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Significance of dobutamine-induced ST-segment elevation and T-wave pseudonormalization in patients with Q-wave myocardial infarction: simultaneous evaluation by dobutamine stress echocardiography and thallium-201 SPECT
Significance of Dobutamine-Induced ST-Segment Elevation and T-Wave Pseudonormalization in Patients With Q-Wave Myocardial Infarction: Simultaneous Evaluation by Dobutamine Stress Echocardiography and Thallium-201 SPECT Yi-Lwun Ho,
MD,
Lung-Chun Lin, MD, Ruoh-Fang Yen, MD, Chau-Chung Wu, Ming-Fong Chen, MD, and Por-Jau Huang, MD
MD,
The clinical significance of stress-induced ST-segment elevation and T-wave pseudonormalization in infarctrelated leads is still controversial. Therefore, we conducted the present study to assess this issue using simultaneous dobutamine stress echocardiography (DSE) and thallium-201 single-photon emission computed tomography. A total of 119 patients with Q-wave myocardial infarction were enrolled in this study. There were 58 patients with (group I) and 61 patients without (group II) dobutamine-induced ST-T changes. Left ventricular ejection fraction was 43 ⴞ 13% in group I and 49 ⴞ 14% in group II (p <0.05). The baseline, low-, and peak-dose global wall motion scores were similar between these 2 groups (26.2 ⴞ 6.1 vs 26.2 ⴞ 6.3 [p ⴝ NS]; 24.1 ⴞ 5.3 vs 23.5 ⴞ 5.7 [p ⴝ NS]; 26.4 ⴞ 5.7 vs 26.7 ⴞ 6.1 [p ⴝ NS]). The sensitivity, specificity, and accuracy of these ST-T changes for detecting residual myocardial viability
and ischemia documented by DSE in all patients were 50%, 53%, and 51% (for viability), and 47%, 48%, and 47% (for ischemia), respectively. The sensitivity, specificity, and accuracy of these ST-T changes for detecting a reversible perfusion defect documented by thallium-201 single-photon emission computed tomography were 51%, 54%, and 52%, respectively. In conclusion, dobutamine-induced ST elevation and/or T-wave pseudonormalization is associated with poor resting left ventricular function. These ST-T changes are not associated with residual myocardial ischemia and viability in the infarct area. Therefore, these electrocardiographic changes alone cannot be reliably considered as distinctive markers in formulating the therapeutic strategy of coronary intervention. 䊚1999 by Excerpta Medica, Inc. (Am J Cardiol 1999;84:125–129)
T
simultaneous DSE and stress radionuclide imaging.7,8 The present study was designed to evaluate the functional significance of dobutamine-induced ST elevation and/or T-wave pseudonormalization in patients with previous Q-wave myocardial infarction (MI) by simultaneous DSE and thallium-201 SPECT.
he clinical significance of stress-induced STsegment elevation and T-wave pseudonormalization in infarct-related leads is still controversial.1–9 The possible mechanisms include ventricular asynergy, residual myocardial ischemia, and contractile reserve within the infarct area.1–9 Because residual myocardial ischemia and viability within the infarct area is important for cardiologists to formulate the strategy of coronary intervention, the significance of these electrocardiographic changes need to be further validated. Dobutamine stress echocardiography (DSE) and thallium-201 single-photon emission computed tomography (SPECT) are sensitive and specific in myocardial ischemia and viability detection.10 –15 Also, both examinations provide complementary information in the assessment of myocardial viability.16 However, there have been few reports about the assessment of these electrocardiographic changes using From the Departments of Internal Medicine (Cardiology) and Nuclear Medicine, National Taiwan University Hospital, Taipei, Taiwan. Manuscript received November 10, 1998; revised manuscript received March 8, 1999, and accepted March 10, 1999. Address for reprints: Por-Jau Huang, MD, Department of Internal Medicine (Cardiology), National Taiwan University Hospital, No. 7, Chung-Shan S. Road, Taipei, Taiwan. ©1999 by Excerpta Medica, Inc. All rights reserved. The American Journal of Cardiology Vol. 84 July 15, 1999
METHODS
Study population: DSE and dobutamine thallium201 SPECT images were simultaneously obtained in 119 patients (108 men and 11 women, mean age 59 ⫾ 12 years) who had history of MI and pathologic Q waves in infarct-related leads. Recent MI (⬍1 month) was noted in 53 patients. The diagnosis of acute MI relied on a typical history of chest pain, a diagnostic increase in serum creatine kinase, and evolutional electrocardiographic changes. Patients were excluded from the study entry if they had resting or unstable angina, uncontrolled hypertension (systolic blood pressure ⬎200 mm Hg, or diastolic pressure ⬎110 mm Hg), or New York Heart Association functional class III or IV symptoms of heart failure. Additional exclusion criteria included a history of sustained ventricular arrhythmia, poor echo windows, or severe aortic stenosis. All patients underwent coronary an0002-9149/99/$–see front matter PII S0002-9149(99)00220-9
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giography within 7 days after DSE and thallium-201 SPECT. Dobutamine infusion protocol: All patients received 250 ml of normal saline as a fluid challenge before the infusion to avoid hypotension and bradycardia occasionally occurring with dobutamine infusion. Dobutamine was given intravenously at rates of 5, 10, 20, 30, and 40 g/kg/min in 3-minute stages. Reasons for termination were: severe hypertension (systolic blood pressure ⬎220 mm Hg or diastolic blood pressure ⬎110 mm Hg), a symptomatic decrease in blood pressure from the predobutamine baseline, prolonged angina, any significant arrhythmias, achievement of 85% of the age-predicted maximal heart rate, or completion of the maximal dose of 40 g/kg/min. Patients were observed for 5 minutes after infusion. Blood pressure, heart rate, symptoms, and electrocardiographic data were recorded at baseline, the last minute of each stage, and at the end of recovery. Calcium channel blockers and  blockers were not discontinued before DSE. Electrocardiographic analysis: ST elevation was defined as new or additional ⱖ1.0 mm elevation at the J point, with a horizontal or upsloping ST-segment lasting 80 ms during stress in ⱖ2 Q-wave leads (the PQ segment was considered the isoelectric line).9 T-wave pseudonormalization was defined as the negative T wave inverted to upright in infarct-related leads.4 To correlate the localization of electrocardiographic abnormalities with scintigraphic, echocardiographic, and angiographic abnormalities, 2 electrocardiographic sites were considered: (1) anterior (leads V1 to V4), which was assigned to the anterior wall, septum, and apex, and to the left anterior descending coronary artery; (2) inferolateral (II, III, aVF, I, aVL, V5, and V6), which was assigned to the lateral and inferoposterior walls, and to the left circumflex and right coronary arteries.7 Interpretation of ST-segment elevation and T-wave pseudonormalization was performed in a blinded manner by 2 independent cardiologists, and disagreement was resolved by consensus. Echocardiography and wall motion analysis: Standard parasternal and apical views were obtained at baseline and at each stage of dobutamine protocol. The left ventricle was divided into 16 segments according to guidelines of the American Society of Echocardiography.17 Images were generated with a Sonos 1500 apparatus (Hewlett-Packard, Andover, Massachusetts) with a 2.0/2.5-MHz probe, digitized and then stored in quad-screen cine loop format with a Freeland Cardiac Workstation (Louisville, Colorado). Images taken during the 5- or 10-g/kg/min infusion were recorded as the low-dose images. Images taken at the highest attainable infusion rate were recorded as the peak-dose images. Wall motion was analyzed by 2 experienced echocardiologists with no knowledge of electrocardiographic, thallium, or angiographic results. The following scoring system was used: segments with normal or hyperkinetic motion were assigned 1, hypokinesia 2, akinesia 3, and dyskinesia 4.17 The wall motion score was derived by summation of individual segment score.10,13 Myocar126 THE AMERICAN JOURNAL OF CARDIOLOGY姞
