Manifestations of 201 Tl Myocardial Single Photon Emission Computed Tomography in Patients with Myocardial Bridge

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1 Manifestations of Tl Myocardial Single Photon Emission Computed Tomography in Patients with Myocardial Bridge Chiung-Zuan Chiu 1, Jun-Jack Cheng 1, Shen-Chang Lin 1, Shih-Huang Lee 1,Peiliang Kuan 1, Kuo-Gi, Shyu 1, Ming-Tsung Chen 2, Yen-Kung Chen 2, Alfred C Liao 2, Yeh-You Shen 2 1 Section of Cardiology, Shin-Kong Wu Ho-Su Memorial Hospital 2 Department of Nuclear Medicine, Shin-Kong Wu Ho-Su Memorial Hospital Background: Myocardial bridge (MB) is an congenital coronary anomaly resulting in systolic narrowing of coronary artery. It may be seen occasionally during coronary angiography (CAG) examinations and may cause clinical symptoms and/or signs of coronary artery disease (CAD). The symptoms/signs include angina pectoris, myocardial infarction, vasospasm, cardiac arrythmia, and sudden cardiac death. Few previous reports stated about the Tl perfusion defects noted in patients with MB, which probably imply the evidence of myocardial ischemia. The purpose of this study is to do a retrospective analysis of Tl images in patients with MB. Methods: From July, 2000 to June, 2003, 63 patients (30 male; mean age 57 ± 10, and range from 33 to 80 years old), with chest pain and/or chest tightness underwent stress test for CAD. Six patients underwent treadmill exercise with Bruce protocol and 57 patients received dipyridamole as pharmacological stress. All patients were followed by image acquisitions done immediately after stress and 4 h later. All underwent CAG subsequently to identify the severity of CAD. Results: In all of the 63 patients, CAG revealed MB. Fifty patients had MB in left descending artery (LAD) (40 at mid portion; 8 at distal portion; 2 at mid and distal portion), 4 in left circumflex artery (LCX), and 1 in right coronary artery (RCA). Seven patients had MB in both LAD and LCX, and 1 patient had MB in both LAD and RCA. Sixty patients (95%) had Tl perfusion defects in either reverse (R), partial reverse (PR), or reverse redistribution (RR) patterns. In the abnormal Tl SPECTs, 103 abnormal perfusion areas were found including 57 R (55%), 40 PR (39%), and 6 RR (6%). In all vessels with MB, 48 (83%) in LAD could see Tl perfusion defects in anterior, septal, and/or apical areas. In addition, 6 of 11 (55%) in LCX could detect defects in lateral or inferior areas, and 2 of 2 (100%) in RCA could detect defects in inferior areas. Conclusions: Myocardial ischemia with abnormal Tl perfusion image can be detected in most patients with MB. MB with ischemic evidence in Tl perfusion image also may be associated with chest pain and/or chest tightness in our patients. Tl perfusion defect may be presented with R, PR, or RR in patients with MB. The significance of three different perfusion defects patterns (R, PR, and RR) may represent the various severity of perfusion insufficiency induced by MB. Key words: myocardial bridge, myocardial ischemia, Tl perfusion image Ann Nucl Med Sci 2005;18:9-16 Received 8/30/2004; revised 11/4/2004; accepted 11/12/2004. For correspondence or reprints contact: Chiung-Zuan Chiu, M.D., Section of Cardiology, Shin-Kong Wu Ho-Su Memorial Hospital, 95 Wen Chan Road, Taipei 111, Taiwan. Tel: (886) ext. 2084, Fax: (886) , juice243@hotmail.com Myocardial bridge (MB) is a congenital anomaly occurred in 15%-85% people on autopsy and 0.5%-16%

2 Chiu CZ et al patients on coronary angiography (CAG). The bridge formation is an anatomic arrangement in which an epicardial coronary artery becomes engulfed for a limited segment by myocardial fibers. In clinical situation, it describes an angiographic entity: a systolic narrowing of a coronary artery, mainly the left anterior descending (LAD) artery, responsible for a milking effect [1-5]. Although it is still controversial whether MB contributes to myocardial ischemia, there are patients who have clinical symptoms and signs of myocardial ischemia associated with MB during exercise and/or rest. MB may be concomitant clinically with myocardial ischemia, coronary spasm, arrhythmia, acute myocardial infarction, and sudden cardiac death [6-9]. Patients with MB may also experience the symptoms of angina pectoris with chest tightness and/or pain. Its clinical presentations