, and accuracy for a peak velocity of °5.5 cm/s to identify an abnormal segment at maximal stress appear in Figures 6 and 7, excluding apical segments. Velocities ú5.5 cm/s with the most commonly used velocity range of { 9.5 cm/s corresponded to a peak velocity coded as yellow or turquoise-green. In apical segments, the accuracy for a peak velocity of 5.5 cm/s to identify an abnormal segment at maximal stress was lower at 59%, with a sensitivity of 34% and a specificity of 95%.
DISCUSSION This study demonstrates that quantitative evaluation of the segmental left ventricular response to dobutamine stress can be accomplished by on-line color-coded tissue Doppler measures of endocardial velocity. Tissue Doppler data were available from a Parasternal short axis relatively large series of consecutive patients and a Anteroseptum 73 (89) 73 (89) Anterior 75 (91) 72 (89) high proportion of segmental sites. Alterations in enLateral 73 (89) 62 (76) docardial velocity induced by dobutamine stress Posterior 76 (93) 62 (76) from multiple segmental sites could be serially asInferior 76 (93) 60 (73) sessed to quantify segmental function. With the exInferoseptum 73 (89) 44 (54) ception of apical segments, the endocardial velocity response to peak stress was significantly blunted in abnormal hypokinetic or akinetic segments, although significant increases in endocardial velocity occurred in both normal and abnormal segments. A peak systolic velocity response of °5.5 cm/s at peak stress was useful in identifying abnormal segments in all but apical segments. Tissue Doppler imaging can quantify left ventricular function by color-coding myocardial velocities. Recent studies have documented the accuracy of tissue Doppler imaging in measuring endocardial velocity by showing a close correlation with more traditional hand-traced M-mode FIGURE 3. Bar graphs of pooled peak systolic endocardial tissue Doppler velocities for techniques.10,11,17,18 This method the parasternal long- and short-axis views of the normal and abnormal segments at baseline and peak dobutamine stress. has also been shown to quantify segmental regional dysfunction dividual tissue Doppler segmental results are listed in patients with coronary artery disease or cardioin Table IV and pooled results by view in Figures 3 myopathy.10,11,19 Other investigators have shown the to 5. Consistent significant increases in segmental utility of tissue Doppler measures of mitral annular responses were seen with peak dobutamine stress in velocity to differentiate constrictive pericarditis from the normal control group. The endocardial velocity restrictive cardiomyopathy.20 This present study exalso significantly increased with peak stress in most tends the utility of quantitative tissue Doppler segabnormal segments. However, the peak velocity in mental analysis to the clinically relevant dobutamine abnormal segments was significantly blunted com- stress echocardiography examination. 73 79 79 79
(89) (86) (96) (96)
78 71 68 77 76 65
(95) (87) (83) (94) (93) (79)
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TABLE IV Segmental Peak Systolic Velocity Data at Maximal Stress Segments Normal Velocity (cm/s)
Segments Normal
Abnormal Velocity (cm/s)
Velocity (cm/s)
No.
Parasternal long axis Basal anteroseptum Midanteroseptum Basal posterior Midposterior
7.08 8.49 7.50 7.05
{ 2.46 { 1.57 { 1.59 { 1.45
3.12 3.21 4.15 3.46
{ 1.67* { 1.79* { 1.95* { 1.20*
(13) (16) (5) (12)
Parasternal short axis Anteroseptum Anterior Lateral Posterior Inferior Inferoseptum
8.74 6.25 5.74 6.83 7.11 6.77
{ 1.14 { 1.60 { 1.26 { 1.85 { 1.60 { 1.91
2.60 2.10 3.00 3.04 4.05 3.20
{ 1.42* { 1.01* { 0.57* { 0.66* { 1.67* { 1.75*
(14) (13) (2) (8) (16) (17)
Abnormal Velocity (cm/s)
No.