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dial ischemia was considered present if new or worsening regional wall motion abnormality was induced by dobutamine.10,13 Therefore, segments were judged to be ischemic when there was an increment of wall motion score ⬎1 grade at any stage of dobutamine infusion compared with the resting stage. Akinesia that directly deteriorated to dyskinesia was not considered a marker of myocardial ischemia.18 Myocardial viability was considered present if wall motion was normal at rest, or if the resting regional wall motion abnormality was reversed or improved under dobutamine infusion.11,13,16 Our interobserver agreement for DSE was 94% ( 0.85, SEM 0.078).14 Dobutamine thallium-201 imaging: Dobutamine was infused intravenously according to the protocol described above. Two to 3 mCi of thallium-201 was injected intravenously at the third minute of peak phase. Another 1 mCi of thallium-201 was reinjected immediately after the 4-hour imaging. SPECT myocardial scintigrams were recorded within 10 minutes (stress phase), at 4 hours (redistribution phase) after injection of thallium-201, and at 20 minutes (reinjection phase) after reinjection of thallium-201 using a large field-of-view gamma camera (CAMSTAR 3000, General Electric, Milwaukee, Wisconsin) equipped with a low-energy, all-purpose collimator. The detector collected data through a 180° arc from the 45° right anterior oblique to the 45° left posterior oblique position. Contiguous transaxial tomograms were reconstructed into 6-mm-thick multiple sections using a filtered back-projection method with a Hanning ramp filter, and using a convolution reconstruction algorithm without attenuation correction. Thereafter, tomographic images along the short and long axes of the left ventricle were reorganized from the set of the transaxial tomograms according to the method described by Borrello et al.19 All SPECT images were interpreted qualitatively by 2 experienced observers who were unaware of the electrocardiographic, echocardiographic, or angiographic results. We used the 16-color scale in image interpretation and the left ventricle was divided into 10 segments.20,21 Thallium201 activity in each segment was scored as 3 (normal), 2 (mildly reduced), 1 (moderately reduced), or 0 (severely reduced or absent). A segment was considered abnormal if its score was ⱕ2.20 Stress images were compared with redistribution and reinjection images to evaluate the presence or absence of reversible or fixed defects.20,22 Reversible perfusion defects were defined as abnormal segments with an increment of tracer uptake ⬎1 grade at the redistribution or reinjection phase compared with the stress phase.20 Myocardial ischemia was considered in segments with reversible perfusion defects.20 A myocardial segment was considered nonviable in the presence of a severe (score ⫽ 0), fixed perfusion defect.22 Our interobserver agreement for SPECT interpretation was 96% ( 0.90, SEM 0.079).23 Our agreement of regional wall motion abnormality/perfusion defect was 81% ( 0.61).15 JULY 15, 1999
TABLE I Clinical Data of Groups I and II Group I (n ⫽ 58)
TABLE II Findings of Dobutamine Stress Echocardiography Group II (n ⫽ 61)
Men/women 50/8 58/3 Age (yr) 59 ⫾ 12 60 ⫾ 12 Anterior/inferior MI 35/23 35/26 Recent MI 28 25 Use of  blockers 35 33 Use of calcium blockers 7 10 Baseline ST-segment 29 21 elevation Amplitude of baseline 1.9 ⫾ 0.6 1.7 ⫾ 0.7 ST elevation (mm) 1-vessel CAD 16 18 Multivessel CAD 42 43 LVEF (%) 43 ⫾ 13 49 ⫾ 14* Baseline HR (beats/min) 73 ⫾ 15 70 ⫾ 13 Baseline systolic BP 121 ⫾ 16 118 ⫾ 20 (mm Hg) Baseline diastolic BP 77 ⫾ 10 75 ⫾ 12 (mm Hg) Baseline double product 8,963 ⫾ 2,528 8,317 ⫾ 2,365 (mm Hg 䡠 beats 䡠 min⫺1) Peak HR (beats/min) 106 ⫾ 16 99 ⫾ 19 Peak systolic BP (mm Hg) 140 ⫾ 26 141 ⫾ 29 Peak diastolic BP (mm Hg) 75 ⫾ 12 73 ⫾ 16 Peak dose double product 14,624 ⫾ 3,282 14,037 ⫾ 3,696 (mm Hg 䡠 beats 䡠 min⫺1) *p ⫽ 0.047. BP ⫽ blood pressure; CAD ⫽ coronary artery disease; HR ⫽ heart rate; LVEF ⫽ left ventricular ejection fraction.
Coronary angiography and left ventriculography:
Coronary angiography and left ventriculography were performed with the Judkins technique. A ⱖ50% diameter stenosis in the coronary artery was considered significant. Left ventricular ejection fraction was calculated by area-length method from the left cineventriculogram. Interobserver agreement of left ventricular ejection fraction in our laboratory was 95% ( 0.89). Statistical analysis: All results are expressed as the mean ⫾ SD. Sensitivity, specificity, positive predictive value, negative predictive value, and accuracy were all calculated with standard formulas. All statistical differences among the groups were obtained by using the Student’s t and chi-square method. The relation between ST-T changes and myocardial ischemia/viability was evaluated by the McNemar test. It was considered statistically significant if the p value was ⬍0.05. Interobserver concordance was determined by calculating the coefficient.
RESULTS
Clinical characteristics (Table I): Fifty-eight of the 119 patients had ST-segment elevation and/or T-wave pseudonormalization (group I) and 61 patients did not have electrocardiographic changes (group II). In group I, 23 patients had T pseudonormalization, 15 patients had ST elevation, and 20 patients had both changes. There was no difference in the number of patients with anterior (35 vs 35) or inferior (23 vs 26) MI in these 2 groups. There was no difference in the number of patients with either recent MI or baseline
DSE Baseline global WMS Low-dose global WMS Peak-dose global WMS Baseline infarct WMS Low-dose infarct WMS Peak-dose infarct WMS Baseline akinetic/dyskinetic segments Peak-dose akinetic/dyskinetic segments Dyskinetic segments at peak dose
Group I 26.2 24.1 26.4 16.1 14.5 15.9 3.5 3.7 0.6
⫾ ⫾ ⫾ ⫾ ⫾ ⫾ ⫾ ⫾ ⫾
6.1 5.3 5.7 5.7 5.7 5.5 2.8 2.6 1.0
Group II 26.2 23.5 26.7 14.7 13.2 15.2 3.1 3.3 0.6
⫾ ⫾ ⫾ ⫾ ⫾ ⫾ ⫾ ⫾ ⫾
6.3 5.7 6.1 6.3 6.2 6.3 2.7 2.7 1.0
WMS ⫽ wall motion scores.
ST-segment elevation in these 2 groups. The amplitudes of baseline ST-segment elevation were also similar (1.9 ⫾ 0.6 vs 1.7 ⫾ 0.7 mm; p ⫽ NS). Left ventricular ejection fraction was 43 ⫾ 13% in group I and 49 ⫾ 14% in group II (p ⬍0.05). There was no difference in the number of patients taking either  blockers or calcium channel blockers in these 2 groups. Findings of dobutamine stress echocardiography:
After dobutamine infusion, the peak-dose heart rate and systolic and diastolic blood pressures were similar between the 2 groups (Table I). Baseline, low-dose, and peak-dose global wall motion scores were also similar in the 2 groups (Table II). The baseline, lowdose, and peak-dose infarct area wall motion scores were similar in the 2 groups. The numbers of baseline and peak-dose akinetic/dyskinetic segments in the 2 groups were also similar. Sensitivity, specificity, and accuracy of dobutamine-induced ST-T changes for detecting residual myocardial ischemia documented by DSE in total patients were 47%, 48%, and 47%, respectively (p ⫽ NS; Table III). There was no association between ST-T changes and residual ischemia documented by DSE in patients with either anterior or inferior MI. Sensitivity, specificity, and accuracy of ST-T changes for detecting residual viable myocardium documented by DSE in total patients were 50%, 53%, and 51%, respectively (p ⫽ NS). There was also no association between ST-T changes and residual myocardial viability documented by DSE in patients with either anterior or inferior MI. Findings of dobutamine thallium-201 single-photon emission computed tomography (Tables IV and V)4: Do-
butamine-induced ST-T changes were not associated with reversible perfusion defects documented by thallium-201 SPECT in total patients (p ⫽ NS). These ST-T changes were also not associated with reversible perfusion defects in patients with either anterior or inferior MI. The prevalence of a normal perfusion pattern, and reversible and fixed perfusion defects in the reciprocal area to MI were similar in the 2 groups (p ⫽ NS). The scores of thallium activity in all fixed perfusion defects were 0.
