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Circulation. 1995;91:1697-1705

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(Circulation. 1995;91:1697-1705.)
© 1995 American Heart Association, Inc.


Articles

Prediction of ReversibleIschemia After Revascularization

Perfusion and Metabolic Studies WithPositron Emission Tomography

Nagara Tamaki, MD; Masahide Kawamoto, MD; Eiji Tadamura, MD; Yasuhiro Magata, PhD; Yoshiharu Yonekura, MD; Ryuji Nohara, MD; Shigetake Sasayama, MD; Kazunobu Nishimura, MD; Toshihiko Ban, MD; Junji Konishi, MD

From the Department of Radiology and Nuclear Medicine (N.T., M.K., E.T., Y.M., Y.Y., J.K.); The Third Division (R.N., S.S.), Department of Internal Medicine; and Department of Cardiovascular Surgery (K.N., T.B.), Kyoto University Faculty of Medicine, Kyoto, Japan.

Correspondence to Nagara Tamaki, MD, Department of Nuclear Medicine, Kyoto University Faculty of Medicine, Shogoin, Sakyo-ku, Kyoto, 606 Japan.


*    Abstract
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*Abstract
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Background Accurate noninvasive determination of myocardial viability is of paramount importance for the clinical identification of patients who will benefit most from revascularization. The preserved metabolic activity in the myocardium, as studied with positron emission tomography (PET), has been considered a gold standard for this purpose. However, recent reports show that moderate hypoperfusion or stress-induced ischemia may represent reversible ischemia. The present study was undertaken to compare the value of perfusion and metabolic studies with PET for predicting improvement in wall motion after revascularization.

Methods and Results Of 61 patients who had regional asynergy and underwent PET before revascularization, 43 patients who had successful revascularization were included in the study. Each patient underwent rest-stress 13N-ammonia perfusion scans and 18F-fluorodeoxyglucose (FDG) scan at rest while in a fasting state. Reversible ischemia was considered to be present when the resting perfusion was >=50% of the peak value, stress-induced hypoperfusion was present, or an increase in FDG uptake was observed. Of 130 asynergy segments, 51 segments had improved wall motion after revascularization. The positive and negative predictive values for improvement in asynergy were 48% and 87% by the rest perfusion study, 63% (P=.05 versus the rest value) and 87% by the rest-stress perfusion study, and 76% (P<.01 versus the rest value) and 92% by the FDG study.

Conclusions FDG PET provided the best predictive value for improvement in wall motion after revascularization. On the other hand, 13N-ammonia PET is useful for predicting nonreversible myocardial scarring when it shows severe hypoperfusion at rest or hypoperfusion without stress-induced ischemia.


Key Words: tomography • ischemia • heart diseases


*    Introduction
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up arrowAbstract
*Introduction
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It is well known that myocardial areas with impaired ventricular function often show improved function after revascularization. Therefore, accurate identification of such reversible ischemic myocardium, "viability assessment," has important clinical implications, especially in patients being considered for interventional therapy.1 2

Many studies have focused on the assessment of tissue viability.3 4 5 6 7 8 9 10 11 Among them, positron emission tomography (PET) using 18F-fluorodeoxyglucose (FDG) has been proved to be the most accurate method of differentiating reversible ischemic myocardium from irreversible scar tissue.10 11 On the other hand, recent investigations have indicated that the 201Tl reinjection method or resting thallium imaging has potential for providing accuracy similar to that obtained with PET.12 13 Areas with relatively preserved 201Tl uptake on the delayed or resting scan may indicate viable myocardium. However, the low-energy photons from 201Tl may not provide accurate distribution of the tracer because of great photon attenuation. Because of the accurate photon attenuation of PET, PET study has the potential for more accurate assessment of myocardial perfusion than 201Tl single-photon emission computed tomography. We hypothesized that a residual perfusion of >50% or the presence of stress-induced ischemia on 13N-ammonia PET scans may predict reversible ischemia as accurately as the preserved glucose metabolism on FDG PET scans. Accordingly, the present study was undertaken to compare the clinical value of 13N-ammonia perfusion studies with that of FDG metabolic studies for prediction of reversible ischemia that is likely to show improved regional wall motion after revascularization.


*    Methods
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up arrowIntroduction
*Methods
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Patient Population
A consecutive sample of 61 patients with chronic myocardial infarction who underwent myocardial perfusion and metabolic studies with PET before revascularization were evaluated. Forty-three of these patients demonstrated successful revascularization on the follow-up angiogram and were included in the study. The remaining 18 patients had inadequate revascularization and were excluded from the study. The 43 patients consisted of 41 men and 2 women (age range, 36 to 72 years; mean, 58.1 years). The left ventricular ejection fraction on contrast ventriculography ranged from 21% to 64%, with a mean of 41%. All of the 43 patients had regional wall motion abnormalities on contrast ventriculography and a history of myocardial infarction with a duration of more than 1 month from onset. Twenty-four patients underwent coronary artery bypass graft surgery (CABG) and 19 patients underwent percutaneous transluminal coronary angioplasty (PTCA) within 4 weeks after the PET study. Two patients had non–insulin-dependent diabetes mellitus. Patients with insulin-dependent diabetes were excluded from the study. All 43 patients gave written, informed consent, and the study was approved by the Kyoto University Ethical Committee.

