Author + information
- Received August 11, 1995
- Revision received July 15, 1996
- Accepted September 16, 1996
- Published online January 1, 1997.
- Stephen Sawada, MD, FACCA,*,
- Gregory Elsner, MDA,
- Douglas S Segar, MD, FACCA,
- Mark O’Shaughnessy, MDA,
- Samer Khouri, MDA,
- Judy Foltz, RNA,
- Patrick D.V Bourdillon, MD, FACCA,
- John R Bates, MDA,
- Naomi Fineberg, PhDA,
- Thomas Ryan, MD, FACCA,
- Gary D Hutchins, PhDA and
- Harvey Feigenbaum, MD, FACCA
- ↵*Dr. Stephen G. Sawada, University Hospital, Room 5420, 550 North University Boulevard, Indianapolis, Indiana 46202.
Objectives. We investigated the patterns of perfusion and metabolism in dysfunctional myocardium whose contractility improved with dobutamine.
Background. Clinical studies have suggested that dobutamine echocardiography can identify hibernating myocardium, but laboratory studies suggest that reduced perfusion limits the response to dobutamine.
Methods. Twenty-five patients with coronary disease and ventricular dysfunction underwent low (5 and 10 μg/kg body weight per min) and high dose (maximum of 50 μg/kg per min) dobutamine echocardiography and positron emission tomography (PET) using nitrogen-13 (N-13) ammonia and fluorine-18 fluorodeoxyglucose (FDG) for imaging of perfusion and metabolism. Wall motion and tracer uptake were scored in 16 left ventricular segments.
Results. Perfusion and metabolism were normal in 56.4%, mildly reduced in 29.1% and mismatched (reduced perfusion, preserved FDG uptake) in 14.5% of dysfunctional segments viable on PET. Wall motion improved with dobutamine in 89 dysfunctional segments (62 at low dose, 27 only at peak dose), and 86 of these (97%) were viable on PET. Improvement in wall motion with dobutamine was more common in segments with normal perfusion and metabolism (56.5%) than in those with mildly reduced tracer uptake (28.5%, p < 0.001) and those with mismatch (32%, p = 0.03). All the segments with a biphasic response were supplied by vessels with ≥70% stenosis, and 88% had normal perfusion and metabolism.
Conclusions. The majority of viable segments with rest dysfunction had normal perfusion and metabolism, suggesting that myocardial stunning was common. Improvement of wall motion at low and high doses of dobutamine was highly correlated with myocardial viability on PET and was more common in myocardium with normal perfusion. A biphasic response to dobutamine identified segments with normal perfusion and metabolism supplied by severely diseased vessels.
(J Am Coll Cardiol 1997;29:55–61)>
Dobutamine echocardiography is a recent addition to the list of imaging methods used for detection of myocardial viability. In experimental and clinical studies, improvement in wall motion with dobutamine stimulation has been found to be a sensitive indicator of stunned but viable myocardium after restoration of blood flow after acute ischemic injury ([1, 2]). In the setting of acute infarction treated with thrombolytic agents, metabolic imaging and dobutamine echocardiography yield similar results in distinguishing viable from infarcted myocardium ().
The phenomenon of myocardial hibernation—a reduction in rest myocardial perfusion resulting in diminished left ventricular contractility—is thought to account for systolic dysfunction in patients who have viable myocardium and chronic, advanced coronary artery disease ([4–6]). The results of recently published clinical studies suggest that dobutamine echocardiography may also be useful for the detection of viable myocardium in these patients with advanced coronary artery disease and reduced left ventricular function ([7–9]). However, some experimental observations suggest that dobutamine stimulation may be less effective for the detection of viability when rest myocardial perfusion is reduced ().
Positron emission tomography (PET), by virtue of its ability to assess myocardial perfusion and metabolism using fluorine-18 fluorodeoxyglucose (FDG), is widely regarded as the most accurate technique for the detection of viable myocardium. A “mismatch” pattern, characterized by a reduction in perfusion tracer uptake with normal or increased uptake of FDG, has been described as the PET correlate of myocardial hibernation ([5, 11]). In this investigation, patients with regional wall motion abnormalities, reduced systolic function and advanced coronary artery disease underwent dobutamine echocardiography and PET to identify the patterns of perfusion and metabolism that occur in dobutamine-responsive myocardium. This study also evaluated the accuracy of rest and dobutamine echocardiography for the detection of myocardial viability using metabolic imaging as the reference standard.
