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CARDIOVASCULAR ANESTHESIA

Does Intraoperative Evaluation of Left Ventricular Contractile Reserve Predict Myocardial Viability? A Clinical Study Using Dobutamine Stress Echocardiography in Patients Undergoing Coronary Artery Bypass Graft Surgery

Jacqueline M. Leung, MD MPH^*, Wayne H. Bellows, MD, and Darwin Pastor^*

*Department of Anesthesia and Perioperative Care, University of California, San Francisco, California; and Department of Cardiovascular Anesthesiology, Kaiser Permanente Medical Center, San Francisco, California

Address correspondence and reprint requests to Jacqueline M. Leung, MD, MPH, University of California, San Francisco, Department of Anesthesia and Perioperative Care, 521 Parnassus Ave., San Francisco, CA 94143-0648. Address e-mail to jmleung{at}itsa.ucsf.edu

	Abstract

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To determine the contractile reserve of the left ventricle during reperfusion as a predictor of myocardial viability in patients undergoing coronary artery bypass graft surgery, we measured the response of left ventricular regional wall motion and thickening by using dobutamine stress echocardiography (DSE) after myocardial revascularization. All patients were monitored with radial and pulmonary arterial catheters, transesophageal echocardiography, standard five-lead clinical electrocardiography, and three-channel Holter electrocardiography. Immediately after separation from cardiopulmonary bypass, dobutamine was administered IV starting at 5 µg · kg^–1 · min^–1, with increases in rate every 3 min to 10, 20, 30, and 40 µg · kg^–1 · min^–1. Within 1 wk after surgery, resting and redistribution thallium-201 myocardial perfusion imaging (thallium studies) was performed to assess the relationship between the intraoperative contractile response and myocardial viability. One-hundred patients completed DSE up to 10 µg · kg^–1 · min^–1, and 85 patients received the larger escalating doses of the DSE. Seventy-two patients had postoperative thallium studies. At the completion of the small-dose dobutamine infusion, 689 (97.7%) of 705 segments had a normal response (improvement), and 16 segments (2.3%) had a positive response (deterioration). During large-dose dobutamine infusion, 577 (95.8%) of 602 segments had a normal response, and 25 segments (4.2%) had a positive response. Myocardial segments that had a positive response during large-dose DSE (48%) were more likely to be considered as nonviable on postoperative thallium studies compared with segments that had a normal response (14.7%) (P < 0.00001). By using thallium studies as the reference standard, the sensitivity of DSE was low (31% and 48% for small- and large-dose DSE, respectively) in predicting nonviable myocardium. However, the specificity was higher (86% and 85% for small- and large-dose DSE, respectively). In a separate analysis of patients who developed new regional wall motion abnormalities (RWMA) in the early intraoperative reperfusion period, 15 (75%) of 20 abnormally contracting myocardial segments had normal postoperative thallium studies. Our results demonstrate that a normal response to DSE is highly specific for viable myocardium; however, a positive response to DSE has low sensitivity in predicting nonviable myocardium. The majority of new postbypass regional wall motion abnormalities appear to be related to stunned myocardium.

IMPLICATIONS: To assess the left ventricular contractile reserve during reperfusion in patients undergoing coronary artery bypass graft surgery, we measured the response of left ventricular regional wall motion and thickening by using dobutamine stress echocardiography (DSE) after myocardial revascularization, with validation by postoperative thallium-201 myocardial perfusion to assess myocardial viability. Our results demonstrate that a normal response to DSE (improvement in function) is highly specific for viable myocardium; however, a positive response to DSE has a low sensitivity in predicting nonviable myocardium. The majority of new postbypass regional wall motion abnormalities appear to be related to stunned myocardium.

	Introduction

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Despite improvements in myocardial protection and surgical techniques, ventricular dysfunction after cardiopulmonary bypass is common (1–3). In addition to global left ventricular dysfunction, regional ventricular dysfunction may also occur after myocardial revascularization (4–6). More importantly, the development of new regional wall motion abnormalities (RWMA) during the postbypass period may be predictive of adverse cardiac outcome (6). Despite the apparent prognostic significance of these postbypass RWMA, the etiology of these changes remains unclear. Abnormal wall motion may result from reversible physiologic changes that produce stunned, hibernating, or ischemic, but still viable, tissue. Alternatively, RWMA may result from irreversible changes leading to nonviable, infarcted tissue. Although the reversibility of these abnormalities may be the key in differentiating viable from nonviable tissue, the natural time course of reversibility is unpredictable.