Apical 4 chamber Basal septum Midseptum Apical septum Basal lateral Midlateral Apical lateral
7.71 7.78 3.77 7.33 5.70 3.30
{ 1.83 { 1.93 { 3.10 { 1.96 { 1.96 { 2.90
2.93 2.99 2.66 3.80 4.05 3.28
{ 1.18* { 1.16* { 1.12 { 0.30* { 0.62 { 1.82
(15) (16) (13) (4) (5) (13)
Apical 2 chamber Basal inferior Midinferior Apical inferior Basal anterior Midanterior Apical anterior
7.96 6.77 5.19 7.17 5.38 4.20
{ 1.68 { 1.69 { 1.87 { 2.11 { 1.74 { 2.92
4.24 3.51 2.81 5.25 4.24 2.97
{ 1.69* { 1.72* { 1.94* { 0.27 { 0.71 { 1.63
(12) (14) (8) (2) (3) (8)
*p õ0.05 versus normal. No. Å number of abnormal segments by routine 2-dimensional criteria.
phy has become widely utilized, variability in the visual interpretation of wall motion assessment has been demonstrated in a recent multicenter study with interinstitutional agreement of only 73%.22 Quantitative standardization of echocardiographic data interpretation, such as establishing velocity thresholds by tissue Doppler imaging for an abnormal segmental response to stress, has the potential to decrease the interobserver variability and increase interinstitutional agreement. Study limitations: An alternative diagnostic evaluation for coronary artery disease, such as coronary angiography, radionuclide perfusion imaging, myocarFIGURE 4. Bar graphs of pooled peak systolic endocardial tissue Doppler velocities for the apical 4-chamber view at basal, midventricular, and apical levels of the normal and dial contrast echocardiography, abnormal segments at baseline and at peak stress. or positron emission tomography was not part of this study. AcThe ischemic cascade is a pathophysiologic con- cordingly, an evaluation of the comparative accuracy tinuum with segmental dysfunction due to myocar- of routine visual wall motion assessment versus tisdial ischemia occurring before either electrocardio- sue Doppler endocardial velocity in the same patient graphic changes or angina pectoris is manifest.21 could not be a part of this study without a third stanThis concept has served as the clinically useful basis dard of reference. Because visual wall motion asof stress echocardiography to detect early signs of sessment has been widely established to identify abischemia.1 – 6 In a recent review of 568 patients who normal segmental left ventricular function with underwent stress echocardiography using routine vi- stress, it represents an acceptable reference standard sual assessment of wall motion, sensitivity was 89%, to evaluate the tissue Doppler technique.1 – 7 It is thespecificity 80%, and overall accuracy 87% for de- oretically possible that tissue Doppler measures of tecting angiographically significant coronary artery endocardial velocity may be superior to visual asdisease.4 In addition, a positive dobutamine-atropine sessment because of its quantitative basis; however, stress echocardiographic study has been shown to be this study is unable to draw this conclusion. A lima very powerful predictor of perioperative cardiac itation of this technique is that the incidence angle events in patients undergoing major vascular sur- of the ultrasound beam affects Doppler velocity gery.5 Although dobutamine stress echocardiogra- calculations.23 Accordingly, endocardial movement 1040
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FIGURE 5. Bar graphs of pooled peak systolic endocardial tissue Doppler velocities for the apical 2-chamber view at basal, midventricular, and apical levels of the normal and abnormal segments at baseline and at peak stress.
FIGURE 6. Sensitivity, specificity, and accuracy for an endocardial velocity of °5.5 cm/s for identifying an abnormal segment at peak stress for parasternal long- and short-axis views.
that is not parallel to the ultrasound beam will have an underestimation of its true velocity, and segments where movement is nearly perpendicular to the angle of imaging can have dropout where the resultant calculation of velocity is zero. Because myocardial contraction includes longitudinal shortening and rotation in addition to circumferential shortening, we observed endocardial excursion to be truly perpendicular to the ultrasound beam only a few times. In addition, the high signal-to-noise ratio from the tissue Doppler shifts results in enhanced sensitivity to detect tissue motion, even in these nearly perpendicular segments. Furthermore, a threshold velocity of °5.5 cm/s at peak stress appeared to distinguish between normal and abnormal segments regardless of segmental site. However, tissue Doppler measures were unable to reliably
FIGURE 7. Sensitivity, specificity, and accuracy for an endocardial velocity of °5.5 cm/s for identifying an abnormal segment at peak stress for the basal and midventricular segments from the apical views.