and changes on electrocardiogram (ECG) overlap with those with coronary artery disease (CAD). So Tl myocardial perfusion imaging may be a tool recommended to identify the severity of myocardial ischemia in patients with MB. Few articles discussed about this issue before. The goal of this study is to do a retrospective analysis about the changes in Tl myocardial perfusion imaging in patients with MB documented by CAG. Materials and Methods Patients From July, 2000 to June, 2003, 63 patients (30 males; mean age 57 ± 10 year-old, and range from 33 to 80 years old), with clinical symptoms of angina pectoris (chest pain and/or chest tightness) received Tl myocardial perfusion SPECT (treadmill exercise stress by Bruce protocol in 6 and dipyridamole pharmacological stress in 57). All patients underwent CAG subsequently to identify the severity of CAD. Twenty patients had abnormal ST-T changes in resting ECG. Twenty-four patients also underwent treadmill exercise test and 22 of them (92%) showed positive findings. All patients underwent left ventriculogram (LVG) and revealed normal left ventricular function. One patient showed apical hypertrophy by LVG. Underlying disease was hypertension in 36 (57%), diabetes millitus in 10 (16%) and hyperlipidemia in 22 (35%). Eight patients were smoker (13%) (Table 1). Coronary Angiography All patients underwent subsequent CAG and LVG either by transradial or transfemoral approach. Myocardial bridge is defined as normal caliber of bridging segment of coronary artery during diastole phase (different from atherosclerotic coronary stenosis noted in diastolic phase) but abruptly narrows of segmental coronary artery with each systole. All patients were found to have MB. Location (left anterior descending [LAD], left circumflex [LCX], right coronary artery [RCA]), region (proximal, middle, distal), and severity (length of MB and percentage of stenosis during systolic narrowing phase) of MB were recorded individually. Two operators reviewed the pictures of CAG during the procedure. A narrowing of the diameter of more than 50% in the systolic phase was considered as significant. Table 1. Basic data in all patients with myocardial bridge (MB) Patients number 63 Mean age (range) 57±10 (33-80) Male (%) 30 (48%) Underlying disease DM (%) 10 (16%) Hypertension (%) 36 (57%) Hyperlipidemia (%) 22 (35%) Smoking (%) 8 (13%) DM: diabetes millitus ; Hyperlipidemia: total cholesterol > 220 mg/dl Tl Myocardial Perfusion SPECT Same day stress-delay image sets were obtained on either physiological (treadmill) or pharmacological (dipyridamole) stress protocols in individual cases. Six patients underwent treadmill exercise with Bruce protocol and 57 patients received dipyridamole as a pharmacological stress agent, generally at a rate of 0.14 mg kg -1, intravenously for a 4-min period. Intravenous injection of Tl (111 MBq) was administrated accordingly at the peak of the exercise or at 6 min on pharmacological stress. The image acquisitions were done immediately after stress and 4 h later, and no diet limitation in the interval between two images. A Tl SPECT was performed with the patient in the supine position under a right angle dual heads camera (Varicam, Millennium VG, GE, Milwaukee, USA) equipped Ann Nucl Med Sci 2004;18:9-16 Vol. 18 No. 1 March

3 Tl manifestations in patients with myocardial bridge Tl with low energy and general purpose collimators. Both stress and delay Tl images were acquired by a matrix with a 1.3 zoom through 180 (90 for each head) rotation at 3 per step, 18 s per projection for stress, and 24 s per projection for redistribution per angle step. The detector collected data from the 45 right anterior oblique to the 45 left posterior oblique position. Images were reconstructed using the filter back-projection method and a Butterworth filter. Background subtraction and attenuation correction were not used. In the SPECT image interpretation analysis, we divided the short axis views into fifteen segments, the vertical long axis views into seven segments, and the horizontal long axis views into seven segments. A three-dimensional display was also used to assist in interpretation. In addition, a polar map (bull s eye) analysis of the counting rate density was displayed to compare stress and redistribution slices. Two nuclear medicine physicians using visual inspection