Thallium and indium antimyosin dual-isotope single-photon emission tomography in acute myocardial infarction to identify patients at further ischaemic risk

European Journal of

Nuclear Medicine Original article

Thallium and indium antimyosin dual-isotope single-photon emission tomography in acute myocardial infarction to identify patients at further ischaemic risk Heiko Schoeder ~, Hubert Topp 2, Michael Friedrich 1, Annegret Jatzkewitz 1, Martin Roser 2

1 Department of Radiology/Nuclear Medicine, Urban Hospital Berlin, Berlin, Germany 2 Department of Cardiology, Urban Hospital Berlin, Berlin, Germany

Received 12 June and in revised form 15 December 1993

Abstract. Dual-isotope single-photon emission tomography (SPET) with indium-111 antimyosin and thallium- 201 chloride was performed in 54 patients with acute myocardial infarction (AMI) to detect the location and extent of myocardial necrosis (antimyosin) and viable myocardium (2°1T1). All patients underwent intravenous thrombolytic therapy with either streptokinase (1.5 million units/90 rain) or tissue plasminogen activator (80 rag/90 rain). Sensitivity in detecting MI was 91% (49/54 patients). With regard to dual-isotope SPET patterns, patients were devided into three groups: match, i.e. antimyosin uptake in segments with thallium defect (n = 8); mismatch, i.e. no uptake of either of the nuclides in corresponding segments (presence of perfusion abnormalities in the absence of antimyosin uptake) (n = 5); and overlap, i.e. thallium uptake in segments with uptake of antimyosin (n = 41). Coronary angiography and thallium exercise tests were performed in 40 and 45 patients, respectively, 5-14 days after MI. Exercise-induced ischaemia occurred in 66% of patients with overlap, 14% with match and 0% with mismatch (P <0.05 for overlap vs other groups). If, however, major in-hospital complications (sudden cardiac death, severe arrhythmias; five overlap, three overlap in addition to match/mismatch, two match, two mismatch) were included in the statistical analysis, there was no significant difference between the three groups (P = NS). Thus, although the dual-isotope pattern "overlap" identifies a subgroup of patients with a substantial amount of residual viable tissue after MI and a high probability of exercise-induced ischaemia, this criterion is of limited value in assessing short-term prognosis. Nevertheless, in cases of doubt it may help to decide which patients should undergo coronary revascularization.

Correspondence to: H. Schoeder, Department of Radiology/Nu- clear Medicine, Krankenhaus Am Urban Berlin, D-10967 Berlin, Germany

Key words: Double-nuclide single-photon tomography - Indium-111 antimyosin - Thallium-201 chloride - Acute myocardial infarction - Ischaemic risk

Eur J Nucl Mcd (1994) 21:415-422

Introduct ion

Today intravenous thrombolytic therapy is the treatment of choice for patients with acute myocardial infarction (AMI) [14] . However, the role and timing of percutane- ous transluminal coronary angioplasty (PTCA) in these patients are still under discussion [5-11]. Therefore it seems necessary to identify those patients who are at higher risk for further in-hospital ischaemic events at an early juncture, when exercise testing or pharmacological stress testing cannot yet be performed.

Antimyosin is a Fab fragment of a murine monoclonal antibody. Injected intravenously it binds to human myosin which is exposed after irreversible damage of myocytes due to ischaemia [12, 14]. If labelled with ra- dioisotopes [13, 14], areas of myocardial necrosis may be evaluated with nuclear imaging. Radiolabelled antimyosin antibodies have been used for detection of myocardial necrosis in patients with myocarditis [15, 16], cardiomyopathy [ 17] and myocardial infarction [ 18-22] as well as for detection of transplant rejection [23]. Pre- vious studies have shown that myocardial infarct size can be accurately estimated from antimyosin planar [20, 21] and single-photon emission tomography (SPET) studies [12, 14, 18, 22] with high sensitivity and specificity. A large multicentre trial [19] confirmed the latter preliminary results. In addition, it has been shown that immunoscintigraphy with antimyosin is able to confirm an MI in the absence of ECG changes [22, 23].

The aim of the present study was to evaluate (1) whether there is a clear correlation between the presence

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of an area at risk as shown by dual-isotope SPET and short-term prognosis and (2) whether dual-isotope imaging would aid in the se lect ion of further therapeut ic ap- p roaches for pat ients with AMI .