PET Studies
PET studies were performed using a whole-body PET camera (Positologica III [n=30] or PCT 3600W [n=13], Hitachi Medico Co). The Positologica III has four rings that provide seven tomographic slices at 16-mm intervals. The intrinsic spatial resolution in the tomographic plane was 7.6 mm full-width half-maximum (FWHM) at the center, and the axial resolution was 12 mm FWHM.14 The PCT 3600W has eight rings that provide 15 tomographic slices at 7-mm intervals, and the intrinsic resolution was 4.6 mm FWHM. The effective resolution of these PET cameras after reconstruction was 11 mm and 10 mm FWHM, respectively.

Each patient was kept in a fasting condition for at least 5 hours during the study. After accurate positioning of the patient under the PET camera using the ultrasound technique, we performed transmission scanning for 15 to 20 minutes to obtain accurate correction of photon attenuation. Then, 80 to 300 MBq (2.2 to 8.1 mCi) of FDG was injected with the patient at rest. Approximately 60 minutes later, a glucose metabolic scan was performed for 10 to 15 minutes.

The perfusion study was performed separately within 1 week of the FDG study. Approximately 400 to 600 MBq (10.8 to 16.2 mCi) of 13N-ammonia was injected at rest, and resting perfusion scanning was started 3 minutes later.

Two hours later, patients performed graded exercise using a supine ergometer; they started at 25 W with 25-W increments every 3 minutes. The exercise continued until the patient experienced fatigue, severe chest pain, dyspnea, more than 0.2 mV of ST-segment depression, or 85% of the age-predicted maximal heart rate. Another dose of 13N-ammonia was injected at peak exercise, and the exercise was continued for an additional 30 to 60 seconds. The stress perfusion scan was performed 3 minutes after tracer administration.15 16 17

From a series of transverse slices, oblique tomograms perpendicular to the long and short axes of the left ventricular myocardium were also reconstructed for three-dimensional analysis of the tracer distribution.18

Image Analysis
In each patient, resting and stress perfusion images were normalized to the normal reference regions. Coronary angiography was reviewed to determine that the reference regions corresponded to a myocardial segment supplied by a vessel without significant stenosis. The left ventricular myocardium was divided into five segments (anterior, septal, apical, inferior, and lateral) to calculate the mean regional perfusion as percent activity of the maximal counts in the normal reference regions by using the circumferential profile analysis of four to six short-axis slices of the 13N-ammonia distribution. Segments with perfusion above the lower limit of the normal values were considered to be normal. The lower limit was determined as the mean -2 SD of the perfusion profile for each segment from 12 healthy subjects who had less than 5% likelihood of coronary artery disease.16 17 Segments with perfusion below the lower limit were defined as hypoperfused segments. In addition, stress and resting perfusions were compared using the circumferential profile analysis based on the corresponding short-axis slices. Segments with a stress perfusion of more than 10% lower than the resting perfusion on the profile analysis were considered as stress-induced hypoperfusion.17

The FDG uptake was quantitatively measured as the body weight (BW)–corrected percent of the injected dose per 100 g of tissue (% ID/100 g) in each segment19 according to the following equation:



where CT is the myocardial tissue activity of FDG (cpm/mL), BW is the patient's body weight, and CF is the calibration factor between millicuries on the curie meter and counts per minute per milliliter on the PET images.19 FDG images were shown as a parametric display as FDG uptake index (not normalized uptake) to define the ischemic myocardium as increased FDG uptake. Because of heterogeneity of FDG uptake in normal myocardium, the normal range of FDG uptake was defined as the mean±2 SD of the FDG uptake in eight healthy subjects.13 Hypoperfused segments with an increase in FDG uptake above the normal range were defined as PET ischemia, whereas those with no increase in FDG uptake were defined as PET scarring.11 13 19

Wall Motion Analysis
Analysis of the regional wall motion was performed within 4 weeks of the PET study before revascularization and repeated at 4 to 8 weeks after revascularization. Each patient underwent biplane contrast ventriculography in right anterior oblique and left lateral projections to assess regional wall motion before and after revascularization. In three patients who could not undergo the contrast ventriculography, radionuclide ventriculography was performed in the anterior and left anterior oblique projections after intravenous injection of 740 MBq (20 mCi) of 99mTc red blood cells. The left ventricle was divided into anterior, apical, inferior, septal, and lateral segments. Wall motion was visually assessed in a blinded fashion by three experienced observers and scored using a five-point grading system (normal, mild hypokinesis, severe hypokinesis, akinesis, and dyskinesis).17 When the wall motion score improved by one or more points after intervention, the segment was considered to show improved wall motion.11 17 In the study of patients who underwent CABG, the septal segment was excluded from the wall motion analysis because of frequent paradoxical motion after surgery.