DISCUSSION Identifying the area of infarcted myocardium with depressed but potentially reversible contractile func-
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TABLE III Sensitivity, Specificity, and Accuracy of Dobutamine-induced ST-T–Segment Changes for Detecting Residual Myocardial Ischemia and Viable Myocardium Documented by DSE Residual Myocardial Ischemia
Sensitivity Specificity Accuracy
Residual Viable Myocardium
Total
Anterior MI
Inferior MI
Total
Anterior MI
Inferior MI
34/73 (47%) 22/46 (48%) 56/119 (47%)
18/38 (47%) 15/32 (47%) 33/70 (47%)
16/35 (46%) 7/14 (50%) 23/49 (47%)
37/74 (50%) 24/45 (53%) 61/119 (51%)
18/38 (47%) 15/32 (47%) 33/70 (47%)
19/36 (53%) 9/13 (69%) 28/49 (57%)
TABLE IV Sensitivity, Specificity, Positive Predictive Value, Negative Predictive Value, and Accuracy of DobutamineInduced ST-T–Segment Changes for Detecting Presence of Reversible Perfusion Defect Documented by Thallium-201 SPECT Anterior MI Sensitivity Specificity Positive predictive Negative predictive Accuracy
21/37 19/33 21/35 19/35 40/70
(57%) (58%) (60%) (54%) (57%)
Inferior MI 12/28 10/21 12/23 10/26 22/49
Total
(43%) 33/65 (48%) 29/54 (52%) 33/58 (38%) 29/61 (45%) 62/119
(51%) (54%) (57%) (48%) (52%)
TABLE V Prevalence of Fixed Perfusion Defect, Reversible Perfusion Defect, and Normal Pattern in Reciprocal Area to Myocardial Infarction Between Groups I and II Thallium Pattern in Reciprocal Area Fixed perfusion defect Reversible perfusion defect No perfusion defect Total
Group I
Group II
8 23 27 58
10 24 27 61
tion helps to predict the prognosis of patients with coronary artery disease and chronic left ventricular dysfunction.24 Therefore, stress-induced ST elevation and T-wave pseudonormalization of infarct-related leads have generated great interest among cardiologists in that residual myocardial ischemia and viability have been proposed to be plausible mechanisms of these electrocardiographic phenomena. The incidence of dobutamine-induced ST-segment elevation ranges from 41% to 55% and our results are similar to these reports.9,25 Lombardo et al5 observed that dobutamine-induced ST-T changes were indicative of contractile reserve in infarct-related leads when these changes developed with low-dose dobutamine. Dobutamine-induced T-wave pseudonormalization has been also reported to be a sign of viable myocardium in patients with Q-wave MI and an indicator of myocardial ischemia in patients with non–Q-wave MI.6,7 In contrast, there have been several reports suggesting that the mechanism of ST-segment elevation may be due to mechanical rather than to residual myocardial ischemia or viability in most patients.2,8,9,25–28 Either exercise or dobutamine-induced ST-segment elevation during radionuclide studies has been attributed to stress-induced left ventricular asynergy rather than ischemia.26,27 Dobutamine-induced ST-segment elevation has also been reported not to be associated with a higher incidence and extent of viable or jeop128 THE AMERICAN JOURNAL OF CARDIOLOGY姞
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ardized myocardium defined by DSE.8,9,25 The results of the present study are compatible with these reports.8,9,25–27 Our patients with dobutamine-induced ST-T changes had worse left ventricular ejection fraction than those without these changes (p ⬍0.05). The presence of residual myocardial ischemia and viability was not different in patients with or without ST-T changes. The sensitivity, specificity, and accuracy of these ST-T changes to diagnose either reversible perfusion defects in thallium-201 imaging or viable myocardium in DSE were relatively poor. These data are compatible with results reported by Ricci et al.9 In the present study, the prevalence of a normal pattern, and fixed and reversible perfusion defects in thallium imaging in the reciprocal area (to MI) were all similar in the 2 groups. Therefore, these electrocardiographic changes could not be attributed to the ischemic event in the reciprocal area (to MI) and could not be interpreted as markers of more extensive coronary artery disease. Similar observations were also obtained by Haines et al.2 In normal patients, the action potential duration of the endocardial region is longer than that of the epicardial region, and ventricular repolarization is from epicardium to endocardium. The action potential duration may be shortened in the presence of myocardial injury, and electrical gradients are created in different directions rather than in the direction from epicardium to endocardium.29 Stress (either exercise or dobutamine) further enhanced the distortion of left ventricular geometry caused by MI. Therefore, the magnitude and directions of the electrical gradients vary and result in ST-T changes. Residual myocardial ischemia and viability can also change the duration of action potential and interfere with the direction of electrical gradients. Therefore, we cannot exclude the possibility that myocardial ischemia and viability may contribute to additional ST-T changes in some patients.9 However, dobutamine-induced ST-T changes cannot reliably be considered as distinctive markers in formulating the therapeutic strategy of coronary intervention. Because of the safety considerations, our patients received 250 ml of normal saline as a fluid challenge before dobutamine infusion to avoid hypotension and bradycardia. As in our previous study,30 the incidence of hypotension and bradycardia decreases and the diagnostic accuracy is compatible with previous reports.10,30 Both preload increase and dobutamine infusion enhance systolic performance of the left venJULY 15, 1999
tricle. Therefore, the effects of this preload alternation on the diagnostic accuracy of DSE is minimal. Our study has several limitations. First, we did not evaluate the timing of dobutamine-induced ST-T changes. The duration may carry potential clinical significance. Second, using visual analysis rather than quantitative analysis to detect perfusion defects may reduce the sensitivity of dobutamine thallium201 imaging. Third, myocardial viability and ischemia were evaluated by DSE and reinjection protocol of thallium-201 in this study. However, these techniques have been widely accepted as accurate tools in assessing myocardial ischemia and viability.11,12 Therefore, the possibility of under- or overestimation of wall motion recovery after revascularization may be minimal. 1. Bruce RA, Fisher LD, Pettinger M, Weiner DA, Chaitman BR. ST segment elevation with exercise: a marker for poor ventricular function and poor prognosis. Circulation 1988;77:897–905. 2. Haines DE, Beller GA, Watson DD, Kaiser DL, Sayre SL, Gibson RS. Exercise-induced ST-segment elevation 2 weeks after uncomplicated myocardial infarction: contributing factors and prognostic significance. J Am Coll Cardiol 1987;9:996 –1003. 3. Margonato A, Chierchia SL, Xuereb RG, Xuereb M, Fragasso G, Cappelletti A, Landoni C, Luciganani G, Fazio F. Specificity and sensitivity of exerciseinduced ST segment elevation for detection of residual viability: comparison with fluorodeoxyglucose and positron emission tomography. J Am Coll Cardiol 1995; 25:1032–1038. 