Materials and methods

Patient selection. Fifty-four patients with AMI were studied. En- trance criteria included chest pain >30 min, 12-lead ECG with ST elevation of >0.2 mV in at least two leads and typical enzyme ele- vations [creatine kinase (CK) >300 U/l]. All patients underwent intravenous thrombolytic therapy with either streptokinase (SK; 1.5 million U/1 h) or tissue plasminogen activator (tPA; 100 mg/90 min) 1-6 h after infarct onset.

The patient group consisted of 36 men and 18 women with a mean age of 54 years (28-83 years). The acute infarct location, proven by ECG, was anterior in 28 and posterior or inferoposteri- or in the remaining 26. Twenty-one of the 54 patients had a Q-wave MI. Three patients had had a previous MI in other segments, 1-2 years earlier (dual-isotope findings in those segments were ignored in the statistical analysis). No patient had un- dergone a previous study with monoclonal antibodies. Informed consent to participation in the study was obtained from all patients.

Antibody preparation. Myoscint (Centocor, Leyden, The Nether- lands) is a murine monoclonal antibody fragment (0.5 mg in a sterile, pyrogen-free solution) conjugated with diethylene triamine penta-acetic acid. For radiolabelling the antibody solution was mixed with indium-111 chloride (Amersham, Braunschweig, Ger- many) and incubated at room temperature for about 15 rain. Thin- layer chromatography showed the binding rate to be more than 93%. 80-100 MBq indium antimyosin was injected intravenously 3-7 (mean 5) days after MI.

Imaging. Forty-eight hours after intravenous administration of 11~In antimyosin patients were brought to the Department of Nu- clear Medicine and injected with 80-100 MBq thallium-201 chloride. Myocardial dual-isotope SPET was performed 10-15 min later. An APEX 409-A ECT camera (Elscint, Haifa, Israel) with a special medium-energy collimator (Mullekom, Nuclear Fields, The Netherlands) was used and three energy peaks were selected: 69 keV for 2°1T1, and 172 keV and 245 keV for rain, all peaks having a low- and a high-energy window of 15%. Matrix size was 64 x 64. Data acquisition was performed from 60 ° RAO to 120 ° LPO in steps of 6 ° with an acquisition time of 60 s per step. The total count number was about 10 million in each study. The whole ECT procedure took approximately 40 min.

A Hanning filter was used for filtered backprojection and short and long (horizontal and vertical) axis slices with a slice thickness of two pixels were reconstructed. Phantom studies had shown an energy cross-over of 12% from 2°1T1 into II~In windows and vice versa.

Data analysis. Twelve representative slices (four from each slice direction) were chosen for data analysis and divided into segments in a clockwise direction as follows: horizontal long slices: septal, anterior, lateral; vertical long slices: anterior, apical, posterior; short axis: anterior, anterolateral, posterolateral, posterior, poste- roseptal, anteroseptal. All images were read by two independent observers, with an interobserver agreement of 94%. The following classification was used [25]: match: antimyosin uptake in seg-

ments with thallium defect; mismatch: no uptake of either of the nuclides in corresponding segments, i.e. presence of perfusion abnormalities in the absence of antimyosin uptake; overlap: thallium uptake in segments with uptake of ~ In antimyosin. Regions with overlap were defined as myocardium at risk.

In addition to localization, intensity of uptake was evaluated with a semiquantitative index from 1+ to 3+, in which 1+ was faint uptake and 3+ an uptake equal to or higher than hepatic activity. In cases in which the opinion of the two observers differed, an agreement was reached. This was most frequently the case in patients with only faint uptake of antimyosin (1+), who were then classified as mismatch.

In a large previous study [24] no human anti-mouse antibodies (HAMA) could be found in 125 serum samples from 50 patients. Therefore we did not perform serum analysis to detect levels of HAMA. In our study there were no adverse effects strictly related to antimyosin injection.

Exercise test. Of the 54 patients, 45 underwent a ;°XT1 bicycle exercise test. The test was performed 10-23 (mean 14) days after MI. Patients were injected with 80-100 MBq 2°lT1 chloride at peak heart rate. Care was taken to reach submaximal heart rate (85% of age-predicted maximal heart rate) to improve image quality and to avoid misinterpretation. End-points other than heart rate included severe angina or excessive dyspnoea and significant arrhythmias. The SPET studies were performed 5-10 rain and 5 h later. Image analysis was based on visual interpretation of images and lung uptake as well as bull's eye quantification and washout analysis.