Statistical Analysis
Comparisons of the predictive value of each study were performed with {chi}2 analysis or Fisher's exact test. A value of P<.05 was considered statistically significant.


*    Results
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*Results
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There were a total of 130 asynergic segments before revascularization. After revascularization, 51 of the segments showed improvement in the wall motion abnormality, whereas the remaining 79 segments did not show improved wall motion.

Among the 130 asynergic segments, the resting 13N-ammonia PET study showed normoperfusion with 80% or more of the maximal value in the whole myocardium in 1 segment, mild hypoperfusion with 70% to 80% of the maximal value in 21 segments, hypoperfusion with 60% to 70% of the maximal value in 38 segments, hypoperfusion with 50% to 60% of the maximal value in 38 segments, hypoperfusion with 40% to 50% of the maximal value in 21 segments, and severe hypoperfusion with less than 40% of the maximal value in 11 segments (Table 1Down). To compare the improvement in wall motion after revascularization (Table 2Down), these segments were divided into two groups: those with perfusion of more than 50% and those with perfusion of less than 50% of the peak value. Of 98 segments with mild-to-moderate hypoperfusion with at least 50% of the peak value, 47 segments showed improved wall motion (Figs 1Down and 2Down) and 51 segments did not show improved wall motion after revascularization. On the other hand, of 32 segments with severe hypoperfusion with less than 50% of the normal value, only 4 segments showed improved wall motion and the remaining 28 segments did not show improved wall motion after revascularization (Fig 3Down) ({chi}2=12.7, P<.001). The positive and negative predictive values of the resting perfusion study for improvement in asynergy were 48% and 87%, respectively.


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Table 1. Number of Asynergy Segments Showing Severity of Hypoperfusion at Rest and Improvement in Regional Wall Motion After Revascularization


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Table 2. Number of Asynergy Segments With Improvement in Regional Wall Motion After Revascularization in Relation to Resting Myocardial Perfusion





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Figure 1. Studies of a 57-year-old man who had a history of inferior-wall infarction 3 months earlier. His coronary angiograms showed 100% occlusion in the left anterior descending coronary artery and 99% stenosis in the left circumflex artery. A, Four corresponding short-axis slices of [13N]-ammonia perfusion at rest (top) and stress (middle) and [18F]-fluorodeoxyglucose (FDG) images (bottom) before coronary artery bypass graft surgery show mild-to-moderate hypoperfusion (70% to 55%) at rest with stress-induced ischemia in anterior and inferolateral regions with increase in FDG uptake. End-diastolic (left) and end-systolic (right) images of contrast ventriculogram before (B) and after (C) surgery. Severely hypokinetic wall motion is seen in inferior regions before the surgery that normalized after the surgery.





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Figure 2. Studies of a 58-year-old man who had a history of inferior-wall myocardial infarction 2 months earlier. Since the patient's coronary angiograms showed 90% to 100% stenosis of all three major arteries, he was scheduled to receive coronary artery bypass graft surgery. A, Four corresponding short-axis slices of [13N]-ammonia perfusion at rest (top) and stress (middle) and [18F]-fluorodeoxyglucose (FDG) images (bottom) before coronary artery bypass graft surgery show mild hypoperfusion (65%) at rest with stress-induced ischemia in inferolateral region. An increase in FDG uptake is noted in the same area. End-diastolic (left) and end-systolic (right) images of contrast ventriculogram before (B) and after (C) surgery. Akinetic wall motion is seen in inferior regions that strikingly improved after the surgery.





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Figure 3. Studies of a 62-year-old man who had an old history of anterior- and inferior-wall myocardial infarction at 2 years and 9 months earlier, respectively. Because his coronary angiograms showed 90% to 100% stenosis of all three major arteries, he was scheduled to receive coronary artery bypass graft surgery. A, Four corresponding short-axis slices of [13N]-ammonia perfusion at rest (top) and stress (middle) and [18F]-fluorodeoxyglucose (FDG) images (bottom) before coronary artery bypass graft surgery show severe hypoperfusion (40%) at rest without significant stress-induced ischemia in anterior region. No increase in FDG uptake is noted. End-diastolic (left) and end-systolic (right) images of contrast ventriculogram before (B) and after (C) surgery. Akinetic wall motion with aneurysm is seen in anterior and apical regions that did not improve after the surgery.