During surgery, the only clinically feasible indicators of viability are regional wall motion and systolic wall thickening detected by echocardiography. The differential response at small doses of dobutamine infusion can be used to distinguish viable (but dysfunctional) from necrotic myocardium and establish tissue viability. When used at a small dose (up to 10 µg · kg^–1 · min^–1), dobutamine produces a marked inotropic effect on normal myocardium. Reversible dysfunction, such as stunned myocardium, is recruited with improvement in wall thickening, whereas nonviable myocardium should produce no change. At larger infusion doses, because of the increase in myocardial oxygen demand, the jeopardized myocardium may become dysfunctional, resulting in either new or worsening RWMA.

Therefore, the goals of our study were to determine the contractile reserve of left ventricular regional function in the postbypass reperfusion period by using intraoperative dobutamine stress echocardiography (DSE) and to determine whether the contractile response during DSE is predictive of myocardial viability, by using postoperative rest-redistribution thallium-201 myocardial perfusion studies (thallium studies) as the "gold standard." We hypothesized that viable myocardium could be differentiated from nonviable myocardium depending on the response to dobutamine stress testing.

	Methods

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The study was approved by the Committee on Human Research and the Radiation Safety Committee from the University of California, San Francisco, and Kaiser Permanente Medical Center, San Francisco, and informed consent was obtained from all study patients. The inclusion criteria were patients scheduled for elective coronary artery bypass grafting (CABG) surgery between 1994 and 1997. The exclusion criteria were patients with esophageal disease or prior esophageal surgery, precluding the safe insertion of the esophageal probe; sensitivity to dobutamine; or known arrhythmogenic potential.

One hour before surgery, patients received lorazepam 1–4 mg by mouth and morphine sulfate (up to 0.1 mg/kg) IM. All cardiac medications were continued until the time of operation. Anesthesia was induced by IV administration of boluses of sufentanil (up to 5 µg/kg) and midazolam (up to 0.1 mg/kg), with isoflurane as needed. Anesthesia throughout the intraoperative period was maintained by infusion of sufentanil (1–2 µg · kg^–1 · h^–1), and isoflurane was titrated as necessary to modulate the anesthetic depth. Vecuronium was used for muscle relaxation. Heart rate (HR) and systolic blood pressure (SBP) were controlled within ±20% of the preoperative baseline.

Cardiopulmonary bypass was conducted by using a membrane oxygenator with hemodilution and mild systemic hypothermia. Multidose cold blood with potassium cardioplegia and topical saline/ice slush were used for myocardial protection during cardiopulmonary bypass. Mean arterial blood pressure (MAP) was maintained between 40 and 80 mm Hg.

Distal anastomoses were usually performed first during continuous aortic cross-clamping, followed by proximal vein grafting during partial aortic occlusion. The pericardium was left open in all patients. The quality of the bypass grafts was assessed by surgeons before the dobutamine infusion. The grafts were graded qualitatively as 1, 2, 3, or 4, which represented poor, fair, very good, and excellent revascularization, respectively (6,7).

Postbypass HRs were maintained at 110 bpm, and SBP was maintained between 90 and 130 mm Hg. The use of inotropes and vasodilators was not controlled but was recorded.

Routine clinical monitors included a five-lead electrocardiograph (ECG), radial artery and pulmonary artery catheters, and multiplane transesophageal echocardiography (TEE). All patients received 100% inspired oxygen. Ventilation was controlled to maintain PaO₂ >70 mm Hg and PaCO₂ between 35 and 45 mm Hg.

ECG ST segment changes were monitored in real time by an investigator during the DSE. In addition, all patients were monitored with a three-channel Holter ECG recorder (Del Mar Model 459; Del Mar Avionics, Irvine, CA; frequency response, 0.05–100 Hz). For Holter monitoring, three bipolar leads—CC5, modified CM5, and ML—were used (8). During offline analysis, each ECG recording on Holter tapes was scanned visually with an ECG analysis system (Del Mar Model 750). All normal QRS complexes were identified, and all abnormal QRS complexes (e.g., ventricular ectopic beats and conduction abnormalities) were excluded. All possible ST segment changes consistent with ischemia were reviewed and verified by two investigators who were blinded to patient identity and outcome. An ischemic episode was defined as a reversible ST segment shift from baseline of a 0.1-mV depression at J + 60 ms or a 0.2-mV increase at the J point lasting for at least 1 min (9). The time after the J point chosen to measure ST segment depression was adjusted to exclude the T wave during tachycardia.