4. Schneider CA, Helmig AK, Baer FM, Horst M, Erdmann E, Sechtem U. Significance of exercise-induced ST-segment elevation and T-wave pseudonormalization for improvement of function in healed Q-wave myocardial infarction. Am J Cardiol 1998;82:148 –153. 5. Lombardo A, Loperfido F, Pennestri F, Rossi E, Patrizi R, Cristinziani G, Catapano G, Maseri A. Significance of transient ST-T segment changes during dobutamine testing in Q wave myocardial infarction. J Am Coll Cardiol 1996; 27:599 – 605. 6. Salustri A, Garyfallidis P, Elhendy A, Ciavatti M, Cornel JH, Gemelli A, Ten Cate FJ, Roelandt JRTC, Fioretti PM. T-wave normalization during dobutamine echocardiography for diagnosis of viable myocardium. Am J Cardiol 1995;75: 505–507. 7. Elhendy A, Geleijnse L, Salustri A, van Domburg RT, Cornel JH, Arnese CM, Roelandt JRT, Fioretti PM. T-wave normalization during dobutamine stress testing in patients with non-Q wave myocardial infarction. Eur Heart J 1996;17: 526 –531. 8. Elhendy A, Geleijnse ML, Roelandt JRTC, van Domburg RT, Cornel JH, Ten Cate FJ, Postma-Tjoa J, Reijs AEM, El-Said GM, Fioretti PM. Evaluation by quantitative 99m-technetium MIBI SPECT and echocardiography of myocardial perfusion and wall motion abnormalities in patients with dobutamine-induced ST-segment elevation. Am J Cardiol 1995;76:441– 448. 9. Ricci R, Bigi R, Galati A, Bandini P, Coletta C, Fiorentini C, Lumia F, Occhi G, Ceci V. Dobutamine-induced ST-segment elevation in patients with acute myocardial infarction and the role of myocardial ischemia, viability, and ventricular dyssynergy. Am J Cardiol 1997;79:733–737. 10. Sawada SG, Segar DS, Ryan T, Brown SE, Dohan AM, William R, Fineberg NS, Armstrong WF, Feigenbaum H. Echocardiographic detection of coronary artery disease during dobutamine infusion. Circulation 1991;83:1605–1614. 11. Pierard LA, De Landsheere CM, Berthe C, Rigo P, Kulbertus HE. Identification of viable myocardium by echocardiography during dobutamine infusion in patients with myocardial infarction after thrombolytic therapy: comparison with positron emission tomography. J Am Coll Cardiol 1990;15:1021–1031. 12. Dilsizian V, Rocco TP, Freedman NMT, Leon MB, Bonow RO. Enhanced detection of ischemic but viable myocardium by the reinjection of thallium after stress-redistribution imaging. N Engl J Med 1990;323:141–146.
13. Kao HL, Wu CC, Ho YL, Chen WJ, Lee CM , Chen MF, Liou CS, Lee YT. Dobutamine stress echocardiography predicts early wall motion improvement after elective percutaneous transluminal coronary angioplasty. Am J Cardiol 1995;76:652– 656. 14. Ho YL, Wu CC, Huang PJ, Lin LC , Chieng PW, Chen WJ, Chen MF, Lee YT. Assessment of coronary artery disease in women by dobutamine stress echocardiography: comparison with thallium-201 single-photon emission computed tomography and exercise electrocardiography. Am Heart J 1998;135:655– 662. 15. Huang PJ, Ho YL, Wu CC, Chia CL, Chen MF, Chieng PU, Lee YT. Simultaneous dobutamine stress echocardiography and thallium-201 perfusion imaging for the detection of coronary artery disease. Cardiology 1997;88:556 – 562. 16. Baumgartner H, Porenta G, Lau YK, Wutte M, Klaar U, Mehrabi M, Siegel RJ, Czernin J, Laufer G, Sochor H, Schelbert H, Fishbein MC, Maurer G. Assessment of myocardial viability by dobutamine echocardiography, positron emission tomography and thallium-201 SPECT: correlation with histopathology in explanted hearts. J Am Coll Cardiol 1998;32:1701–1708. 17. Schiller NB, Shah PM, Crawford M, DeMaria A, Devereux R, Feigenbaum H, Gutgesell H, Reichek N, Sahn D, Schnittger I, Silverman AH, Tajik AJ. American Society of Echocardiography Committee on standards, subcommittee on quantitation of two-dimensional echocardiograms: recommendations for quantitation of the left ventricle by two-dimensional echocardiography. J Am Soc Echocardiogr 1989;2:358 –367. 18. Arnese M, Fioretti PM, Cornel JM, Postma-Tjoa, Reijs AE, Roelandt JRTC. Akinesia becoming dyskinesia during high dose dobutamine stress echocardiography: a marker of myocardial ischemia or a mechanical phenomenon? Am J Cardiol 1994;73:896 – 899. 19. Borrello JA, Clinthorne NH, Rogers WL, Thrall JH, Keyes JW Jr. Oblique angle tomography: a reconstruction algorithm for transaxial tomographic data. J Nucl Med 1981;22:471– 473. 20. Huang PJ, Yen RF, Chieng PU, Chen ML, Su CT. Do -blockers affect the diagnostic sensitivity of dobutamine stress thallium-201 single photon emission computed tomographic imaging? J Nucl Cardiol 1998;5:34 –39. 21. Iskandian AS, Heo J, Askenase A, Segal BL, Helfant RH. Thallium imaging with single photon emission computed tomography. Am Heart J 1987;114:852– 865. 22. Arnese M, Cornel JH, Salustri A, Maat APWM, Elhendy A, Reijs AEM, Ten Cate FJT, Keane D, Balk AHMM, Roelandt JRTC, Fioretti PM. Prediction of improvement of regional left ventricular function after surgical revascularization: a comparison of low-dose dobutamine echocardiography with 201Tl singlephoton emission computed tomography. Circulation 1995;91:2748 –2752. 23. Ho F-M, Huang P-J, Liau C-S, Lee F-K, Chieng P-U, Su C-T, Lee Y-T. Dobutamine stress echocardiography compared with dipyridamole thallium-201 single-photon emission computed tomography in detecting coronary artery disease. Eur Heart J 1995;16:570 –575. 24. Barilla F, Gheorghiade M, Alam M, Khaja F, Goldstein S. Low-dose dobutamine in patients with acute myocardial infarction identifies viable but not contractile myocardium and predicts the magnitude of improvement in wall motion abnormalities in response to coronary revascularization. Am Heart J 1991;122:1522–1531. 25. Lanzarini L, Fetiveau R, Poli A, Cavalotti C, Griffini M, Previtali M. Significance of ST-segment elevation during dobutamine stress echocardiography in patients with acute myocardial infarction treated with thrombolysis. Eur Heart J 1996;17:1008 –1014. 26. Coma-Canella I, del Val Gomez M, Terol I, Rodrigo F, Castro JM. Radionuclide studies in patients with stress-induced ST-segment elevation after acute myocardial infarction. Am Heart J 1994;128:459 – 465. 27. Lahiri A, Balasubramanian V, Craig MWM, Grawley J, Raftery EB. Exercise-induced ST segment elevation: electrocardiographic, angiographic, and scintigraphic evaluation. Br Heart J 1980;43:582–588. 28. Gewirtz H, Sullivan M, O’Reilly G, Winter S, Most AS. Role of myocardial ischemia in the genesis of stress-induced ST-segment elevation in previous anterior myocardial infarction. Am J Cardiol 1983;51:1289 –1293. 29. Kubota I, Hanashima K, Ideda K, Tsuiki K, Yasui S. Detection of diseased coronary artery by exercise ST-T maps in patients with effort angina pectoris, single-vessel disease, and normal ST-T wave on electrocardiogram at rest. Circulation 1989;80:120 –127. 30. Ho YL, Wu CC, Lin LC, Tseng WK, Chen WJ, Huang PJ, Lee YT. Localizing individual coronary artery obstructions with the dobutamine stress echocardiography. Cardiology 1997;88:197–202.