The stress perfusion study was performed approximately 2 hours after the resting perfusion study. Stress-induced hypoperfusion was observed in 68 of the 130 asynergic segments (Table 3Down). Forty-three of them showed improved wall motion (Figs 1Up and 2Up), yielding a positive predictive value of 63%. On the other hand, no stress-induced hypoperfusion was observed in the remaining 62 asynergic segments. Only 8 segments showed improved wall motion after revascularization, whereas the remaining 54 segments did not (Fig 3Up) ({chi}2=34.5, P<.001). Thus, the negative predictive value was 87%. When the segments with mild-to-moderate hypoperfusion (at least 50% of the peak value) were selected for analysis, improvement in the asynergy was observed in 40 of the 62 segments with stress-induced hypoperfusion, whereas improvement was seen in only 7 of the 36 segments without stress-induced hypoperfusion ({chi}2=18.5, P<.001). Thus, the positive and negative predictive values were similar (65% and 81%, respectively).


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Table 3. Number of Asynergy Segments With Improvement in Regional Wall Motion After Revascularization in Relation to Stress-Induced Hypoperfusion

Among the 130 asynergic segments, FDG PET showed an increase in FDG uptake in 59 segments but no increase in 71 segments (Table 4Down). Forty-five of the 59 segments exhibiting an increase in FDG uptake showed improved regional wall motion after revascularization (Figs 1Up and 2Up), whereas only 6 of the 71 segments showing no increase in FDG uptake improved (Fig 3Up) ({chi}2=62.2, P<.001). Thus, the positive and negative predictive values of the FDG findings were 76% and 92%, respectively.


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Table 4. Number of Asynergy Segments With Improvement in Regional Wall Motion After Revascularization in Relation to Myocardial FDG Uptake

The overall accuracy of the prediction of improvement in asynergy was 58% (65 of 130) in the resting perfusion study, 75% (97 of 130) in the rest-stress perfusion study, and 85% (110 of 130) in the FDG study (P<.05 within each study).


*    Discussion
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up arrowAbstract
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*Discussion
down arrowReferences
 
The present data indicate the importance of myocardial perfusion and metabolic PET imaging in differentiating reversible ischemia from nonreversible myocardial scarring. Among the various available parameters of PET perfusion and metabolism, FDG PET may provide the best accuracy for predicting reversibility of regional wall motion abnormalities after revascularization. On the other hand, severe hypoperfusion (less than 50% of the peak value) and hypoperfusion with no stress-induced ischemia on 13N-ammonia PET scans are likely to represent irreversible myocardial damage that shows no improvement in asynergy after revascularization. In contrast, PET patterns with mild reduction of perfusion showed poor predictive value for functional recovery after revascularization.

Although a number of prior clinical studies have shown that glucose metabolic imaging is superior to the assessment of myocardial perfusion alone in identifying reversible ischemia, to our knowledge this is the first study that addressed the usefulness of PET evaluation of the relative reduction in myocardial perfusion in identifying viable tissue.

Value of Perfusion Imaging
Previous experimental studies indicated that a certain threshold of myocardial perfusion is required to maintain tissue viability.21 22 23 24 25 Segments with very low flow below this threshold may show decreased exogenous glucose use, which may represent irreversible myocardial scarring. The present data indicate that none of the segments with perfusion of less than 40% of the maximal value at rest recovered regional function after revascularization. The present data are in agreement with the results of a 201Tl study of stress-delayed scanning,26 rest-redistribution scanning,27 or reinjection scanning.28 However, PET perfusion studies should be more accurate in assessing regional perfusion than 201Tl studies because of accurate correction of photon attenuation and scattering. Therefore, 13N-ammonia PET might be more suitable for defining the threshold of perfusion in vivo.

Our results are in agreement with those reported by Duvernov et al,29 who showed that severely hypoperfused segments with less than 40% of the normal value did not show improved regional wall motion. In addition, our previous PET study demonstrated that none of the segments with severe hypoperfusion (less than 45% of the peak value) had regional myocardial glucose use of more than 0.3 µmol · min-1 · g-1, suggesting that a certain minimal threshold of residual perfusion is required to maintain glucose metabolism.25

The threshold determined in these studies appears to be much higher than the experimental value. Because myocardial perfusion images in vivo may contain a significant amount of noise and background activity compared with in vitro tissue counting, the perfusion in ischemic tissue in vivo is likely to be overestimated. Although PET images contained much less background activity than the 201Tl single-photon emission computed tomography or planar images, there appears to be no definite method of accurately correcting for background activity on PET. In addition, ischemic tissue in human studies should be quite different from that in experimental infarct models, considering the collateral circulation and duration of ischemic insult.

On the other hand, there was much variation in the changes in wall motion after revascularization in the areas with moderate hypoperfusion. Improvement in wall motion was observed in only 50% of the segments with perfusion of at least 50% of the peak value. It is important to note that detection of residual viable myocardium may not be equal to detection of reversible ischemia. A myocardial segment with a mixture of healthy and scar tissues without ischemia may not show improved regional function after revascularization, although the residual perfusion in such areas may be relatively well maintained. In such circumstances, other indicators, such as the 201Tl redistribution or perfusion-metabolic mismatch, may be required for accurate identification of reversible ischemia.