1.1 Patient selection.
The Indiana University PET facility began operation in February 1993. Between February and November 1993, 53 patients with coronary artery disease and wall motion abnormalities were evaluated for myocardial viability at the facility. Twenty-six patients who also underwent dobutamine echocardiography for assessment of myocardial viability comprised the study group. The viability studies were performed at the discretion of the referring physician and written informed consent was obtained for dobutamine echocardiography. One subject who had a change in clinical status between the two imaging studies was excluded.
In the remaining 25 patients (4 women, 21 men) the mean age was 58 ± 10 years and the average time between the studies was 13 ± 21 days. All patients had reduced left ventricular systolic function (ejection fraction 32 ± 9% [range 15% to 49%]). Eighteen patients had a history of prior myocardial infarction. Five with a recent infarction (<4 weeks) underwent PET from 5 to 11 days after the event. Eleven patients had diabetes mellitus and 13 had hypertension. Twenty-three patients were receiving medication to treat ischemia (nitrates in 22 patients, beta-blockers in 7 and calcium antagonists in 6). Twelve patients had angina, and four of these had worsened symptoms at the time of evaluation. No patients had unstable angina. Nineteen patients had mild heart failure symptoms (New York Heart Association functional class I or II), and six had more severe symptoms (functional class III or IV).
1.2 Positron emission tomography.
Patients were requested to fast for 4 to 6 h before the PET study. Oral glucose (50 g) was administered before beginning the study. In patients with diabetes mellitus, studies were performed with the patients on their usual diet and medications. Plasma glucose levels were monitored during the study, and if necessary, intravenous insulin was administered to reduce glucose levels and enhance FDG uptake. Positron emission tomography was performed using a whole-body tomograph (Siemens 951/31R). A 15-min transmission scan was performed after positioning the patient. A 20-mCi dose of nitrogen-13 (N-13) ammonia was administered intravenously for assessment of myocardial perfusion. Beginning 5 min after injection, images were obtained for a 20-min period. After decay of the ammonia, 10 mCi of FDG was administered. Thirty minutes after injection, images were acquired for a 20-min period. For those patients with glucose intolerance, FDG imaging was delayed until the plasma glucose level was reduced by insulin administration. After treatment, glucose levels were comparable between subjects with and without glucose intolerance (106 ± 25 mg/dl vs. 110 ± 27 mg/dl, p = 0.72). The image data were reconstructed using a Hanning filter (cutoff frequency 0.35 cycles/pixel) to transaxial images, which were resliced into a series of short-axis and long-axis images.
1.3 Dobutamine echocardiography.
Echocardiograms were performed using commercially available equipment (Hewlett Packard Sonos 1500, Advanced Technology Laboratories UM4). The modified Simpson method was used to obtain the ejection fraction from the apical four-chamber view of the baseline study in 24 subjects. In one subject the ejection fraction was determined by visual assessment of the contrast ventriculogram.
Intravenous dobutamine was infused in incremental fashion starting at a dose of 5 μg/kg body weight per min. The dose was increased to 10 μg/kg per min after 3 min and then by 10-μg/kg per min increments every 3 min. End points for the infusion included 1) extensive new or worsening wall motion abnormalities; 2) chest pain; 3) ≥2 mm ST segment depression or elevation; 4) significant side effects, arrhythmias or hypotension as determined by the operator; 5) ≥85% of the age-predicted maximal heart rate; and 6) maximal dose of 50 μg/kg per min. Intravenous atropine was administered in patients who had minimal increases in heart rate at doses ≥30 μg/kg per min. Echocardiographic images using parasternal and apical windows were recorded on videotape and digitally acquired in a quad screen format at baseline, at 5 and 10 μg/kg per min and at peak dose in 21 patients, and at baseline, 10 μg/kg per min and peak dose in 4 other patients ().