Immediately after tracheal intubation, a probe tipped with a 5-MHz phased-array transducer (Hewlett Packard or Acuson) was introduced into the esophagus. After a thorough cardiac examination was completed, the transducer was positioned and maintained at the level of the midpapillary muscles to obtain a short-axis view of the left ventricle for continuous clinical intraoperative monitoring.

Immediately after separation from cardiopulmonary bypass, dobutamine was administered IV into a central venous catheter starting at 5 µg · kg^–1 · min^–1, with increases in rate every 3 min to 10, 20, 30, and 40 µg · kg^–1 · min^–1. Small-dose DSE was defined as doses 10 µg · kg^–1 · min^–1, and large-dose DSE was considered as doses >10 µg · kg^–1 · min^–1 (10). The infusion was stopped if any of the following end points was reached: maximum dobutamine infusion dose (40 µg · kg^–1 · min^–1) achieved, 85% maximum predicted HR based on age (220 – age = maximum predicted HR), development of significant ventricular arrhythmias (ventricular tachycardia [3 bpm] or increases in ventricular ectopic beats), development of severe hypertension (SBP >180 mm Hg or diastolic blood pressure (DBP) >100 mm Hg), development of hypotension (a decrease in SBP of >20 mm Hg from preoperative baseline), development of new or worsening RWMA by continuous TEE monitoring, or ECG ST segment depression of 0.1 mV or ST elevation of 0.1 mV by clinical ECG monitoring.

Two-dimensional TEE was performed during the prebypass and postbypass periods, immediately after separation from cardiopulmonary bypass, before dobutamine infusion, and at each dose of dobutamine in the mid-transgastric short-axis, midesophageal longitudinal long-axis, midesophageal four-chamber, and midesophageal two-chamber views (11). These imaging planes resulted in a 16-segment model recommended by the Subcommittee on Quantification of the American Society of Echocardiography (ASE) Standards Committee (12). The images were continuously recorded on a -in. videotape for subsequent review. In addition, TEE images were digitally stored in loop format so that a corresponding cardiac cycle at each infusion dose of dobutamine could be displayed in a quad-screen format for evaluation. Myocardial segments were analyzed both in real time and offline for systolic wall thickening and endocardial wall motion by using the same criteria. The left ventricle was divided into segments based on the recommendations of the ASE Standards Committee (13). Regional wall motion and thickening of each segment were graded by using a semiquantitative system previously used by our group and other investigators (6,14,15). A five-point scoring system was used in which 1 indicated normal wall motion and systolic thickening >30%, 2 indicated mildly hypokinetic and systolic thickening 10%–30%, 3 indicated severely hypokinetic and systolic thickening <10%, 4 indicated akinetic and systolic thickening 0%, and 5 indicated dyskinetic and wall bulges outward during systole. All TEE data were analyzed by two investigators by consensus, and discrepancy was arbitrated by a third investigator (6). New RWMA in the postbypass reperfusion period were defined as deterioration of wall motion and thickening of any segment by one or more grades compared with the prebypass baseline measurement (6).

The DSE data were reviewed offline in a blinded fashion as follows: the DSE was considered normal if all segments that were normal at baseline (immediately after reperfusion) showed a normal or hyperdynamic response with increased systolic wall thickening and wall motion. A normal response during DSE was evidence of the presence of contractile reserve. In contrast, a positive test was considered as new or worsening regional wall motion by one grade or more. Results from DSE were validated with postoperative thallium studies. In addition, biphasic contractile function—improvement at small dose and worsening at peak dose—was also measured (16).

HR and radial and pulmonary artery SBP and DBP were continuously monitored and downloaded onto a laptop computer. In addition, cardiac output and pulmonary artery occlusion pressure were measured immediately after separation from cardiopulmonary bypass but before dobutamine infusion and at every incremental dose of dobutamine. All measurements were obtained at end-expiration.