Although resting perfusion studies may be useful for identifying viable myocardium on the basis of the residual myocardial perfusion, stress perfusion studies may add important clinical data for detecting stress-induced ischemia. Detection of stress-induced ischemia is one method of detecting reversible ischemia. Data from our previous study30 indicated that stress-rest 13N-ammonia PET scans identified stress-induced ischemia more frequently than did stress-delayed 201Tl scans. In addition, reversible ischemic myocardium after CABG was more accurately identified by PET perfusion studies than by the 201Tl studies.17 Furthermore, segments showing stress-induced ischemia are often associated with an increase in FDG uptake in PET studies.31 32

Although supine ergometer exercise was applied, adequate exercise levels were obtained, as described previously.30 PET imaging started 3 minutes after the tracer injection, and there was no motion artifact in any of the patients. Our results indicated that segments without stress-induced ischemia were least likely to show improved regional function, and therefore this was considered to be a highly specific sign of irreversible damage. On the other hand, hypoperfused segments associated with stress-induced ischemia may not always show improved regional function. The positive predictive value (60%) was not very satisfactory. Similar predictive values for stress-perfusion studies were obtained when segments with mild-to-moderate hypoperfusion at rest were selected for analysis.

Because 13N-ammonia images represent the relative myocardial perfusion, areas with stress-induced hypoperfusion indicate a decrease in the flow reserve compared with other, normal areas. It is well known that ischemic tissues distal to stenotic coronary arteries show a decrease in flow reserve.33 However, areas with decreased flow reserve may not necessarily represent ischemic myocardium. A recent preliminary report showed that changes in the perfusion reserve may be unrelated to residual glucose metabolism as a marker of tissue viability.34 A prospective study may be warranted to evaluate whether a decrease in the flow reserve is a good indicator for identifying reversible ischemia in patients undergoing revascularization.

Value of Metabolic Imaging
PET has emerged as an excellent technique for assessing myocardial viability in patients with left ventricular dysfunction since it can demonstrate preserved glucose metabolism in regions with reduced perfusion.10 11 20 In ischemic myocardium, ß-oxidation of fatty acids in the mitochondria is suppressed, and the myocytes compensate for the loss of oxidative potential by shifting toward greater glucose use to generate high-energy phosphates.35 36 Thus, analysis of the glycolytic process could play an important role in assessing myocyte viability.

Previous preliminary reports showed that a perfusion-metabolic mismatch may be an excellent indicator for predicting recovery of myocardial function after revascularization.10 11 37 38 The present data are consistent with these findings. In particular, areas with no increase in FDG uptake were least likely to improve, yielding a high negative predictive value (78% to 92%). On the other hand, the positive predictive value may not be as high (72% to 82%). One of the major reasons is that recovery of regional function may not be completed within 4 to 8 weeks after revascularization. Prolonged postischemic ventricular dysfunction is often observed after revascularization.39 40 Such prolonged dysfunction may be associated with a sustained increase in FDG uptake in postischemic areas.11 37

The present study provided slightly better predictive values than did a previous study.11 Several reasons may be considered. First, the number of patients enrolled in the present study was greater. Second, those who had inadequate revascularization on the follow-up angiogram were excluded from the present study. The present study included 19 previously reported cases and 24 new cases. Third, the FDG uptake was quantitatively measured in each segment.19 Therefore, an increase in FDG uptake can be defined more accurately than in the previous report. In addition, the present study includes a comparison of the predictive value obtained with FDG PET with those obtained with rest perfusion and rest-stress perfusion studies.

The prediction of reversible ischemia by metabolic analysis was slightly better than that by perfusion analysis. In areas with moderate hypoperfusion, it will be important to differentiate ischemic and compromised myocardium from a mixture of healthy and scar tissues. This differentiation may be more accurately performed by combined perfusion-metabolic imaging than by only perfusion imaging at rest. In addition, an increase in tracer uptake, as in the case of FDG uptake, may be easier to interpret than a decrease in tracer distribution as perfusion imaging.

On the other hand, FDG uptake is known to differ depending on the dietary condition.41 42 In the postprandial condition, increased use of glucose by the healthy myocardium would result in an increase in FDG uptake with a relative decrease in its uptake in the ischemic myocardium. As a result, the extent of tissue viability may be underestimated. In contrast, in the fasting condition, as was used in the present study, preferential use of fatty acids by the healthy myocardium occurred. Therefore, extensive necrosis with a small amount of ischemic tissue may show intense uptake of FDG compared with the healthy myocardium; thus, it may overestimate the viable tissue. In addition, a recent report suggests heterogeneous uptake of FDG by the healthy myocardium in the fasting state.43 To resolve these limitations, we quantitatively measured FDG uptake for parametric display of FDG uptake to identify segments with FDG uptake above the normal range as PET ischemia.19 The current criteria may overcome the limitation of using the FDG distribution in the fasting state.