1.4 Analysis of PET images.
Before initiation of this study, the interobserver variability of visual assessment of the PET images was determined by having two experienced observers independently interpret the perfusion and metabolism studies of 20 patients evaluated at our PET facility. The interobserver agreement for distinguishing normal and reduced perfusion was 84%. The interobserver agreement for determination of viability based on FDG uptake was 92%. For the purposes of this study, a single observer who had no knowledge of the clinical data and the results of echocardiography visually assessed and scored the uptake of N-13 ammonia and FDG in 16 left ventricular segments. The scheme used for segmentation of the left ventricle has been previously described (). Assessment of tracer uptake was made primarily from three resliced short-axis images at the base of the left ventricle, at the midpapillary muscle level and at the apex. The posterior junction of the right and left ventricles, visible on the N-13 ammonia images, was used to define the location of the basal and midinferior segments, and the locations of the remaining basal and midventricular segments were determined using the posterior and anterior (when visualized) junctions of the ventricles as reference points.
Tracer uptake was graded using a four-point scale: 1 = normal; 2 = mildly reduced; 3 = moderately reduced; 4 = severely reduced or absent and equal to background activity (). For the purposes of this study, myocardial segments with FDG scores ≥3 were considered to be nonviable and were designated as having transmural infarction. Segments with normal or mildly reduced FDG uptake were considered viable. These segments were divided into three groups: Segments with normal FDG uptake (=1) in the presence of reduced N-13 ammonia uptake (≥2), or mildly reduced FDG uptake (≤2) in the presence of moderate or severely reduced N-13 ammonia uptake (≥3) were defined as having perfusion-metabolism mismatch. Segments with FDG and N-13 ammonia uptake (=2) were defined as having a pattern of nontransmural infarction. Segments that had N-13 ammonia and FDG scores = 1 were designated as the normal N-13 ammonia, normal FDGgroup. After completion of this study, a quantitative method for determining tracer uptake was developed and used to validate the visual scoring technique. Circumferential profiles of tracer uptake were derived in 15 subjects using the semiautomated analysis program. Tracer uptake in 16 segments of the left ventricle was determined after normalization of both the N-13 ammonia and FDG images to the region having maximal ammonia uptake.
1.5 Analysis of echocardiographic images.
Two observers, who had no knowledge of the clinical data and results of PET imaging, rendered a consensus analysis of wall motion at rest and with dobutamine infusion in 16 left ventricular segments. Wall motion was graded as 1 = normal, hyperkinetic with dobutamine; 2 = mildly hypokinetic, <5 mm inward systolic motion; 2.5 = severely hypokinetic minimal inward systolic motion and wall thickening; 3 = akinetic, absence of inward motion and wall thickening; 4 = dyskinetic. Improvement in segmental wall motion by one grade or more (including severe to mild hypokinesis) was considered significant. For the purposes of comparison with the PET results, myocardial segments with scores ≤2.5 at rest or with dobutamine infusion were considered viable.
1.6 Coronary angiography.
Coronary angiography was performed in all subjects. An experienced angiographer who had no knowledge of the results of PET and echocardiographic imaging determined percent diameter stenosis by caliper measurement or visual estimation. Significant coronary artery disease was defined by ≥50% reduction in lumen diameter of an epicardial coronary artery or major branch vessel. Severe disease was defined by ≥70% stenosis of a major vessel.
1.7 Statistical analysis.
A preliminary analysis was performed to determine if a segment by segment analysis of the data was appropriate in the absence of any consistent intra-patient correlations of the segment data. A total of 120 possible correlations between the 16 left ventricular segments were examined for each stage of the dobutamine echocardiographic study and for the perfusion and metabolism data. The proportion of segment pairs that had no statistically significant correlation (p ≥ 0.05) was 73%, and in the remainder with significant correlations both positive and negative correlations were found. Because there were no consistent correlations, the segment was used as the unit of analysis.
Continuous variables are reported as mean values ± SD. Mean values between different groups were compared using the ttest statistic. The Fisher exact test was used to analyze categorical variables. The correlation between PET and echocardiography for assessment of myocardial segment viability was expressed as percent agreement and value of kappa. The McNemar test was used in the analysis of discordant PET and echocardiographic results. A p value <0.05 was considered significant.