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MD,
Lung-Chun Lin, MD, Ruoh-Fang Yen, MD, Chau-Chung Wu, Ming-Fong Chen, MD, and Por-Jau Huang, MD
MD,
The clinical significance of stress-induced ST-segment elevation and T-wave pseudonormalization in infarctrelated leads is still controversial. Therefore, we conducted the present study to assess this issue using simultaneous dobutamine stress echocardiography (DSE) and thallium-201 single-photon emission computed tomography. A total of 119 patients with Q-wave myocardial infarction were enrolled in this study. There were 58 patients with (group I) and 61 patients without (group II) dobutamine-induced ST-T changes. Left ventricular ejection fraction was 43 ⴞ 13% in group I and 49 ⴞ 14% in group II (p <0.05). The baseline, low-, and peak-dose global wall motion scores were similar between these 2 groups (26.2 ⴞ 6.1 vs 26.2 ⴞ 6.3 [p ⴝ NS]; 24.1 ⴞ 5.3 vs 23.5 ⴞ 5.7 [p ⴝ NS]; 26.4 ⴞ 5.7 vs 26.7 ⴞ 6.1 [p ⴝ NS]). The sensitivity, specificity, and accuracy of these ST-T changes for detecting residual myocardial viability
and ischemia documented by DSE in all patients were 50%, 53%, and 51% (for viability), and 47%, 48%, and 47% (for ischemia), respectively. The sensitivity, specificity, and accuracy of these ST-T changes for detecting a reversible perfusion defect documented by thallium-201 single-photon emission computed tomography were 51%, 54%, and 52%, respectively. In conclusion, dobutamine-induced ST elevation and/or T-wave pseudonormalization is associated with poor resting left ventricular function. These ST-T changes are not associated with residual myocardial ischemia and viability in the infarct area. Therefore, these electrocardiographic changes alone cannot be reliably considered as distinctive markers in formulating the therapeutic strategy of coronary intervention. 䊚1999 by Excerpta Medica, Inc. (Am J Cardiol 1999;84:125–129)
T
simultaneous DSE and stress radionuclide imaging.7,8 The present study was designed to evaluate the functional significance of dobutamine-induced ST elevation and/or T-wave pseudonormalization in patients with previous Q-wave myocardial infarction (MI) by simultaneous DSE and thallium-201 SPECT.
he clinical significance of stress-induced STsegment elevation and T-wave pseudonormalization in infarct-related leads is still controversial.1–9 The possible mechanisms include ventricular asynergy, residual myocardial ischemia, and contractile reserve within the infarct area.1–9 Because residual myocardial ischemia and viability within the infarct area is important for cardiologists to formulate the strategy of coronary intervention, the significance of these electrocardiographic changes need to be further validated. Dobutamine stress echocardiography (DSE) and thallium-201 single-photon emission computed tomography (SPECT) are sensitive and specific in myocardial ischemia and viability detection.10 –15 Also, both examinations provide complementary information in the assessment of myocardial viability.16 However, there have been few reports about the assessment of these electrocardiographic changes using From the Departments of Internal Medicine (Cardiology) and Nuclear Medicine, National Taiwan University Hospital, Taipei, Taiwan. Manuscript received November 10, 1998; revised manuscript received March 8, 1999, and accepted March 10, 1999. Address for reprints: Por-Jau Huang, MD, Department of Internal Medicine (Cardiology), National Taiwan University Hospital, No. 7, Chung-Shan S. Road, Taipei, Taiwan. ©1999 by Excerpta Medica, Inc. All rights reserved. The American Journal of Cardiology Vol. 84 July 15, 1999
METHODS
Study population: DSE and dobutamine thallium201 SPECT images were simultaneously obtained in 119 patients (108 men and 11 women, mean age 59 ⫾ 12 years) who had history of MI and pathologic Q waves in infarct-related leads. Recent MI (⬍1 month) was noted in 53 patients. The diagnosis of acute MI relied on a typical history of chest pain, a diagnostic increase in serum creatine kinase, and evolutional electrocardiographic changes. Patients were excluded from the study entry if they had resting or unstable angina, uncontrolled hypertension (systolic blood pressure ⬎200 mm Hg, or diastolic pressure ⬎110 mm Hg), or New York Heart Association functional class III or IV symptoms of heart failure. Additional exclusion criteria included a history of sustained ventricular arrhythmia, poor echo windows, or severe aortic stenosis. All patients underwent coronary an0002-9149/99/$–see front matter PII S0002-9149(99)00220-9
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giography within 7 days after DSE and thallium-201 SPECT. Dobutamine infusion protocol: All patients received 250 ml of normal saline as a fluid challenge before the infusion to avoid hypotension and bradycardia occasionally occurring with dobutamine infusion. Dobutamine was given intravenously at rates of 5, 10, 20, 30, and 40 g/kg/min in 3-minute stages. Reasons for termination were: severe hypertension (systolic blood pressure ⬎220 mm Hg or diastolic blood pressure ⬎110 mm Hg), a symptomatic decrease in blood pressure from the predobutamine baseline, prolonged angina, any significant arrhythmias, achievement of 85% of the age-predicted maximal heart rate, or completion of the maximal dose of 40 g/kg/min. Patients were observed for 5 minutes after infusion. Blood pressure, heart rate, symptoms, and electrocardiographic data were recorded at baseline, the last minute of each stage, and at the end of recovery. Calcium channel blockers and  blockers were not discontinued before DSE. Electrocardiographic analysis: ST elevation was defined as new or additional ⱖ1.0 mm elevation at the J point, with a horizontal or upsloping ST-segment lasting 80 ms during stress in ⱖ2 Q-wave leads (the PQ segment was considered the isoelectric line).9 T-wave pseudonormalization was defined as the negative T wave inverted to upright in infarct-related leads.4 To correlate the localization of electrocardiographic abnormalities with scintigraphic, echocardiographic, and angiographic abnormalities, 2 electrocardiographic sites were considered: (1) anterior (leads V1 to V4), which was assigned to the anterior wall, septum, and apex, and to the left anterior descending coronary artery; (2) inferolateral (II, III, aVF, I, aVL, V5, and V6), which was assigned to the lateral and inferoposterior walls, and to the left circumflex and right coronary arteries.7 Interpretation of ST-segment elevation and T-wave pseudonormalization was performed in a blinded manner by 2 independent cardiologists, and disagreement was resolved by consensus. Echocardiography and wall motion analysis: Standard parasternal and apical views were obtained at baseline and at each stage of dobutamine protocol. The left ventricle was divided into 16 segments according to guidelines of the American Society of Echocardiography.17 Images were generated with a Sonos 1500 apparatus (Hewlett-Packard, Andover, Massachusetts) with a 2.0/2.5-MHz probe, digitized and then stored in quad-screen cine loop format with a Freeland Cardiac Workstation (Louisville, Colorado). Images taken during the 5- or 10-g/kg/min infusion were recorded as the low-dose images. Images taken at the highest attainable infusion rate were recorded as the peak-dose images. Wall motion was analyzed by 2 experienced echocardiologists with no knowledge of electrocardiographic, thallium, or angiographic results. The following scoring system was used: segments with normal or hyperkinetic motion were assigned 1, hypokinesia 2, akinesia 3, and dyskinesia 4.17 The wall motion score was derived by summation of individual segment score.10,13 Myocar126 THE AMERICAN JOURNAL OF CARDIOLOGY姞