In the present study, we did not correct for a partial volume effect, which may lead to underestimation of the 13N-ammonia and FDG uptake in the asynergic segments. An accurate and feasible method for making this correction may further improve the accuracy of the prediction. Echocardiography has been commonly used to correct the partial volume effect. However, this technique may not be reproducible, and the measured segment may not correspond well to the PET segment.

Furthermore, background activity was not subtracted, which may affect observed PET perfusion defect severity measurement. An accurate correction of such noise may permit more definite distinction to be made between viable and nonviable myocardium.

Another study limitation was the use of ungated PET imaging, which may underestimate regional tracer distribution in asynergic segments compared with those with normal function.44 However, ungated scanning remains a common PET acquisition method at most clinical PET centers.

Clinical Implications
Accurate noninvasive determination of myocardial viability is of paramount importance for the clinical identification of patients who will benefit most from revascularization. This investigation confirmed that a perfusion-metabolism mismatch on PET can accurately identify reversible dysfunction in the ischemically compromised myocardium. Furthermore, this investigation addressed the usefulness of severity of myocardial hypoperfusion in identifying such reversibility. In particular, areas of severe hypoperfusion at rest or hypoperfusion without stress-induced ischemia on PET may represent irreversible damage. However, such findings were seen less frequently than no FDG uptake. In this respect, FDG PET may provide the best accuracy in predicting the reversibility of regional wall motion abnormalities. However, when 13N-ammonia PET shows severe myocardial hypoperfusion at rest or no stress-induced ischemia, revascularization therapy will be of no use.


*    Acknowledgments
 
This study was supported in part by a grant-in-aid for General Scientific Research from the Ministry of Education, Science and Culture, Tokyo, Japan. We gratefully acknowledge the valuable comments of Susumu Shindo, MD; Norio Takahashi, MD; Shinji Ono, MD; Kazumi Okuda, MD; and Tatsuo Torizuka, MD. We also thank Emiko Komori, Toru Fujita, and the Cyclotron Staff for their technical assistance.

Received August 12, 1994; revision received August 16, 1994; accepted September 28, 1994.


*    References
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up arrowAbstract
up arrowIntroduction
up arrowMethods
up arrowResults
up arrowDiscussion
*References
 
1. Bodenheimer MM, Banka VS, Hermann GA, Trout RG, Pasdar H, Helfant RH. Reversible asynergy. Circulation. 1976;53:792-796. [Abstract/Free Full Text]

2. Brundage BH, Massie BM, Botvinick EH. Improved regional ventricular function after successful surgical revascularization. J Am Coll Cardiol. 1984;3:902-908. [Abstract]

3. Pohost GM, Zir LM, Moore RH, McKusick KA, Guiney TE, Beller GA. Differentiation of transiently ischemic from infarcted myocardium by serial imaging after single dose of thallium-201. Circulation. 1977;55:294-302. [Abstract/Free Full Text]

4. Rozanski A, Berman DS, Gray R, Raymond M, Maddahi J, Pantaleo N, Waxman A, Swan HJC, Matloff J. Use of thallium-201 redistribution scintigraphy in the preoperative differentiation of reversible and nonreversible myocardial asynergy. Circulation. 1981;64:936-944. [Abstract/Free Full Text]

5. Rozanski A, Berman D, Gray R, Diamond G, Raymond M, Prause J, Maddahi J, Swan HJC, Matloff J. Preoperative prediction of reversible myocardial asynergy by postexercise radionuclide ventriculography. N Engl J Med. 1982;307:212-216. [Abstract]

6. Gibson RS, Watson DD, Taylor GJ, Crosby IK, Wellons HL, Holt ND, Beller GA. Prospective assessment of regional myocardial perfusion before and after coronary revascularization surgery by quantitative thallium-201 scintigraphy. J Am Coll Cardiol. 1983;1:804-815. [Abstract]

7. 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. [Abstract]

8. Ohtani H, Tamaki N, Yonekura Y, Mohiuddin IH, Hirata K, Ban T, Konishi J. Value of thallium-201 reinjection after delayed SPECT imaging for predicting reversible ischemia after coronary artery bypass grafting. Am J Cardiol. 1990;66:394-399. [Medline] [Order article via Infotrieve]

9. Pierard LC, DeLandsheere 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. [Abstract]

10. Tillisch J, Brunken R, Marshall R, Schwaiger M, Madelkern M, Phelps ME, Schelbert H. Reversibility of cardiac wall-motion abnormalities predicted by positron tomography. N Engl J Med. 1986;314:884-888. [Abstract]

11. Tamaki N, Yonekura Y, Yamashita K, Saji H, Magata Y, Senda M, Konishi Y, Hirata K, Ban T, Konishi J. Positron emission tomography using fluorine-18 deoxyglucose in evaluation of coronary artery bypass grafting. Am J Cardiol. 1989;64:860-865. [Medline] [Order article via Infotrieve]

12. Bonow RO, Dilsizian V, Cuocolo A, Bacharach SL. Identification of viable myocardium in patients with coronary artery disease and left ventricular dysfunction: comparison of thallium scintigraphy with reinjection and PET imaging with 18F-fluorodeoxyglucose. Circulation. 1991;83:26-37. [Abstract/Free Full Text]