2.1 Dobutamine infusion and coronary angiography.
Low and peak dose echocardiographic studies were completed in all 25 subjects without complications. No patient had sustained arrhythmia or prolonged ischemia resulting from dobutamine infusion. Five patients received sublingual nitroglycerin or esmolol, or both, to treat induced ischemia. The peak dose of dobutamine was 40 ± 10 μg/kg per min (range 20 to 50), and eight subjects received atropine. The mean heart rate at baseline was 77 ± 15 beats/min and 130 ± 14 beats/min at peak dose. The rate-pressure product was 8,980 ± 2,265 mm Hg × beats/min at baseline, and 17,256 ± 4,316 mm Hg × beats/min at peak dose.
Twenty-one patients (84%) had multivessel and four had single-vessel disease. Nineteen patients (76%) had ≥70% stenosis of at least one coronary artery.
2.2 Positron emission tomography and dobutamine echocardiography.
Tracer uptake was quantitatively assessed in 15 patients to determine if the visual scoring system used in this study reliably distinguished different groups of segments, including those with reduced perfusion and those with mismatch. Significantly greater N-13 ammonia uptake was seen in segments with normal (score 1) compared with mildly reduced (score 2) perfusion (83 ± 11% vs. 66 ± 13%, p < 0.001). Fluorine-18 FDG uptake was significantly greater in segments with mildly reduced metabolism (score 2) (73 ± 14%) compared with tracer uptake in those scored as nonviable (scores 3 and 4) (60 ± 14%, p = 0.006). The FDG/N-13 ammonia ratio was significantly greater in segments with mismatch (1.53 ± 0.42) compared with all other viable segments with reduced perfusion (1.05 ± 0.17, p < 0.001).
A total of 31 myocardial segments were excluded from analysis because of inadequate echocardiographic or PET images. Regional wall motion was assessed in the remaining 369 left ventricular segments. Baseline wall motion was abnormal in 247 segments (67%) and normal in 122 segments. Fluorine-18 FDG uptake indicative of myocardial viability was found in 192 dysfunctional segments (78%), and 55 segments were nonviable according to PET criteria.
The perfusion and metabolism patterns in the 192 dysfunctional segments with FDG evidence of myocardial viability are shown in Fig. 1. Segments with normal perfusion and metabolism were most common. Only 14.5% of dysfunctional segments had perfusion-metabolism mismatch. One segment had normal perfusion and mildly reduced FDG uptake, and in subsequent analyses this segment was included in the nontransmural infarction group.
Improvement in wall motion at low doses of dobutamine (5 or 10 μg/kg per min) occurred in 62 (25%) of the 247 dysfunctional segments. An additional 27 (11%) improved at peak dose. Fluorine-18 FDG evidence of myocardial viability was found in 86 (97%) of the 89 segments that had improved wall motion with dobutamine. Wall motion did not improve with dobutamine stimulation in 158 dysfunctional segments. A substantial but significantly smaller proportion of these segments (106 of 158 [67%]) had PET evidence of myocardial viability compared with segments (86 of 89 [97%], p < 0.001) that demonstrated improvement with dobutamine.
Each dysfunctional segment with PET evidence of myocardial viability was assigned to one of three groups based on the pattern of perfusion and metabolism, and the proportion of segments with improvement in wall motion was determined within each group. Fig. 2demonstrates that improvement in wall motion was more common in the group of segments with normal uptake of N-13 ammonia and FDG than in the groups with reduced perfusion that had the patterns of nontransmural infarction or mismatch.
Each dysfunctional segment that improved with dobutamine (n = 89) was assigned to one of four categories that characterized the low dose (5 or 10 μg/kg per min) and peak dose changes in wall motion. Wall motion improved at low dose and was unchanged at peak dose in 35 segments (39%). Ten segments (11%) improved at low dose and continued to improve at peak dose. Another 27 segments (30%) improved only at peak dose, and 17 (19%) had a biphasic response, improving at low dose and worsening at peak dose. The PET results were compared in the four wall motion categories to identify any associations between perfusion-metabolism patterns and wall motion responses (Table 1). The few segments with transmural infarction were found only in the two groups (groups 2 and 3) that demonstrated improvement in wall motion at peak dose. Normal perfusion and metabolism was the most common pattern in each of the wall motion categories. The proportion of segments with normal perfusion and metabolism was highest in the group with a biphasic response (88% vs. 64% of segments in the other three groups, p = 0.08).