analysis independently interpreted all images. The severity of perfusion defects is assessed using a semiquantitative visual scoring system: 0 = normal, 1 = mildly reduced or equivocal, 2 = moderately reduced, 3 = severely reduced. Computer quantification of circumferential count distribution profiles provides a means of quantifying precisely the extent (the number of angles below the lower limit) and the severity (area below the lower limit) of a perfusion defect. This measurement can be expressed as an integrated defect score. Perfusion defects seen at the stress image study, which recovered at the delay image study stage, were accordingly defined as reversible perfusion defects (R). A partial reversible perfusion defect (PR) was considered to be present if defects did not completely recover at the redistribution stage. Those with normal uptake of stress which decreased on delay imaging were defined as reverse redistribution defects (RR). Results All 63 patients experienced chest discomfort (chest tightness and/or chest pain) in clinical situation. CAG in all 63 patients also revealed evident MB (Figure 1). Fifty patients had MB in LAD (40 at mid portion; 8 at distal portion; 2 at mid and distal portion), 4 in LCX, and 1 in RCA. 7 patients had MB in both LAD and LCX and 1 patient in both LAD and RCA (Table 2). Sixty patients (95%) had evident Tl imaging perfusion defects (R, PR, or RR). The distribution and severity of perfusion defects and localization of MB are listed in Table 3. In all the abnormal SPECTs, 103 abnormal perfusion lesions included 57 R (55%), 40 PR (39%), and 6 RR (6%). In all vessels with MB, 48 of 58 (83%) in LAD could see Tl perfusion defects in anterior, septal, and/or apical areas. In addition, 6 of 11 (55%) vessels with MB in LCX could detect Tl perfusion defects in lateral or inferior areas, and 2 of 2 (100%) in RCA could detect Tl perfusion defects in inferior areas. The representative images of MB displayed by perfusion SPECTs and polar maps and their corresponding coronary angiography in systolic and diastolic phases were shown in Figures 2 and 3. Discussion The mechanism of myocardial bridge induced is an interesting issue. As we know, coronary perfusion occurs in Figure 1. Relationship between treadmill exercise test and Tl in patients underwent treadmill- Tl or dipyridamole- Tl Table 2. Locations of myocardial bridge LAD 50 LAD-M 40 LAD-D 8 LAD M+D 2 LCX 4 RCA 1 LAD and LCX 7 LAD and RCA 1 LAD: left anterior descending artery; LCX: left circumflex artery; RCA: right coronary artery; M: middle portion; D: distal portion 2005;18:

4 Chiu CZ et al Table 3. Localization of myocardial bridge (MB) and characteristics of Tl Patients No Myocardial Bridge Tl Imaging Findings 1 LAD-M Ant, Sep; R 2 LAD-M Sep, Inf; PR 3 LAD-M Sep, Api; PR 4 LAD-M Inf; PR 5 LAD-M Sep; R 6 RCA-D Sep, Inf; PR 7 LAD-M normal 8 LAD-D Ant; R, Inf; PR 9 LAD-M Inf; R 10 LAD-D Inf-post; PR 11 LAD-M Ant; R 12 LAD-M, D Sep, Inf; R 13 LAD-M Ant, Sep, Api; R 14 LAD-M Sep; R, Inf; PR 15 LAD-M Ant; PR, Sep; R 16 LAD-D Sep, Inf; PR 17 LAD-M, LCX-M Inf; PR 18 LAD-M Ant; RR, Inf, Lat; R 19 LAD-M Ant, Inf; R 20 LAD-M Inf; PR 21 LAD-M Sep, Inf; PR 22 LAD-D Ant; R 23 LAD-M Sep, Inf; R 24 LAD-M Ant, Sep; R 25 LCX-M normal 26 LAD-M Ant; R, Lat; RR 27 LAD-M Sep, Inf; R 28 LAD-M Ant; R 29 LAD-M Lat; R 30 LAD-D Ant, Sep; R, Api; PR 31 LAD-M Ant; R 32 LCX-M normal 33 LAD-M Ant, Sep, Api; R 34 LAD-D Ant; PR 35 LAD-M Ant, Sep; RR 36 LAD-D Inf; PR 37 LAD-M Ant; R, Inf; RR 38 LAD-M Api, Inf; R 39 LAD-M; LCX-D Ant; RR; Lat; R 40 LAD-M Inf; PR 41 LAD-D Ant; PR 42 LAD-M Ant, Inf, Lat; R 43 LAD-M, D; LCX-M Sep; R, Lat; PR 44 LAD-M, RCA-M Ant, Sep, Inf; PR 45 LAD-M Sep, Api; R 46 LAD-M, LCX-D Ant; R 47 LAD-M Sep, Api; R, Inf; PR 48 LAD-M Inf; PR 49 LAD-M Sep; R, Inf; PR 50 LAD-M, D Inf, RR; Api, PR 51 LAD-M Ant, R 52 LCX-M Lat, Api, PR 53 LCX-M Ant, PR 54 LAD-M, LCX-M Inf, R; Api, PR 55 LAD, LCX Ant, Inf; R 56 LAD-M Inf, Api; R 57 LAD-M Sep, Inf; PR 58 LAD-M Ant, Api; R 59 LAD-M, LCX-M Api; PR 60 LAD-M Ant; R 61 LAD-M Sep, Api; PR 62 LAD-M Sep, Inf; R 63 LAD-M Ant, PR; Lat, R Ant: anterior; Sep: septal; Api: apical; Inf: inferior; Lat: lateral; Post: posterior; R: reversible; PR: partial reversible; RR: reverse redistribution diastolic phase of cardiac cycle and myocardial bridge only causes narrowing of partial segment of