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identify an abnormal segmental response in the apical segments, which remains a limitation of this technique. Other influences on the Doppler segmental velocities are whole heart translation motion, right ventricular volume overload and abnormal electrical activation, which can be easily recognized by routine imaging.24,25 The translational motion from exaggerated respirations with exercise may likely represent a limitation, although this study did not attempt to evaluate tissue Doppler imaging with exercise stress. Furthermore, the possibility of an increase in translational motion with inotropic stimulation was a potential limitation of this study. A method to correct for Doppler angle, translational motion, and ventricular interaction is use of the transmural myocardial velocity gradient.19 This prototype analysis system can mathematically correct for Doppler angle and can subtract whole heart motion from transmural thickening velocity, but was not available for this study. Another limitation of myocardial velocity to quantify regional function is the effect of heart rate. Although heart rate correction algorithms may be developed in the future to overcome this limitation, this is yet to be tested.26 Despite these limitations, tissue Doppler imaging has potential to enhance the quantitative approach to interpretation of dobutamine stress echocardiograms. 1. Sawada SG, Segar DS, Ryan T, Brown SE, Dohan AM, Williams R, Fineberg NS, Armstrong WF, Feigenbaum H. Echocardiographic detection of coronary artery disease during dobutamine infusion. Circulation 1991;83:1605–1614. 2. Marcovitz PA, Armstrong WF. Accuracy of dobutamine stress echocardiography in detecting coronary artery disease. Am J Cardiol 1992;69:1269– 1272. 3. Segar DS, Brown SE, Sawada SG, Ryan T, Feigenbaum H. Dobutamine stress echocardiography correlation with coronary artery lesion severity as determined by quantitative angiography. J Am Coll Cardiol 1992;19:1197–1202. 4. Pellikka PA, Roger VL, Oh JK, Miller FA, Seward JB, Tajik J. Stress echocadiography. Part II. Dobutamine stress echocardiography: techniques, implementation, clinical applications, and correlations. Mayo Clin Proc 1995;70:16– 27. 5. Poldermans D, Arnese M, Fioretti P, Salustri A, Boersma E, Thomson IR, Roelandt JRTC, van Urk H. Improved cardiac risk stratification in major vascular surgery with dobutamine-atropine stress echocardiography. J Am Coll Cardiol 1995;26:648–653. 6. Poldermans D, Fioretti PM, Forster T, Thomson IR, Boersma E, El-said EM, du Bois NAJJ, Roelandt JRTC, van Urk H. Dobutamine stress echocardiography for assessment of perioperative cardiac risk in patients undergoing major vascular surgery. Circulation 1993;87:1506–1512. 7. Schiller NB, Shah PM, Crawford M, DeMaria A, Devereux R, Feigenbaum H, Gutgesell H, Reichek N, Sahn D, Schnittger I, Silverman NH, Tajik AJ. Recommendations for quantitation of the left ventricle by two-dimensional echocardiography. J Am Soc Echocardiogr 1989;2:358–367.