Resting and redistribution thallium myocardial perfusion study was performed within 1 wk after surgery. All patients fasted for at least 4 h before the procedure. Thallium-201 3.5 mCi, as thallous chloride, was injected IV with the patient at rest. Single-photon emission computed tomography (SPECT) images of the heart were acquired within 10–15 min after IV injection of thallium-201. Delayed SPECT imaging of the heart was performed at 4 h after the initial rest image acquisition. A model similar to that used for TEE interpretation was applied to scintigraphic analysis. Myocardial segments were analyzed for their relative regional radioactivity according to an adaptation of the method by Bonow (17) as follows: mild to moderate defects at rest with >50% of peak myocardial radioactivity were considered to be viable, whereas rest defects with <50% of peak activity were considered viable only if demonstrating redistribution or improvement on a subsequent image obtained 4 h later. All thallium images were read by experienced nuclear medicine physicians blinded to the intraoperative DSE results and the clinical course of the patient.

Both 12-lead ECG and myocardial muscle creatine kinase isoenzyme levels were obtained daily for the first two postoperative days. Myocardial infarction was defined as the occurrence of new Q waves (40 ms; 25% R wave) on 12-lead ECG and a myocardial muscle creatine kinase isoenzyme level 50 U/L.

Chi-square analysis with continuity correction or Fisher’s exact test was applied to categorical data (Stata 8.0). Serial measurements of hemodynamic data were analyzed with repeated-measures analysis of variance and group x time interaction. All data are presented as mean ± SD unless stated otherwise. P < 0.05 was considered statistically significant. In addition, the sensitivity and specificity of DSE in identifying viable myocardium were calculated with standard formulas.

	Results

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The clinical characteristics of the study patients are shown in Table 1. Of 115 patients enrolled, 100 patients received dobutamine in the immediate postbypass period. Fifteen patients were excluded from the study before dobutamine infusion for various technical and medical reasons. Of 100 patients receiving dobutamine, 21 required dobutamine 5 or 10 µg · kg^–1 · min^–1 to separate from cardiopulmonary bypass. All 100 patients completed DSE up to 10 µg · kg^–1 · min^–1, and 85 patients received the larger escalating doses of the DSE. Twenty-eight patients did not have postoperative thallium studies because they were transferred early to the referring hospitals, thus precluding the performance of the thallium studies. No complications occurred during DSE. The hemodynamic data measured at baseline (after separation from cardiopulmonary bypass) and during DSE are shown in Table 2. HRs increased progressively with increasing dobutamine doses, whereas pulmonary artery occlusion pressure decreased progressively with increasing dosing. Cardiac index increased with dobutamine dosing; however, increases in HR contributed primarily to the increase in cardiac indices as stroke volume indices remained unchanged with escalating doses of dobutamine infusion. Fractional area change, as measured by intraoperative TEE, was unchanged with escalating doses of dobutamine.

Using thallium studies as the reference standard, the sensitivity of DSE (either small or large dose) was low (31% and 48%, respectively) in predicting nonviable myocardium. However, the specificity was higher (86% and 85% for small- and large-dose DSE, respectively).

During the early reperfusion postbypass period, 20 segments in 15 patients with new contractile abnormalities were observed before the performance of DSE. During small-dose DSE, only 1 segment improved, and 19 segments were considered unchanged. During subsequent large-dose DSE, 3 of 19 segments improved, 9 were considered unchanged, and 8 were not exposed to large-dose DSE. By using thallium studies as the reference standard, the sensitivity of large-dose DSE in predicting myocardial viability in these abnormally contracting segments was 50% (excluding the eight segments that were not exposed to large-dose DSE), specificity was 100%, positive predictive value was 100%, and negative predictive value was 100%. In contrast, small-dose DSE was unable to predict viable myocardium, although the specificity was 74% and the negative predictive value was 93%. From the thallium studies, 15 (75%) of 20 myocardial segments with new RWMA on reperfusion had normal postoperative myocardial perfusion, suggesting that these abnormalities were likely secondary to stunned myocardium. In contrast, 3 (15%) of 20 segments had fixed defects on thallium studies, and were likely nonviable tissue, whereas the remaining 2 (10%) of 20 segments had reversible defects on thallium studies and were considered ischemic but viable myocardium.

Sixteen patients developed ECG changes on Holter monitoring that were suggestive of myocardial ischemia during DSE. However, the concordance of ECG changes and RWMA during DSE was low. Furthermore, ECG changes during DSE were not associated with perfusion defects on postoperative thallium studies: 13.5% of patients with positive thallium results had ECG changes during DSE, compared with 25% who had no ECG changes (P = 0.24).