13. Tamaki N, Ohtani H, Yamashita K, Magata Y, Yonekura Y, Nohara R, Kambara H, Kawai C, Hirata K, Ban T, Konishi J. Metabolic activity in the areas of new fill-in after thallium-201 reinjection: comparison with positron emission tomography using fluorine-18-deoxyglucose. J Nucl Med. 1991;32:673-678. [Abstract/Free Full Text]

14. Senda M, Tamaki N, Yonekura Y, Tanada S, Murata K, Hayashji N, Fujita T, Konishi J, Torizuka K, Ishimatsu K, Takami E. Performance characteristics of Positologica III, a whole body positron emission tomograph. J Comput Assist Tomogr. 1985;9:940-946. [Medline] [Order article via Infotrieve]

15. Tamaki N, Yonekura Y, Senda M, Kureshi SA, Saji H, Kodama S, Konishi Y, Ban T, Kambara H, Kawai C, Torizuka K. Detection of coronary artery disease with 13N-ammonia and high resolution positron-emission computed tomography. Eur J Nucl Med. 1985; 11:246-251.

16. Yonekura Y, Tamaki N, Senda M, Nohara R, Kambara H, Konishi Y, Koide H, Kureshi SA, Saji H, Ban T, Kawai C, Torizuka K. Detection of coronary artery disease with 13N-ammonia and high resolution positron-emission computed tomography. Am Heart J. 1987;113:645-654. [Medline] [Order article via Infotrieve]

17. Tamaki N, Yonekura Y, Yamashita K, Senda M, Saji H, Konishi Y, Hirata K, Ban T, Konishi J. Value of rest-stress myocardial positron tomography using N-13 ammonia for the preoperative prediction of reversible asynergy. J Nucl Med. 1989;30:1302-1310. [Abstract/Free Full Text]

18. Senda M, Yonekura Y, Tamaki N, Saji H, Koide H, Nohara R, Kambara H, Konishi Y, Torizuka K. Interpolating scan and oblique-angle tomograms in myocardial PET using N-13 ammonia. J Nucl Med. 1986;27:1830-1836. [Abstract/Free Full Text]

19. Tamaki N, Yonekura Y, Kawamoto M, Magata Y, Sasayama S, Takahashi N, Nohara R, Kambara H, Kawai C, Konishi J. Simple quantification of regional myocardial uptake of fluorine-18-deoxyglucose in the fasting condition. J Nucl Med. 1991;32:2152-2157. [Abstract/Free Full Text]

20. Marshall RC, Tillisch JH, Phelps ME, Huang SC, Carson R, Henze E, Schelbert HR. Identification and differentiation of resting myocardial ischemia and infarction in man with positron computed tomography, 18F-labeled fluorodeoxyglucose and N-13 ammonia. Circulation. 1983;67:766-778. [Abstract/Free Full Text]

21. Rivas F, Cobb FR, Bache RJ, Greenfield JC. Relationship between blood flow to ischemic regions and extent of myocardial infarction. Circ Res. 1976;38:439-447. [Abstract/Free Full Text]

22. Miura T, Downey JM. Critical collateral blood flow level for salvage of ischemic myocardium. Can J Cardiol. 1989;5:201-215. [Medline] [Order article via Infotrieve]

23. Sochor H, Schwaiger M, Schelbert HR, et al. Relationship between Tl-201, Tc-99m (Sn) pyrophosphate and F-18 2-deoxyglucose uptake in ischemically injured dog myocardium. Am Heart J. 1987;114:1066-1077. [Medline] [Order article via Infotrieve]

24. Kaliff V, Schwalger M, Nguyen N, McClanahan TB, Gallagher KP. The relationship between myocardial blood flow and glucose uptake in ischemic canine myocardium determined with fluorine-18-deoxyglucose. J Nucl Med. 1992;33:1346-1353. [Abstract/Free Full Text]

25. Takahashi N, Tamaki N, Kawamoto M, Yonekura Y, Magata Y, Nohara R, Sasayama S, Konishi J, Yamamoto K, Ishii Y. Glucose metabolism in relation to perfusion in patients with coronary artery disease. Eur J Nucl Med. 1994;21:292-296. [Medline] [Order article via Infotrieve]

26. Yamamoto K, Asada S, Masuyama T, Nanto S, Matsumura Y, Naito J, Hirayama A, Mishima M, Naka M, Sasaki J, Hori M, Kodama K. Myocardial hibernation in the infarcted region cannot be assessed from the presence of stress-induced ischemia: usefulness of delayed image of exercise thallium-201 scintigraphy. Am Heart J. 1993;125:33-40. [Medline] [Order article via Infotrieve]

27. Ragosta M, Beller GA, Watson DD, Kaul S, Gimple LW. Quantitative planar rest-redistribution 201Tl imaging in detection of myocardial viability and prediction of improvement in left ventricular function after coronary bypass surgery in patients with severely depressed left ventricular function. Circulation. 1993;87:1630-1641. [Abstract/Free Full Text]

28. Bonow RO, Dilsizian V, Cuocolo A, Bacharach SL. Identification of viable myocardium in patients with chronic coronary artery disease and left ventricular dysfunction. Circulation. 1991;83:26-37.