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8. Sutherland GR, Stewart MJ, Groundstroem KWE, Moran CM, Fleming A, Guell-Peris FJ, Reimersma RA, Fenn LN, Fox KAA, McDicken WN. Color Doppler myocardial imaging: a new technique for assessment of myocardial function. J Am Soc Echocardiogr 1994;7:441–458. 9. Yamazaki N, Mine Y, Sano A, Hirama M, Miyatake K, Yamagishi M, Tanaka N. Analysis of ventricular wall motion using color-coded tissue Doppler imaging system. Jpn J Appl Phys 1994;33:3141–3146. 10. Miyatake K, Yamagishi M, Tanaka N, Uematsu M, Yamazaki N, Mine Y, Sano A, Hirama M. New method of evaluating left ventricular wall motion by color-coded tissue Doppler imaging: in vitro and in vivo studies. J Am Coll Cardiol 1995;25:717–724. 11. Gorcsan J, Gulati, VK, Mandarino WA, Katz WE. Color-coded measures of myocardial velocity throughout the cardiac cycle by tissue Doppler imaging to quantify regional left ventricular function. Am Heart J 1996;131:1203–1213. 12. Gorcsan J, Strum DP, Mandarino WA, Gulati VK, Pinsky MR. Quantitative assessment of alterations in regional left ventricular contractility by color-coded tissue Doppler echocardiography: comparison with sonomicrometry and pressure-volume relations. Circulation 1997; in press. 13. Gulati VK, Katz WE, Follansbee WP, Gorcsan J. Mitral annular descent velocity by tissue Doppler echocardiography as an index of global left ventricular function. Am J Cardiol 1996;77:979–984. 14. Olsen CO, Rankin JS, Arentzen CE, Ring WS, McHale PA, Anderson RW. The deformational characteristics of the left ventricle in the conscious dog. Circ Res 1981;49:843–855. 15. Wallerson DC, Devereux RB. Reproducibility of quantitative echocardiography: factors affecting variability of imaging and Doppler measurements. Echocardiography 1986;3:219–235. 16. Hinelman RB, Cassidy MM, Landzberg JS, Schiller NB. Reproducibility of quantitative two-dimensional echocardiography. Am Heart J 1988;115:425– 431. 17. Palka P, Lange A, Fleming AD, Sutherland GR, Fenn LN, McDicken WN. Doppler tissue imaging: myocardial wall motion velocities in normal subjects. J Am Soc Echocardiogr 1995;8:659–668. 18. Donovan LD, Armstrong WF, Bach DS. Quantitative Doppler tissue imaging of the left ventricular myocardium: validation in normal subjects. Am Heart J 1995;130:100–104. 19. 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. 20. Garcia MJ, Rodriguez L, Ares M, Griffin BP, Thomas JD, Klein AL. Differentiation of constrictive pericarditis from restrictive cardiomyopathy: assessment of left ventrcicular diastolic velocities in longitudinal axis by Doppler tissue imaging. J Am Coll Cardiol 1996;27:108–114. 21. Nesto RW, Kowalchuk GJ. The ischemic cascade: temporal sequence of hemodynamic, electrocardiographic and symptomatic expressions of ischemia. Am J Cardiol 1987;57:23C–30C. 22. Hoffmann R, Lethen H, Marwick T, Arnese M, Fioretti P, Pingitore A, Picano E, Buck T, Erbel R, Flachskampf FA, Hanrath P. Analysis of interinstitutional observer agreement in interpretation of dobutamine stress echocardiograms. J Am Coll Cardiol 1996;27:330–336. 23. Sahn DJ. Instrumentation and physical factors related to visualization of stenotic and regurgitant jets by Doppler color flow mapping. J Am Coll Cardiol 1988;12:1354–1365. 24. Ryan T, Petrovic O, Dillon JC, Feigenbaum H, Conley MJ, Armstong WF. An echocardiographic index for separation of right ventricular volume and pressure overload. J Am Coll Cardiol l985;59:l8–24. 25. Schnittger I, Keren A, Yock PG, Allen MD, Modry DL, Zusman DR, Mitchell RS, Miller DC, Popp RL. Timing of abnormal septal motion after cardiopulmonary bypass operations. J Thorac Cardiovasc Surg 1986;91:619–623. 26. Colan S, Borow K, Neumann A. The left ventricular systolic stress-velocity of fiber shortening relation: a load independent index of myocardial contractility. J Am Coll Cardiol 1984;4:715–724.
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