Coronary angiography. Selective coronary angiography using the Seldinger technique was performed in 40 patients. Coronary an- giograms were interpreted by two experienced observers without knowledge of the scintigraphic results. Coronary artery stenosis was assessed semiquantitatively and expressed as percent lumen diameter stenosis. Additionally, five patients without significant coronary artery stenosis underwent an ergonovine test to provoke coronary vasospasm.

Statistical analysis. Statistical analysis of the data sets was performed using the chi-square test. A P value of less than 0.05 was considered to indicate statistical significance.

Results

Accuracy

Twenty-one pat ients had a Q-wave and the remain ing 33 pat ients a non-Q wave MI. Of the 54 pat ients , 49 showed clear an t imyos in uptake (sensi t ivi ty 91%).

The remain ing five pat ients showed only b lood pool act ivi ty or faint uptake and were c lass i f ied as mismatch . In these cases there was a clear (a l though s ta t is t ical ly not s ignif icant) corre la t ion be tween negat ive scan and infarct locat ion: four of these five pat ients had an infer ior M I with the r ight coronary ar tery (RCA) or lef t c i r cumf lex ar tery (LCX) as the in fa rc t - re la ted artery.

None of the three pat ients with previous M I ( 1 - 2 years ear l ier) showed an t imyos in uptake in the re la ted segments .

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Table 1. Dual-isotope uptake in relation to MI

Pattern Anterior MI Posterior MI Q-wave MI*

Overlap 11 11 10/22 True overlap 10 9 3/19 Match 6 2 5/ 8 Mismatch 1 4 3/ 5

Values are numbers of patients "P=NS

Uptake patterns

Using the three categories of uptake, eight patients showed match (Fig. 1), five mismatch and 41 an overlap of thallium and Hqn antimyosin. Patients with overlap were further divided into two subgroups: 19 of the 41 showed "true" overlap (Fig. 2), which means there was overlap in all corresponding segments with an intensity of thallium and antimyosin uptake of 2+ or 3+. The remaining 22 patients of this group had matched or mismatched segments in addition to a large number of segments with overlap. More detailed data are provided in Tables 1-3.

There was no significant difference in mean CK levels between the three groups. The only significant difference was related to the subgroup with "true overlap": (1)

Fig. 1. Patient with anterior wall MI. Match of antimyosin (red, anterior and apical wall) and 2°IT1 (white)

Fig. 2a-c. Patient with anterior wall MI. a Short and long axis slices for 2°1T1 from the dual-isotope SPET study, b Same slices showing antimyosin only. e Overprojection of a and b shows "true" overlap of 2°~T1 and t l l i n antimyosin

significantly more patients than in any other gorup had a small MI (CK <500 U/l), (2) consequently, this subgroup showed significantly lower mean CK values, and (3) only three of the 19 patients had a Q-wave MI.

Coronary angiography and revascularization

Forty patients underwent coronary angiography 1-22 days after MI with a mean interval of 10 days between angiography and antimyosin scan. Seven of them had three-vessel disease. In general, there was no significant correlation between the dual-isotope scan pattern and coronary collateral status or infarct-related artery. [Four- teen patients did not agree or were not able to undergo angiography (due to clinical course) at this point in time.]

Two of the five patients who underwent an ergonovine test showed coronary vasospasm in the absence of any significant stenosis. One patient (CKma x 1260 U/I) had a mismatch pattern in the dual-isotope study. She died 4 months later due to cardiogenic shock. The other patient showed 2°1T1 IHIn antimyosin overlap in the lateral and posterolateral wall. During a thallium exercise stress test 12 days later the pattern of non-transmural MI without redistribution could be detected.

Twelve patients with higher risk for further ischaemic


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Table 2. Dual-isotope patterns in relation to CK values, exercise testing and 2°IT1 redistribution

Pattern Mean CK Patients with Exercise test values CKma x < 5 0 0 performed

2O1T1 redistribution

(n) (n)

Overlap 1195 4 18/22 12"*

True overlap 650 12" 16/19 6**

Match 1081 2 7/ 8 1/7

Mismatch 1026 1 4/ 5 0/4

CK values in U/1 * P <0.01 for number of patients with CKmax <500 U/1 in comparison to other groups

** P <0.05 vs match and mismatch

Table 3. Uptake patterns in patients with major complications (n = 12)

Pattern No. True overlap 5 Overlap and match/mismatch 3 (1 death) Match 2 (1 death) Mismatch 2

For definition of major complications, see Results

events, including re-infarction (based on clinical parameters and echo-/angiographic data), were diverted to revascularization procedures: eight patients underwent PTCA [four, left anterior descending artery (LAD); two RCA; one LCX; one, PTCA of a venous graft]. There were no major complications due to PTCA. Four patients underwent a coronary artery bypass graft (CABG) procedure between 3 and 5 weeks after MI.