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dial ischemia was considered present if new or worsening regional wall motion abnormality was induced by dobutamine.10,13 Therefore, segments were judged to be ischemic when there was an increment of wall motion score ⬎1 grade at any stage of dobutamine infusion compared with the resting stage. Akinesia that directly deteriorated to dyskinesia was not considered a marker of myocardial ischemia.18 Myocardial viability was considered present if wall motion was normal at rest, or if the resting regional wall motion abnormality was reversed or improved under dobutamine infusion.11,13,16 Our interobserver agreement for DSE was 94% ( 0.85, SEM 0.078).14 Dobutamine thallium-201 imaging: Dobutamine was infused intravenously according to the protocol described above. Two to 3 mCi of thallium-201 was injected intravenously at the third minute of peak phase. Another 1 mCi of thallium-201 was reinjected immediately after the 4-hour imaging. SPECT myocardial scintigrams were recorded within 10 minutes (stress phase), at 4 hours (redistribution phase) after injection of thallium-201, and at 20 minutes (reinjection phase) after reinjection of thallium-201 using a large field-of-view gamma camera (CAMSTAR 3000, General Electric, Milwaukee, Wisconsin) equipped with a low-energy, all-purpose collimator. The detector collected data through a 180° arc from the 45° right anterior oblique to the 45° left posterior oblique position. Contiguous transaxial tomograms were reconstructed into 6-mm-thick multiple sections using a filtered back-projection method with a Hanning ramp filter, and using a convolution reconstruction algorithm without attenuation correction. Thereafter, tomographic images along the short and long axes of the left ventricle were reorganized from the set of the transaxial tomograms according to the method described by Borrello et al.19 All SPECT images were interpreted qualitatively by 2 experienced observers who were unaware of the electrocardiographic, echocardiographic, or angiographic results. We used the 16-color scale in image interpretation and the left ventricle was divided into 10 segments.20,21 Thallium201 activity in each segment was scored as 3 (normal), 2 (mildly reduced), 1 (moderately reduced), or 0 (severely reduced or absent). A segment was considered abnormal if its score was ⱕ2.20 Stress images were compared with redistribution and reinjection images to evaluate the presence or absence of reversible or fixed defects.20,22 Reversible perfusion defects were defined as abnormal segments with an increment of tracer uptake ⬎1 grade at the redistribution or reinjection phase compared with the stress phase.20 Myocardial ischemia was considered in segments with reversible perfusion defects.20 A myocardial segment was considered nonviable in the presence of a severe (score ⫽ 0), fixed perfusion defect.22 Our interobserver agreement for SPECT interpretation was 96% ( 0.90, SEM 0.079).23 Our agreement of regional wall motion abnormality/perfusion defect was 81% ( 0.61).15 JULY 15, 1999
TABLE I Clinical Data of Groups I and II Group I (n ⫽ 58)
TABLE II Findings of Dobutamine Stress Echocardiography Group II (n ⫽ 61)
Men/women 50/8 58/3 Age (yr) 59 ⫾ 12 60 ⫾ 12 Anterior/inferior MI 35/23 35/26 Recent MI 28 25 Use of  blockers 35 33 Use of calcium blockers 7 10 Baseline ST-segment 29 21 elevation Amplitude of baseline 1.9 ⫾ 0.6 1.7 ⫾ 0.7 ST elevation (mm) 1-vessel CAD 16 18 Multivessel CAD 42 43 LVEF (%) 43 ⫾ 13 49 ⫾ 14* Baseline HR (beats/min) 73 ⫾ 15 70 ⫾ 13 Baseline systolic BP 121 ⫾ 16 118 ⫾ 20 (mm Hg) Baseline diastolic BP 77 ⫾ 10 75 ⫾ 12 (mm Hg) Baseline double product 8,963 ⫾ 2,528 8,317 ⫾ 2,365 (mm Hg 䡠 beats 䡠 min⫺1) Peak HR (beats/min) 106 ⫾ 16 99 ⫾ 19 Peak systolic BP (mm Hg) 140 ⫾ 26 141 ⫾ 29 Peak diastolic BP (mm Hg) 75 ⫾ 12 73 ⫾ 16 Peak dose double product 14,624 ⫾ 3,282 14,037 ⫾ 3,696 (mm Hg 䡠 beats 䡠 min⫺1) *p ⫽ 0.047. BP ⫽ blood pressure; CAD ⫽ coronary artery disease; HR ⫽ heart rate; LVEF ⫽ left ventricular ejection fraction.
Coronary angiography and left ventriculography:
Coronary angiography and left ventriculography were performed with the Judkins technique. A ⱖ50% diameter stenosis in the coronary artery was considered significant. Left ventricular ejection fraction was calculated by area-length method from the left cineventriculogram. Interobserver agreement of left ventricular ejection fraction in our laboratory was 95% ( 0.89). Statistical analysis: All results are expressed as the mean ⫾ SD. Sensitivity, specificity, positive predictive value, negative predictive value, and accuracy were all calculated with standard formulas. All statistical differences among the groups were obtained by using the Student’s t and chi-square method. The relation between ST-T changes and myocardial ischemia/viability was evaluated by the McNemar test. It was considered statistically significant if the p value was ⬍0.05. Interobserver concordance was determined by calculating the coefficient.
RESULTS
Clinical characteristics (Table I): Fifty-eight of the 119 patients had ST-segment elevation and/or T-wave pseudonormalization (group I) and 61 patients did not have electrocardiographic changes (group II). In group I, 23 patients had T pseudonormalization, 15 patients had ST elevation, and 20 patients had both changes. There was no difference in the number of patients with anterior (35 vs 35) or inferior (23 vs 26) MI in these 2 groups. There was no difference in the number of patients with either recent MI or baseline
DSE Baseline global WMS Low-dose global WMS Peak-dose global WMS Baseline infarct WMS Low-dose infarct WMS Peak-dose infarct WMS Baseline akinetic/dyskinetic segments Peak-dose akinetic/dyskinetic segments Dyskinetic segments at peak dose
Group I 26.2 24.1 26.4 16.1 14.5 15.9 3.5 3.7 0.6
⫾ ⫾ ⫾ ⫾ ⫾ ⫾ ⫾ ⫾ ⫾
6.1 5.3 5.7 5.7 5.7 5.5 2.8 2.6 1.0
Group II 26.2 23.5 26.7 14.7 13.2 15.2 3.1 3.3 0.6
⫾ ⫾ ⫾ ⫾ ⫾ ⫾ ⫾ ⫾ ⫾
6.3 5.7 6.1 6.3 6.2 6.3 2.7 2.7 1.0
WMS ⫽ wall motion scores.
ST-segment elevation in these 2 groups. The amplitudes of baseline ST-segment elevation were also similar (1.9 ⫾ 0.6 vs 1.7 ⫾ 0.7 mm; p ⫽ NS). Left ventricular ejection fraction was 43 ⫾ 13% in group I and 49 ⫾ 14% in group II (p ⬍0.05). There was no difference in the number of patients taking either  blockers or calcium channel blockers in these 2 groups. Findings of dobutamine stress echocardiography:
After dobutamine infusion, the peak-dose heart rate and systolic and diastolic blood pressures were similar between the 2 groups (Table I). Baseline, low-dose, and peak-dose global wall motion scores were also similar in the 2 groups (Table II). The baseline, lowdose, and peak-dose infarct area wall motion scores were similar in the 2 groups. The numbers of baseline and peak-dose akinetic/dyskinetic segments in the 2 groups were also similar. Sensitivity, specificity, and accuracy of dobutamine-induced ST-T changes for detecting residual myocardial ischemia documented by DSE in total patients were 47%, 48%, and 47%, respectively (p ⫽ NS; Table III). There was no association between ST-T changes and residual ischemia documented by DSE in patients with either anterior or inferior MI. Sensitivity, specificity, and accuracy of ST-T changes for detecting residual viable myocardium documented by DSE in total patients were 50%, 53%, and 51%, respectively (p ⫽ NS). There was also no association between ST-T changes and residual myocardial viability documented by DSE in patients with either anterior or inferior MI. Findings of dobutamine thallium-201 single-photon emission computed tomography (Tables IV and V)4: Do-
butamine-induced ST-T changes were not associated with reversible perfusion defects documented by thallium-201 SPECT in total patients (p ⫽ NS). These ST-T changes were also not associated with reversible perfusion defects in patients with either anterior or inferior MI. The prevalence of a normal perfusion pattern, and reversible and fixed perfusion defects in the reciprocal area to MI were similar in the 2 groups (p ⫽ NS). The scores of thallium activity in all fixed perfusion defects were 0.