Fluorine-18 FDG evidence of myocardial viability was present in all segments that exhibited a biphasic response. The worsening of wall motion at peak dose suggested that these segments had stress-induced ischemia and were likely to be supplied by vessels with significant obstruction. The frequency of severe disease (≥70% diameter reduction) in vessels supplying segments with a biphasic response was compared with the frequency of severe disease supplying segments in the three remaining categories that did not have stress-induced ischemia. Every segment having a biphasic response was supplied by a vessel with severe stenosis (Fig. 3). The frequency of severe stenosis in each of the groups without stress-induced ischemia was significantly less than in the group with a biphasic response.
2.3 Correlation of metabolic imaging and echocardiography for detection of myocardial viability.
The correlation between metabolic imaging and echocardiography for identification of myocardial viability and nonviability in the 369 segments analyzed is shown in Table 2. Segment viability was defined by the presence of any inward motion on the baseline or dobutamine echocardiographic study. The PET criterion for segment viability was an FDG score ≤2. There was significant agreement between PET and echocardiography for identification of viable and nonviable segments (76.1% of segments, kappa = 0.362). Among discordant segments, more were designated viable on PET and nonviable on echocardiography compared with the number that were considered nonviable on PET and viable on echocardiography (70 vs. 18 segments, p < 0.001).
3.1 Perfusion and metabolism patterns.
The persistent dysfunction that is seen in patients with chronic and advanced coronary artery disease is usually attributed to myocardial hibernation. This phenomenon is characterized by a reduction in rest myocardial perfusion and a concomitant reduction in myocardial contractility. Hibernating myocardium may be identified by PET on the basis of perfusion-metabolism mismatch, the reduction of N-13 ammonia uptake in the presence of preserved FDG uptake ([5, 11]). In our study perfusion-metabolism mismatch was present in <15% of dysfunctional segments that had PET evidence of myocardial viability. In the majority of segments, both N-13 ammonia and FDG uptake were scored as normal. These findings were unexpected in this study group, which was composed primarily of patients with severe, chronic disease and reduced ejection fraction. Previous studies utilizing PET for detection of myocardial viability have focused primarily on the analysis of mismatched segments. However, in one of these studies normal perfusion and metabolism was also a common finding (61%) in dysfunctional but viable segments (). In a study by vom Dahl et al. (), mismatched segments also comprised a minority (37%) of the dysfunctional segments with preserved metabolism. Persistent contractile dysfunction in segments with normal perfusion may result from stunning caused by repetitive episodes of ischemia ([5, 16]). In these studies of patients who have advanced coronary artery disease, the frequency of segments with normal perfusion suggests that the phenomenon of stunning may play a significant role in the pathogenesis of persistent ventricular dysfunction.
3.2 Detection of myocardial viability in normal and hypoperfused segments.
The results of recent clinical studies have suggested that dobutamine echocardiography has good sensitivity for the detection of myocardial viability, even in patients with severe coronary artery disease and left ventricular dysfunction ([8, 9]). However, experimental evidence suggests that dobutamine stimulation is less effective for the detection of viability when rest myocardial perfusion is severely reduced (). In this situation, augmentation of contractility may be prevented by a critical reduction in oxygen supply. Alternatively, the magnitude of augmentation may be very transient or below the threshold of detection by noninvasive imaging ([4, 17]). In our study, improvement of wall motion was more commonly observed in segments that had normal perfusion compared with those with mismatch and those with an equivalent, mild reduction in both perfusion and metabolism. The lack of improvement in segments with mismatch could be attributed to the reduction in baseline perfusion. These results would support the findings of Panza et al. (), who reported that the frequency of improvement with dobutamine declined in proportion to the severity of perfusion abnormality. Our results differ somewhat from the data reported by Perrone-Filardi et al. (), who found that dobutamine stimulation maintained sensitivity (88%) for viability in segments with thallium-201 uptake <80% of maximal uptake. The disparity in these results may be due to the different criteria used for defining hypoperfused segments and the exclusive enrollment of subjects with reduced left ventricular systolic function in our study.