Exercise testing and risk stratification

Forty-five patients underwent a thallium bicycle exercise test. Twenty-two showed thallium redistribution; 18 of them had an overlap and one had a match in the dual- isotope study. The remaining three patients (match or mismatch pattern) showed ischaemia in other vascular territories (Fig. 3a).

For statistical analysis, 2°~T1 redistribution in vascular territories not related to the AMI and dual-isotope pattern was excluded (Fig. 3b). Thus, considering exercise- induced ischaemia in only the acutely infarcted and adjacent myocardial segments (n = 19), 18/19 patients with 2°lT1 redistribution showed overlap in the dual-isotope study. On the other hand, 16 of 26 patients without thallium redistribution also showed overlap of thallium and antimyosin (Fig. 3b).

Ten patients did not undergo the exercise test: two

due to deaths (one match, one overlap), five with unstable angina, heart failure or third-degree valve disease (four overlap, one mismatch) and three due to other causes (all three with overlap).

Major complications (re-infarction, asystole, ventricular fibrillation, postinfarct angina) occurred in 12 patients. Eight of them had a scan pattern of either overlap or overlap in addition to matched/mismatched segments (Table 3). Two subjects died during their hospital stay, both due to cardiogenic shock (one match, one overlap).

Risk stratification with reference to antimyosin uptake showed the following results: of 41 patients with overlap, 34 underwent exercise testing, 53% (18/34) with and 47% (16/34) without thallium redistribution in corresponding segments. Four of five patients with mismatch underwent exercise testing; none of them showed ischaemia in mismatched segments but two had ischaemia in adjacent segments. Exercise testing was also performed in seven of eight patients with match, one of whom showed thallium redistribution. In addition, two patients demonstrated ischaemia in segments adjacent to areas with match (Table 2).

In summary, patients with overlap of 2°1T1 and l~lIn antimyosin significantly more often showed exercise-induced ischaemia than those of the other subgroups (P < 0.05; Fig. 3). If, however, major complications are included in this statistical analysis, there is no significant difference between the three patient groups, as is shown in Fig. 4.

Discussion

False-negative studies

Small inferior MI and high residual blood pool activity have been discussed as possible reasons for false-negative antimyosin studies [14, 24, 25]. Although our SPET studies were performed 48 h after antibody injection, all


A

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70

60

50

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419

16 overlap

4 mismatch

6 match

18 overlap

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I s c h e m i a 19

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/ 111~.;.~11 ii~,i b l i ~ . a ;. CJ.i G V ;~ i i ;~ . . ; tl~¢ ~ i i a i 3 / i i i ~ i i i i l l

Fig. 3a,b. Exercise-induced ischaemia in relation to dual-isotope patterns (only segments with overlap, match and mismatch included) (P <0.05 for overlap vs match/mismatch)

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80

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1i3

five patients without antimyosin uptake showed high residual blood pool activity. Their maximum CK values were between 350 and 1260 U/1. Four of these five patients had an inferior/posterior MI with the RCA as the infarct-related artery. Two patients had significant collateral vessels. Another patient had a patent infarct-related RCA and no collateral vessels. During angiography with ergonovine testing performed 9 days after MI (i.e. 3 days after dual-isotope study) he developed a coronary vasospasm. Therefore a vasospasm or thrombotic artery occlusion with subsequent thrombolysis (either spontane- ously or due to treatment) might have been the cause of MI in this patient.

Lack of collateral vessels and/or persistent occlusion of the infarct-related artery may also cause false-negative studies [14, 24, 25]. In this study, however, there was no correlation between antimyosin uptake and vessel patency or collateral status.

Dual-isotope studies

Some reports on dual-isotope imaging with 2°1T1 and ~11In antimyosin have been published [12, 19, 20, 25, 26].