coronary artery during systolic phase. Previous studies stated that there is not only systolic luminal diameter reduction in the MB segment, but also persistent reduction in diastolic diameter with delayed relaxation in diastole. Early diastolic coronary flow may also decrease in patients with MB [10,11]. It is the reason why MB can also induce myocardial ischemia and clinical symptoms and/or signs of CAD. Other study postulated that endothelial damage in MB may result in vasospasm or thrombus formation. Endothelial dysfunction is a major contributor to the initiation, progression, and clinical complications of atherosclerotic disease [12]. MB can become more severe in some situations, such as rapid heart beats, exercise, or the use of nitroglycerin [13-15]. Previous reports showed high incidence of MB in LAD. In our series, 90% (57/63) of MB occurs in LAD. In rare situation MB can be also detected in LCX and RCA. In our study, 95% (60/63) of patients had different patterns (R, PR, or RR) of perfusion defects in Tl imaging. R and PR represent different severity of myocardial ischemia induced by stress agent or test, and total or partial reverse of the ischemia after recovery of stress. RR is a more complex situation, defined as worsening of a perfusion defect during redistribution phase and its clinical significance is still controversial. It may be served a sign of myocardial viability, namely a previously damaged area with Ann Nucl Med Sci 2004;18:9-16 Vol. 18 No. 1 March

5 Tl manifestations in patients with myocardial bridge Tl A B A B C C D D Figure 2. (A) Coronary angiography in right anterior oblique (RAO) view shows systolic narrowing of middle portion of left anterior descending (LAD) artery (thin black arrow) in a patient with myocardial bridge (MB) in LAD. (B) Diastolic phase of coronary angiography shows patent coronary artery (thick black arrow) without MB. (C) Polar maps (bull s-eye display) shows perfusion defect in LAD territory. (D) Tl perfusion imaging shows partial reversible (PR) perfusion defect in anterior and septal areas. Figure 3. (A) Coronary angiography in true lateral view shows systolic narrowing and myocardial bridge in middle portion of LAD (thin black arrow). (B) Diastolic phase in the same patient shows patent coronary artery without myocardial bridge (thick black arrow). (C) Polar maps (bull s-eye display) shows perfusion defect in LAD territory. (D) Tl perfusion imaging shows reversible (R) perfusion defect in anterior and septal areas. some myocardial necrosis but with reserved perfusion. The jeopardized myocardial cells may have transient Tl uptake but not prolonged uptake over 4 h. In our study, 94% of patients had R or PR phenomenon, which may represent real myocardial ischemia in areas of perfusion defects. 6% of patients had RR perfusion defects, which may be due to the so called jeopardized phenomenon [16,17]. As we know, different areas of perfusion defects may imply myocardial ischemia in different coronary artery. In our study, 83% of patients with MB in LAD had perfusion defects in anterior, septal, and/or apical areas. 55% of patients with MB in LCX had perfusion defects in lateral and inferior areas, and 100% 2005;18:

6 Chiu CZ et al of patients with MB in RCA had perfusion defects in inferior area. So we think that there was high correlation between the coronary arteries with MB and their perfusion defects in LAD and RCA territories. However, some perfusion defects not correlated with coronary artery with MB may be associated with the location (proximal, middle, or distal), severity (length and/or percentage of diameter reduction during systole), artifact imaging in Tl looking like perfusion defect, or bias in the interpretation of Tl between investigators. Myocardial dysfunction induced by MB may be exacerbated by exercise or pharmacological (dobutamine) stress with abnormal regional wall in left ventricle detected by stress echocardiography [18]. So, further study using such as gated SPECT with 99m Tc-sestamibi perfusion agent to detect wall motion and ejection fraction in left ventricle may be worthwhile. Dobutamine stress echocardiography (DSE) may also be used as a tool to detect left ventricular function and wall motion abnormality, and to do a comparison with the results of 99m Tc-sestamibi SPECT [19,20]. Conclusion Myocardial ischemia