29. Duvernov C, Rothley J, Sitomer J, vonDahl J, Melon P, Laubenbacher C, Schwaiger M. Relationship of blood flow and functional outcome after coronary revascularization. J Nucl Med. 1993;34:155P. Abstract.

30. Tamaki N, Yonekura Y, Senda M, Yamashita K, Koide H, Saji H, Hashimoto T, Fudo T, Kambara H, Kawai C, Konishi J. Value and limitation of stress thallium-201 single-photon emission computed tomography: comparison with nitrogen-13 ammonia positron tomography. J Nucl Med. 1988;29:1181-1188. [Abstract/Free Full Text]

31. Fudo T, Kambara H, Hashimoto T, Hayashi M, Nohara R, Tamaki N, Yonekura Y, Senda M, Konishi J, Kawai C. F-18 deoxyglucose and stress N-13 ammonia positron emission tomography in anterior healed myocardial infarction. Am J Cardiol. 1988;61:1191-1197. [Medline] [Order article via Infotrieve]

32. Yonekura Y, Tamaki N, Kambara H, Senda M, Saji H, Ban T, Kawai C, Konishi J. Detection of metabolic alteration in ischemic myocardium by F-18 fluorodeoxyglucose uptake with positron emission tomography. Am J Cardiac Imag. 1988;2:122-132.

33. Gould KL, Kirkeeide R, Buchi M. Coronary flow reserve as a physiologic measure of stenosis severity. J Am Coll Cardiol. 1990;15:459-474. [Abstract]

34. Czernin J, Porenta P, Muller P, Rosenqvist G, Krivokapich J, Mody F, Phelps ME, Schelbert HR. Measurements of blood flow and flow reserve fails to discriminate between viable and non-viable myocardium. J Nucl Med. 1992;33:856. Abstract.

35. Liedke AJ. Alterations of carbohydrate and lipid metabolism in the acutely ischemic heart. Prog Cardiovasc Dis. 1972;15:289-329. [Medline] [Order article via Infotrieve]

36. Opie LH. Effects of regional ischemia on metabolism of glucose and fatty acids: relative rates of aerobic and anaerobic energy production during myocardial infarction and comparison with effects of anoxia. Circ Res. 1976;38(suppl I):I-52-I-74.

37. Nienaber CA, Brunken R, Sherman CT, Yeatman LA, Gambhir SS, Krivokapich J, Demer LL, Ratib O, Child JS, Phelps ME, Schelbert HR. Metabolic and functional recovery of ischemic human myocardium after coronary angioplasty. J Am Coll Cardiol. 1991;18:966-978. [Abstract]

38. Marwick TH, Nemec JJ, Lafont A, Salcedo EE, MacIntyre WJ. Prediction by postexercise fluoro-18 deoxyglucose positron emission tomography of improvement in exercise capacity after revascularization. Am J Cardiol. 1992;69:854-859. [Medline] [Order article via Infotrieve]

39. Braunwald E, Kloner RA. The stunned myocardium: prolonged postischemic ventricular dysfunction. Circulation. 1982;66:1146-1149. [Abstract/Free Full Text]

40. Matsuzaki M, Gallagher KP, Kemper WS, White F, Ross J Jr. Sustained regional dysfunction produced by prolonged coronary stenosis: gradual recovery after reperfusion. Circulation. 1983; 68:170-182.

41. Tamaki N, Yonekura Y, Konishi J. Myocardial FDG PET studies with the fasting, oral glucose-loading or insulin clamp methods. J Nucl Med. 1992;33:1263-1268. Editorials.

42. Berry JJ, Baker JA, Pieper KS, Hanson MW, Hoffman JM, Coleman RE. The effect of metabolic milieu on cardiac PET imaging using fluorine-18-deoxyglucose and nitrogen-13-ammonia in normal volunteers. J Nucl Med. 1991;32:1518-1525. [Abstract/Free Full Text]

43. Gropler RJ, Siegel BA, Lee KJ, Moerlein SM, Perry DJ, Bergmann SR, Geltman EM. Nonuniformity in myocardial accumulation of fluorine-18-fluorodeoxyglucose in normal fasted humans. J Nucl Med. 1990;31:1749-1756. [Abstract/Free Full Text]

44. Parodi O, Schelbert HR, Schwaiger M, Hansen H, Selin C, Hoffman EJ. Cardiac emission tomography: underestimation of regional tracer concentrations due to wall motion abnormalities. J Comput Assist Tomogr. 1984;6:1083-1092.




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