Scanning techniques and interpretation of distribution patterns

Some remarks are necessary with respect to the study by Johnson et al. [25], to our knowledge one of the largest studies dealing with the same topic and performed in one centre: Our dual-isotope SPET scanning technique yielded excellent image quality in most patients. This rules out the possibility that technically inadequate scans were the reason for lack of antimyosin uptake in five patients. Superior image quality was related to the use of three energy peaks (instead of the two peaks used by Johnson et al. [23]) and a special medium-energy collimator. The better count statistics (mean total count 10 million in our study) contribute to superior image quality. Furthermore, only 26 of 42 patients of Johnson's study population underwent coronary angiography, either during their hospital stay or within 6 weeks (in comparison to 40 of 54 in our study, all within 3 weeks after MI). It is well known that spontaneous thrombolysis occurs in a high percentage of patients with AMI. Therefore results of coronary angiography performed 6 weeks after MI cannot be correlated with dual-isotope scan patterns obtained some days after MI.

In this initial study Johnson et al. [25] found the following uptake patterns: match (n = 14), mismatch (n = 23), overlap (n = 5). In a recent study [26] these authors reported on a larger study group of 87 patients. In accordance with their basic concept (mismatch and overlap as indicators for higher ischaemic risk), patients were again classified as follows: 28 match, 59 mismatch and/or


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overlap. A subanalysis of the latter group demonstrates that only ten patients had an overlap pattern ("true" overlap in our terms). This is quite different from our results (41 patients; see Results section). However, there is a simple explanation for this difference: Only 10 of 87 patients in Johnson's study received thrombolytic therapy; CKma x or other parameters to (semi)quantify infarct size are not reported. In accordance with our more aggressive treatment and due to the fact that most patients with AMI had arrived in the coronary care unit within 6 h, they all received thrombolytic therapy. SK or tPA infusion were started 0.2-12 (mean 2.7) h after MI. Thrombolytic therapy shortens the time to reperfusion and therefore reduces myocardial infarct size [2, 3, 27, 28]. Therefore in our study there were a considerable number of patients with smaller MI (CKma x < 500 U/l). In addition, since AMI is a dynamic process [29-31], most patients in this study (following early thrombolytic therapy) showed overlap of 2°~T1 and antimyosin (i.e. disseminated or non-transmural instead of transmural MI).

Risk stratification

Ischaemia in the border zone of an MI (the area at risk) may lead to electrical instability [31]. In patients with an overlap of 2°IT1 and antimyosin, areas of myocardial necrosis are mixed with still viable tissue. It was the aim of this study to evaluate whether this residual viable myocardium is at higher ischaemic risk due to possible re- occlusion of an infarct-related artery with subsequent infarct expansion. In addition, one would expect such patients to be at a higher risk of other ischaemic events, e.g. severe ventricular arrhythmias. If this is the case, dual-isotope imaging would be a method to identify such a high-risk subgroup at an early stage.

In our study there were 41 patients with overlap; 34 of them underwent exercise testing and 53% showed thallium redistribution in corresponding segments. In comparison, only one of 13 patients with either match or mismatch showed ischaemia in those segments (P < 0.05 for overlap vs match and mismatch; Fig. 3b).

Of the nine subjects not undergoing exercise testing, seven showed overlap of 2°1T1 and antimyosin. Probably exercise-induced ischaemia would have been present in most of these patients; exercise tests were not done because of their unstable coronary status. If, however, major complications (Table 3) are included in the statistical analysis in addition to thallium redistribution, significant differences are no longer present between the three patient groups (Fig. 4). In addition, the majority of this study population (following thrombolytic therapy) showed overlap of 2°1T1 and antimyosin, approximately 50% of them without thallium redistribution in the exercise study. Thus, the question remains as to who are the subjects at higher ischaemic risk in whom early angiography and revascularization should be performed. Nev-

ertheless, the results confirm our working hypothesis, i.e. that early thrombolytic therapy and coronary artery recanalization produce more patients with non-transmural MI but residual myocardial ischaemia.

Some other attempts have been made to perform a risk stratification of post-AMI patients with antimyosin. In planar antimyosin studies, van Vlies et al. [21] used a count density index (CDI; infarct zone of the heart/left lung). They found a direct correlation between CDI and regional wall motion abnormalities at hospital discharge: patients with only mild regional akinesia had a significantly lower CDI than those with severe akinesia [21]. Recently, Senior et al. [32] studied 29 patients with AMI using a new 99mTc antimyosin Fab complex in comparison to rain antimyosin. The question of which radionuclide would be the ideal one for antimyosin imaging is beyond the scope of this article. This paper [32], however, is of interest because the authors performed antimyosin radionuclide ventriculography (A-RNV), as in their earlier studies [19, 20]. They reported eight patients with wall motion abnormalities in the A-RNV beyond the area of Fab uptake. Although A-RNV seems to be a uni- que method for obtaining additional information (probably also with regard to prognosis), we think it is too early to define myocardial stunning only on the basis of these authors' results.