Six patients (6%) met the ECG and enzyme criteria for postoperative myocardial infarction. Of these six patients, one completed the DSE with a normal response, four had deterioration on a large dose of dobutamine, and one had no improvement with DSE. Overall, the response to DSE was not related to the occurrence of postoperative myocardial infarction by ECG and enzyme criteria. Six percent of patients who had deterioration on small-dose DSE (5–10 µg · kg^–1 · min^–1) developed perioperative myocardial infarction, versus 5.8% of patients who had a normal response during small-dose DSE (P = 0.90). Similarly, 4.5% of patients who had deterioration on larger doses of DSE (>10 µg · kg^–1 · min^–1) developed perioperative myocardial infarction, versus 6.3% of patients who had a normal response during larger-dose DSE (P = 0.76).

	Discussion

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Most previous studies have used preoperative DSE to predict improvement of myocardial function after revascularization (16,18). Of those that investigated intraoperative DSE, most are limited by the lack of an alternate and independent method to verify the changes in ventricular function (19,20). Also, no prior study used the combination of small- and large-dose DSE to evaluate regional ventricular function.

Our study demonstrates that the differential response to dobutamine infusion during the early reperfusion period provides useful insight regarding myocardial viability; however, there are limitations. For myocardial segments that improve during DSE, sufficient coronary flow and metabolic reserve are likely present to sustain increased contractility at testing. The validation by postoperative myocardial perfusion studies demonstrates viable myocardium. Although an infrequent occurrence, myocardial segments that show deterioration during DSE are likely associated with nonviable myocardium. However, the overall sensitivity of either small- or large-dose DSE in predicting nonviable myocardium is low. Several possibilities may explain this observation. First, there is evidence that the segmental response to myocardial revascularization largely depends on the recovery of adjacent segments (21). If there had been tethering adjacent to akinetic and nonviable segments, the tethered segments may have been considered to be dysfunctional, when they may in fact actually be viable tissue. Second, a study in patients with ischemic cardiomyopathy undergoing CABG surgery found that evaluation at 9–12 months after surgery demonstrated that perfusion was preserved more frequently than contractile reserve in approximately 22% of patients (22). Whether myocardial segments that demonstrate a positive response during intraoperative DSE but have normal perfusion on thallium studies ultimately recover in function is uncertain and needs further long-term testing. For all the study patients, we performed a one-year postoperative follow-up to determine survival. We found that neither small-dose nor large-dose DSE could predict long-term survival and that only patients who had fixed defects on postoperative thallium studies tended to have decreased survival, compared with those who had normal thallium study results. These results suggest that dysfunctional myocardial segments with intact perfusion do not decrease long-term survival.

In a small number of patients who presented with new RWMA before the dobutamine infusion, most of the segments that were dysfunctional during surgery were found to be viable on postoperative thallium studies, despite the lack of improvement of contractile function with dobutamine stimulation. It is possible that stunned myocardium is not consistently recruited by small-dose inotropic stimulation, but only by a larger dose, and that this may occur later in the postoperative period. In experimental models of acute ischemia, a dose-dependent increase in systolic thickening with dobutamine can be observed (23). In addition, in patients with postischemic ventricular dysfunction, segments that ultimately recover function after revascularization may not respond during DSE, despite preserved 18-F-2-fluoro-2-deoxy-D-glucose uptake on positron emission tomography (24). Therefore, the lack of response during dobutamine infusion (particularly small doses) is not necessarily a result of infarcted myocardium. In fact, as evidenced from our study, additional myocardium can further be recruited during large-dose dobutamine infusion. Furthermore, the viability of hypokinetic segments is highly influenced by tethering from adjacent segments, which may have a contrasting level of function (25). In the study by Chia et al. (25), small-dose DSE correctly identified only 65% of myocardial segments that ultimately improved after myocardial revascularization.

In contrast, a normal response to DSE (improvement in function) is highly specific in excluding nonviable myocardium. A previous study in patients for myocardial revascularization agrees with our finding that DSE underestimates viability, because late follow-up studies often show substantial improvement of function (26). Nuclear techniques are more sensitive in assessing hibernating myocardium because patients with no apparent contractile reserve may show other signs of viability, such as glucose usage (27). A study in patients with chronic coronary artery disease also demonstrated that contractile reserve detection by dobutamine SPECT was significantly less sensitive but more specific than perfusion quantification (28).