with abnormal Tl perfusion image can be detected in most patients with MB. MB with ischemic evidence in Tl perfusion image may be also associated with chest pain and/or chest tightness in our patients. According the positive Tl findings in MB, we can conclude that MB can cause the same symptoms and/or signs like coronary artery stenosis. Tl perfusion defects in patients with MB may be presented as R, PR, or RR pattern. References 1. Angelini P, Trivellato M, Donis J, Leachman RD. Myocardial bridges: a review. Prog Cardiovasc Dis 1983;26: Kramer JR, Kitazume H, Proudfit WL, Sones FM Jr. Clinical significance of isolated coronary bridges: benign and frequent condition involving the left anterior descending artery. Am Heart J 1982;103: Lauer WJ, Carlson TA. Images in cardiovascular medicine. Myocardial bridging. Circulation 1998;98: Mehra MR. Crossing the vasculopathy bridge from morphology to therapy: a single center experience. J Heart Lung Transplant 2000;19: Kalaria VG, Koradia N, Breall JA. Myocardial Bridge: a clinical review. Catheter Cardiovasc Interv 2002;57: Ortega-Carnicer J, Fernandez-Medina V. Impending acute myocardial infarction during severe exercise associated with a myocardial bridge. J Electrocardiol 1999;32: Morales AR, Romanelli R, Boucek RJ. The mural left anterior descending coronary artery, strenuous exercise and sudden death. Circulation 1980;62: Agirbasli M, Martin GS, Stout JB, Jennings HS 3rd, Lea JW 4th, Dixon JH Jr. Myocardial bridge as a cause of thrombus formation and myocardial infarction in a young athlete. Clin Cardiol 1997;20: de Winter RJ, Kok WE, Piek JJ. Coronary atherosclerosis within a myocardial bridge, not a benign condition. Heart 1998;80: Ishii T, Asuwa N, Masuda S, Ishikawa Y. The effects of a myocardial bridge on coronary atherosclerosis and ischaemia. J Pathol 1998;185: Berry JF, von Mering GO, Schmalfuss C, Hill JA, Kerensky RA. Systolic compression of the left anterior descending coronary artery: a case series, review of the literature, and therapeutic options including stenting. Catheter Cardiovasc Interv 2002;56: Kuhn FE, Reagan K, Mohler ER 3rd, Satler LF, Lu DY, Rackley CE. Evidence for endothelial dysfunction and enhanced vasoconstriction in myocardial bridges. Am Heart J 1991;122: Ahmad M, Merry SL, Haibach H. Evidence of impaired myocardial perfusion and abnormal left ventricular function during exercise in patients with isolated systolic narrowing of the left anterior descending coronary artery. Am J Cardiol 1981;48: Masuda T, Ishikawa Y, Akasaka Y, Itoh K, Kiguchi H, Ishii T. The effect of myocardial bridging of the coronary artery on vasoactive agents and atherosclerosis localization. J Pathol 2001;193: Hongo Y, Tada H, Ito K, Yasumura Y, Miyatake K, Yamagishi M. Augmentation of vessel squeezing at coronary-myocardial bridge by nitroglycerin: study by quan- Ann Nucl Med Sci 2004;18:9-16 Vol. 18 No. 1 March

7 Tl manifestations in patients with myocardial bridge Tl titative coronary angiography and intravascular ultrasound. Am Heart J 1999;138: Takeishi Y, Sukekawa H, Fujiwara S, Ikeno E, Sasaki Y, Tomoike H. Reverse redistribution of technetium-99msestamibi following direct PTCA in acute myocardial infarction. J Nucl Med 1996;37: Faraggi M, Karila-Cohen D, Brochet E, et al. Relationship between resting Tl reverse redistribution, microvascular perfusion, and functional recovery in acute myocardial infarction. J Nucl Med 2000;41: Mouratidis B, Lomas FE, McGill D. Thallium- myocardial SPECT in myocardial bridging. J Nucl Med 1995;36: Buell U, Dupont F, Uebis R, et al. 99 Tc m -methoxyisobutyl-isonitrile SPECT to evaluate a perfusion index from regional myocardial uptake after exercise and at rest. Results of a four hour protocol in patients with coronary heart disease and in controls. Nucl Med Commun 1990;11: Rivitz SM, Yasuda T. Predictive value of dipyridamole thallium imaging in a patient with myocardial bridging but without fixed obstructive coronary artery disease. J Nucl Med 1992;33: ;18:

8 Chiu CZ et al (myocardial bridge; MB) (coronary angiography; CAG) / ( ± ) 6 57 dipyridamole ( ) (95%) - (reverse [R], partial reverse [PR], or reverse redistribution [RR]) - SPECT R (55%) 40 PR (39%) 6 RR (6%) 83% (48/58) 55% (6/11) 100% (2/2) R PR RR R PR RR ;18: (02) (02) juice243@hotmail.com Ann Nucl Med Sci 2005;18:9-16 Vol. 18 No. 1 March