Knapp et al. [33] have also tried to differentiate between patients with AMI and stunned or hibernating myocardium using 99mTc-methoxyisobutylisonitrile/111In antimyosin dual-isotope imaging.

Limitations

The question arises as to why nearly 50% of patients with the overlap scan pattern did not show a thallium defect in the exercise study. There are two possible reasons: (1) Some patients had only small non-transmural MI and recanalized infarct arteries (in addition, one patient underwent exercise testing only a few days after emergency PTCA); thus, small areas of necrosis might have been masked by a large amount of viable myocardi- urn. (2) Thallium re-injection was not routinely performed in these patients. It has been shown that conven- tional thallium exercise studies (stress imaging, redistribution imaging 3-4 h later) are often inaccurate in dif- ferentiating ischaemic but still viable myocardium from scar [34-40]. Some studies have demonstrated a normali- zation of thallium uptake after re-injection [34, 38, 40] and an improvement in regional wall motion in segments with "irreversible" thallium defects after revascularization [39].

Certainly, routine thallium re-injection would have determined exercise-induced ischaemia in a subset of those patients who demonstrated no thallium redistribution in the 3-h imaging. However, in accordance with the relevant guidelines [41, 42], this procedure was performed in only two patients because of discordance be-


tween (a) coronary angiography and dual-isotope SPET pattern and (b) results of thallium exercise study. Both patients had a further, significant fill-in of 2°~T1 after reinjection.

Some groups have tried to quantify the amount of myocardial necrosis: heart-lung ratio, for example, is a simple method and yields semiquantitative information [15, 17, 21]. Others have tried to quantify the amount of necrotic tissue in grams [22]. Of course, patients with a larger MI have a worse prognosis. However, it still has to be determined whether quantification of necrotic tissue yields new information in comparison to the traditional methods and whether it should have any influence on further treatment.

Although prolonged uptake and localization of antimyosin weeks to months after MI have been reported [43], this phenomenon is insignificant in our study due to the fact that most patients had no previous MI and three patients with prior MI (in other segments) showed no antimyosin uptake in those segments.

Clinical implications: Which patients are candidates for revascularization ?

Any revascularization is only indicated in patients with a significant amount of ischaemic (still viable) myocardium. Today thallium scintigraphy with re-injection remains the easiest and a cost-effective method of detecting viable myocardium [34, 41, 42]. Dual-isotope imaging, on the other hand, is far from being a universal approach to answer this question. The potential advantage of this method lies in its potential to clearly define areas of necrosis and viable myocardium that is not stunned or hibernating [33]. This additional information may help to define at an early stage the best treatment strategy in some patients with AMI. Thus, in patients with significant coronary artery stenosis and large overlap of thallium and antimyosin, a more aggressive approach would be preferable, whereas a more conservative form of management would be indicated in patients with match of 2°1T1 and antimyosin. The same would apply to patients with coronary artery stenosis of doubtful significance: if PTCA is associated with higher risk (due to localization and distance of the lesion) and dual-isotope imaging shows only match (necrosis) in the related segments, conservative management should be implemented.

The study reported here is being continued. It still has to be established in how many patients with AMI dual- isotope SPET provides significant additional information with regard to prognosis and further therapy.

Conclusion

1. The advantages of myocardial dual-isotope SPET in- clude (a) clear anatomical orientation, (b) SPET studies can be performed in a reasonably short time, i.e. about

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40 rain, (c) detection of overlap between thallium (showing viable myocardium) and rain antimyosin (as an indi- cator of myocardial necrosis). 2. Thus, this procedure may allow earlier stratification of patients into subgroups. With regard to revascularization, it helps to define a subgroup of patients in whom PTCA or CABG is clearly indicated. 3. On the other hand, clear stratification of patients with AMI is not yet possible on the basis of thallium/lllIn antimyosin SPET alone. 4. To date this method yields only a small amount of additional information in comparison with clinical vari- ables, coronary angiography and (thallium) exercise testing. 5. A further study, including long-term follow-up, is needed to confirm the preliminary results of this study.

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Thallium and indium antimyosin dual-isotope single-photon emission tomography in acute myocardial infarction to identify patients at further ischaemic risk