DISCUSSION Identifying the area of infarcted myocardium with depressed but potentially reversible contractile func-
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TABLE III Sensitivity, Specificity, and Accuracy of Dobutamine-induced ST-T–Segment Changes for Detecting Residual Myocardial Ischemia and Viable Myocardium Documented by DSE Residual Myocardial Ischemia
Sensitivity Specificity Accuracy
Residual Viable Myocardium
Total
Anterior MI
Inferior MI
Total
Anterior MI
Inferior MI
34/73 (47%) 22/46 (48%) 56/119 (47%)
18/38 (47%) 15/32 (47%) 33/70 (47%)
16/35 (46%) 7/14 (50%) 23/49 (47%)
37/74 (50%) 24/45 (53%) 61/119 (51%)
18/38 (47%) 15/32 (47%) 33/70 (47%)
19/36 (53%) 9/13 (69%) 28/49 (57%)
TABLE IV Sensitivity, Specificity, Positive Predictive Value, Negative Predictive Value, and Accuracy of DobutamineInduced ST-T–Segment Changes for Detecting Presence of Reversible Perfusion Defect Documented by Thallium-201 SPECT Anterior MI Sensitivity Specificity Positive predictive Negative predictive Accuracy
21/37 19/33 21/35 19/35 40/70
(57%) (58%) (60%) (54%) (57%)
Inferior MI 12/28 10/21 12/23 10/26 22/49
Total
(43%) 33/65 (48%) 29/54 (52%) 33/58 (38%) 29/61 (45%) 62/119
(51%) (54%) (57%) (48%) (52%)
TABLE V Prevalence of Fixed Perfusion Defect, Reversible Perfusion Defect, and Normal Pattern in Reciprocal Area to Myocardial Infarction Between Groups I and II Thallium Pattern in Reciprocal Area Fixed perfusion defect Reversible perfusion defect No perfusion defect Total
Group I
Group II
8 23 27 58
10 24 27 61
tion helps to predict the prognosis of patients with coronary artery disease and chronic left ventricular dysfunction.24 Therefore, stress-induced ST elevation and T-wave pseudonormalization of infarct-related leads have generated great interest among cardiologists in that residual myocardial ischemia and viability have been proposed to be plausible mechanisms of these electrocardiographic phenomena. The incidence of dobutamine-induced ST-segment elevation ranges from 41% to 55% and our results are similar to these reports.9,25 Lombardo et al5 observed that dobutamine-induced ST-T changes were indicative of contractile reserve in infarct-related leads when these changes developed with low-dose dobutamine. Dobutamine-induced T-wave pseudonormalization has been also reported to be a sign of viable myocardium in patients with Q-wave MI and an indicator of myocardial ischemia in patients with non–Q-wave MI.6,7 In contrast, there have been several reports suggesting that the mechanism of ST-segment elevation may be due to mechanical rather than to residual myocardial ischemia or viability in most patients.2,8,9,25–28 Either exercise or dobutamine-induced ST-segment elevation during radionuclide studies has been attributed to stress-induced left ventricular asynergy rather than ischemia.26,27 Dobutamine-induced ST-segment elevation has also been reported not to be associated with a higher incidence and extent of viable or jeop128 THE AMERICAN JOURNAL OF CARDIOLOGY姞
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ardized myocardium defined by DSE.8,9,25 The results of the present study are compatible with these reports.8,9,25–27 Our patients with dobutamine-induced ST-T changes had worse left ventricular ejection fraction than those without these changes (p ⬍0.05). The presence of residual myocardial ischemia and viability was not different in patients with or without ST-T changes. The sensitivity, specificity, and accuracy of these ST-T changes to diagnose either reversible perfusion defects in thallium-201 imaging or viable myocardium in DSE were relatively poor. These data are compatible with results reported by Ricci et al.9 In the present study, the prevalence of a normal pattern, and fixed and reversible perfusion defects in thallium imaging in the reciprocal area (to MI) were all similar in the 2 groups. Therefore, these electrocardiographic changes could not be attributed to the ischemic event in the reciprocal area (to MI) and could not be interpreted as markers of more extensive coronary artery disease. Similar observations were also obtained by Haines et al.2 In normal patients, the action potential duration of the endocardial region is longer than that of the epicardial region, and ventricular repolarization is from epicardium to endocardium. The action potential duration may be shortened in the presence of myocardial injury, and electrical gradients are created in different directions rather than in the direction from epicardium to endocardium.29 Stress (either exercise or dobutamine) further enhanced the distortion of left ventricular geometry caused by MI. Therefore, the magnitude and directions of the electrical gradients vary and result in ST-T changes. Residual myocardial ischemia and viability can also change the duration of action potential and interfere with the direction of electrical gradients. Therefore, we cannot exclude the possibility that myocardial ischemia and viability may contribute to additional ST-T changes in some patients.9 However, dobutamine-induced ST-T changes cannot reliably be considered as distinctive markers in formulating the therapeutic strategy of coronary intervention. Because of the safety considerations, our patients received 250 ml of normal saline as a fluid challenge before dobutamine infusion to avoid hypotension and bradycardia. As in our previous study,30 the incidence of hypotension and bradycardia decreases and the diagnostic accuracy is compatible with previous reports.10,30 Both preload increase and dobutamine infusion enhance systolic performance of the left venJULY 15, 1999
tricle. Therefore, the effects of this preload alternation on the diagnostic accuracy of DSE is minimal. Our study has several limitations. First, we did not evaluate the timing of dobutamine-induced ST-T changes. The duration may carry potential clinical significance. Second, using visual analysis rather than quantitative analysis to detect perfusion defects may reduce the sensitivity of dobutamine thallium201 imaging. Third, myocardial viability and ischemia were evaluated by DSE and reinjection protocol of thallium-201 in this study. However, these techniques have been widely accepted as accurate tools in assessing myocardial ischemia and viability.11,12 Therefore, the possibility of under- or overestimation of wall motion recovery after revascularization may be minimal. 1. Bruce RA, Fisher LD, Pettinger M, Weiner DA, Chaitman BR. ST segment elevation with exercise: a marker for poor ventricular function and poor prognosis. Circulation 1988;77:897–905. 2. Haines DE, Beller GA, Watson DD, Kaiser DL, Sayre SL, Gibson RS. Exercise-induced ST-segment elevation 2 weeks after uncomplicated myocardial infarction: contributing factors and prognostic significance. J Am Coll Cardiol 1987;9:996 –1003. 3. Margonato A, Chierchia SL, Xuereb RG, Xuereb M, Fragasso G, Cappelletti A, Landoni C, Luciganani G, Fazio F. Specificity and sensitivity of exerciseinduced ST segment elevation for detection of residual viability: comparison with fluorodeoxyglucose and positron emission tomography. J Am Coll Cardiol 1995; 25:1032–1038. 