Few patients in our study exhibited a biphasic response to dobutamine infusion (improvement in function at small dose and deterioration at large dose). This finding contrasts with that occurring in animal studies, in which small-dose dobutamine-induced improvement of systolic wall thickening is accompanied by a parallel increase in distal coronary flow (29). However, at larger doses of dobutamine, systolic wall thickening deteriorates because of the increase in myocardial oxygen demand (increases in HR and MAP), and the jeopardized myocardium may become dysfunctional, resulting in either new or worsening RWMA. Because our study was performed in patients who had just undergone myocardial revascularization, it is likely that large-dose DSE did not result in more biphasic responses in which the RWMA deteriorate because the increase in myocardial oxygen demand was met by an increase in coronary vascular reserve.

Our study demonstrates that contractile reserve elicited by inotropic stimulation in the reperfusion period provides insight regarding subsequent viability. A normal response during DSE (improvement in contractile reserve) is highly specific for viable myocardium and is the most frequently observed finding. However, because a positive response during DSE (deterioration) is not particularly sensitive for infarcted myocardium, assessment of inotropic contractile reserve alone should not be the sole method for assessing myocardial viability in the postbypass reperfusion period.

How do we extend our results to the clinical setting in which a new RWMA is encountered during reperfusion? If the myocardial segment improves its contractile function in response to dobutamine stimulation, the myocardium is viable, and the etiology of the initial dysfunction is likely stunned myocardium. However, if the myocardial segment shows no immediate increase in contractile function during dobutamine stimulation, larger doses may be necessary. If deterioration in function is observed with larger doses, then recurrent ischemia is a likely etiology. Importantly, postoperative follow-up assessment of the left ventricular function and myocardial perfusion may be necessary to determine the reversibility of RWMA. Given our finding that dobutamine produces a dose-dependent increase in left ventricular performance primarily by increasing HR, an alternate drug with more inotropic than chronotropic properties may be indicated to recruit the potentially stunned myocardium.

Because of the early postoperative transfer of a number of patients, postoperative thallium studies were not available in these patients, thus decreasing the number of patients available for analysis. Also, not all myocardial segments described in the 16-segment left ventricular model were visualized in every patient or at each time point of measurement, thus limiting the total available number of myocardial segments for review. Because of individual anatomic variation, not all views can be obtained in all patients (11).

Not all the study patients received preoperative ß-adrenergic blockade. However, the response to DSE and the results from the postoperative thallium studies did not differ between patients who received versus those who did not receive preoperative ß-adrenergic blockade.

It is not feasible to perform intraoperative DSE with immediate follow-up by postoperative thallium studies because patients need to be stabilized in the intensive care unit before being sent to a nonmonitoring environment for the thallium studies. As a result, we cannot eliminate the small possibility that graft stenosis or occlusion may have occurred during the early postoperative period before the performance of the thallium studies.

Finally, we studied only patients presenting for elective CABG surgery. Patients presenting for emergency surgery may have a different contractile response from those observed in this study.

In conclusion, our results demonstrate that in the early reperfusion period, a normal response during DSE with an increase in contractile function is highly specific for viable myocardium. However, myocardial segments that are not readily recruited by inotropic stimulation are not necessarily indicative of infarcted myocardium. In fact, stunned myocardium may be the more likely etiology. Although DSE has been demonstrated to be a sensitive test in predicting myocardium at risk in patients with coronary artery disease, its usefulness in predicting nonviable myocardium in the reperfusion period is relatively small, because a substantial proportion of myocardium may not demonstrate immediate contractile improvement in this early reperfusion period.

	Acknowledgments

 
Supported in part by National Institutes of Health Grant 1K24 AG00948.

We are grateful to Dr. Nelson Schiller (Cardiology, Department of Medicine, University of California, San Francisco) for consultation on the initial study design. We thank the physicians in the Department of Anesthesia & Perioperative Care, University of California, San Francisco, and the Departments of Cardiovascular Anesthesiology and Cardiovascular Surgery, Kaiser Permanente Medical Center, San Francisco, for their cooperation in making the study possible. We also thank physicians in the Nuclear Medicine Departments from both institutions (Drs. Morita and Chin) for interpreting the thallium perfusion studies.

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