4. Schneider CA, Helmig AK, Baer FM, Horst M, Erdmann E, Sechtem U. Significance of exercise-induced ST-segment elevation and T-wave pseudonormalization for improvement of function in healed Q-wave myocardial infarction. Am J Cardiol 1998;82:148 –153. 5. Lombardo A, Loperfido F, Pennestri F, Rossi E, Patrizi R, Cristinziani G, Catapano G, Maseri A. Significance of transient ST-T segment changes during dobutamine testing in Q wave myocardial infarction. J Am Coll Cardiol 1996; 27:599 – 605. 6. Salustri A, Garyfallidis P, Elhendy A, Ciavatti M, Cornel JH, Gemelli A, Ten Cate FJ, Roelandt JRTC, Fioretti PM. T-wave normalization during dobutamine echocardiography for diagnosis of viable myocardium. Am J Cardiol 1995;75: 505–507. 7. Elhendy A, Geleijnse L, Salustri A, van Domburg RT, Cornel JH, Arnese CM, Roelandt JRT, Fioretti PM. T-wave normalization during dobutamine stress testing in patients with non-Q wave myocardial infarction. Eur Heart J 1996;17: 526 –531. 8. Elhendy A, Geleijnse ML, Roelandt JRTC, van Domburg RT, Cornel JH, Ten Cate FJ, Postma-Tjoa J, Reijs AEM, El-Said GM, Fioretti PM. Evaluation by quantitative 99m-technetium MIBI SPECT and echocardiography of myocardial perfusion and wall motion abnormalities in patients with dobutamine-induced ST-segment elevation. Am J Cardiol 1995;76:441– 448. 9. Ricci R, Bigi R, Galati A, Bandini P, Coletta C, Fiorentini C, Lumia F, Occhi G, Ceci V. Dobutamine-induced ST-segment elevation in patients with acute myocardial infarction and the role of myocardial ischemia, viability, and ventricular dyssynergy. Am J Cardiol 1997;79:733–737. 10. Sawada SG, Segar DS, Ryan T, Brown SE, Dohan AM, William R, Fineberg NS, Armstrong WF, Feigenbaum H. Echocardiographic detection of coronary artery disease during dobutamine infusion. Circulation 1991;83:1605–1614. 11. Pierard LA, De Landsheere CM, Berthe C, Rigo P, Kulbertus HE. Identification of viable myocardium by echocardiography during dobutamine infusion in patients with myocardial infarction after thrombolytic therapy: comparison with positron emission tomography. J Am Coll Cardiol 1990;15:1021–1031. 12. Dilsizian V, Rocco TP, Freedman NMT, Leon MB, Bonow RO. Enhanced detection of ischemic but viable myocardium by the reinjection of thallium after stress-redistribution imaging. N Engl J Med 1990;323:141–146.
13. Kao HL, Wu CC, Ho YL, Chen WJ, Lee CM , Chen MF, Liou CS, Lee YT. Dobutamine stress echocardiography predicts early wall motion improvement after elective percutaneous transluminal coronary angioplasty. Am J Cardiol 1995;76:652– 656. 14. Ho YL, Wu CC, Huang PJ, Lin LC , Chieng PW, Chen WJ, Chen MF, Lee YT. Assessment of coronary artery disease in women by dobutamine stress echocardiography: comparison with thallium-201 single-photon emission computed tomography and exercise electrocardiography. Am Heart J 1998;135:655– 662. 15. Huang PJ, Ho YL, Wu CC, Chia CL, Chen MF, Chieng PU, Lee YT. Simultaneous dobutamine stress echocardiography and thallium-201 perfusion imaging for the detection of coronary artery disease. Cardiology 1997;88:556 – 562. 16. Baumgartner H, Porenta G, Lau YK, Wutte M, Klaar U, Mehrabi M, Siegel RJ, Czernin J, Laufer G, Sochor H, Schelbert H, Fishbein MC, Maurer G. Assessment of myocardial viability by dobutamine echocardiography, positron emission tomography and thallium-201 SPECT: correlation with histopathology in explanted hearts. J Am Coll Cardiol 1998;32:1701–1708. 17. Schiller NB, Shah PM, Crawford M, DeMaria A, Devereux R, Feigenbaum H, Gutgesell H, Reichek N, Sahn D, Schnittger I, Silverman AH, Tajik AJ. American Society of Echocardiography Committee on standards, subcommittee on quantitation of two-dimensional echocardiograms: recommendations for quantitation of the left ventricle by two-dimensional echocardiography. J Am Soc Echocardiogr 1989;2:358 –367. 18. Arnese M, Fioretti PM, Cornel JM, Postma-Tjoa, Reijs AE, Roelandt JRTC. Akinesia becoming dyskinesia during high dose dobutamine stress echocardiography: a marker of myocardial ischemia or a mechanical phenomenon? Am J Cardiol 1994;73:896 – 899. 19. Borrello JA, Clinthorne NH, Rogers WL, Thrall JH, Keyes JW Jr. Oblique angle tomography: a reconstruction algorithm for transaxial tomographic data. J Nucl Med 1981;22:471– 473. 20. Huang PJ, Yen RF, Chieng PU, Chen ML, Su CT. Do -blockers affect the diagnostic sensitivity of dobutamine stress thallium-201 single photon emission computed tomographic imaging? J Nucl Cardiol 1998;5:34 –39. 21. Iskandian AS, Heo J, Askenase A, Segal BL, Helfant RH. Thallium imaging with single photon emission computed tomography. Am Heart J 1987;114:852– 865. 22. Arnese M, Cornel JH, Salustri A, Maat APWM, Elhendy A, Reijs AEM, Ten Cate FJT, Keane D, Balk AHMM, Roelandt JRTC, Fioretti PM. Prediction of improvement of regional left ventricular function after surgical revascularization: a comparison of low-dose dobutamine echocardiography with 201Tl singlephoton emission computed tomography. Circulation 1995;91:2748 –2752. 23. Ho F-M, Huang P-J, Liau C-S, Lee F-K, Chieng P-U, Su C-T, Lee Y-T. Dobutamine stress echocardiography compared with dipyridamole thallium-201 single-photon emission computed tomography in detecting coronary artery disease. Eur Heart J 1995;16:570 –575. 24. Barilla F, Gheorghiade M, Alam M, Khaja F, Goldstein S. Low-dose dobutamine in patients with acute myocardial infarction identifies viable but not contractile myocardium and predicts the magnitude of improvement in wall motion abnormalities in response to coronary revascularization. Am Heart J 1991;122:1522–1531. 25. Lanzarini L, Fetiveau R, Poli A, Cavalotti C, Griffini M, Previtali M. Significance of ST-segment elevation during dobutamine stress echocardiography in patients with acute myocardial infarction treated with thrombolysis. Eur Heart J 1996;17:1008 –1014. 26. Coma-Canella I, del Val Gomez M, Terol I, Rodrigo F, Castro JM. Radionuclide studies in patients with stress-induced ST-segment elevation after acute myocardial infarction. Am Heart J 1994;128:459 – 465. 27. Lahiri A, Balasubramanian V, Craig MWM, Grawley J, Raftery EB. Exercise-induced ST segment elevation: electrocardiographic, angiographic, and scintigraphic evaluation. Br Heart J 1980;43:582–588. 28. Gewirtz H, Sullivan M, O’Reilly G, Winter S, Most AS. Role of myocardial ischemia in the genesis of stress-induced ST-segment elevation in previous anterior myocardial infarction. Am J Cardiol 1983;51:1289 –1293. 29. Kubota I, Hanashima K, Ideda K, Tsuiki K, Yasui S. Detection of diseased coronary artery by exercise ST-T maps in patients with effort angina pectoris, single-vessel disease, and normal ST-T wave on electrocardiogram at rest. Circulation 1989;80:120 –127. 30. Ho YL, Wu CC, Lin LC, Tseng WK, Chen WJ, Huang PJ, Lee YT. Localizing individual coronary artery obstructions with the dobutamine stress echocardiography. Cardiology 1997;88:197–202.
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