In our study segments that had mild reductions in both perfusion and metabolism were also less likely to improve with dobutamine, compared with segments with normal perfusion. Segments with mild reductions in both perfusion and metabolism may fail to augment when there has been sufficient subendocardial necrosis. The data of vom Dahl et al. (), showing that these segments are unlikely to improve in function after revascularization, support the hypothesis of infarction of the subendocardium, the portion of myocardium contributing most to contractility ().
3.3 Wall motion responses and perfusion-metabolism patterns.
Four patterns of low and peak dose changes in wall motion were identified in segments that improved with dobutamine. Segments with FDG uptake indicative of transmural infarction were confined to the groups of segments demonstrating improvement at the peak dose of dobutamine. In a study of patients with chronic coronary artery disease, Afridi et al. () demonstrated that revascularization infrequently results in improved wall motion of dysfunctional segments that augment at peak doses of dobutamine. Our data suggest that the majority of these segments have some viable tissue, and in a small proportion (8%), tethering may account for the appearance of viability during dobutamine stimulation.
A biphasic response to dobutamine, with improvement of wall motion at low doses and subsequent worsening at peak dose, is thought to occur in viable myocardium that becomes ischemic with stress. Afridi et al. () reported that the biphasic response was the wall motion pattern that best predicted segments that had improved function after revascularization. Their data suggest that the biphasic response identifies segments with substantial contractile reserve. Our results are consistent with this hypothesis, as nearly all segments with a biphasic response had normal perfusion, suggesting transmural viability. The proportion of segments with normal perfusion was lower in every other category of wall motion response, suggesting a lower frequency of transmural viability in these categories. In our study, all segments that had a biphasic response were subtended by a vessel with ≥70% stenosis, lending credence to the hypothesis that the peak dose deterioration of wall motion is a sign of induced ischemia. Additionally, the observation that the biphasic response occurs in normally perfused segments suggests that the rest dysfunction in these segments could be due to stunning.
3.4 Echocardiography versus PET for detection of myocardial viability.
In our study, improvement of wall motion with dobutamine was a specific finding for preserved FDG uptake. However, improvement with dobutamine was not a sensitive marker for preserved FDG uptake, as 19% of all segments had PET evidence of viability but were considered nonviable according to echocardiographic criteria. Baer et al. () have previously reported that dobutamine stimulation underestimates the number of segments with preserved FDG uptake. The amount of viable tissue required to determine the presence of metabolic activity is likely to be less than that required for detection of contractile reserve. In our study, a larger proportion of segments with preserved FDG uptake failed to improve with dobutamine. In contrast to the group studied by Baer et al. (), all of our subjects had global systolic dysfunction and extensive coronary artery disease and regional wall motion abnormalities. Dobutamine stimulation may be less sensitive when there are extensive areas of akinesia in combination with reduced perfusion (). Additionally, other systemic disorders, such as diabetes, may have contributed to ventricular dysfunction. In nonischemic cardiomyopathy metabolic activity may be preserved, but contractile function may be exhausted ().
3.5 Study limitations.
This study employed the standard protocol for assessment of myocardial viability and detection of ischemia used in our laboratory. Echocardiographic imaging was performed during two low dose stages (5 and 10 μg/kg per min) and a peak dose stage (mean 40 ± 10 μg/kg per min) of dobutamine infusion. The majority of viable segments may be detected using these two low dose stages, but other investigators have demonstrated the incremental value of additional low dose stages (7.5 μg/kg per min) and intermediate doses (15 and 20 μg/kg per min) for detection of viability ([10, 17, 19]). We may have underestimated the number of augmenting segments by not capturing and analyzing intermediate dose stages.
This study used visual analysis for both wall motion and tracer uptake. The results of quantitative analysis in a subset of patients suggested that visual assessment of tracer uptake defined different groups of segments. Qualitative analysis of wall motion remains the standard in clinical practice.
For the purposes of this study, we categorized the results of perfusion and metabolism imaging into several patterns. Perfusion-metabolism mismatch may identify hibernating myocardium, but stunned tissue and admixtures of viable and necrotic tissue may also be found in regions of mismatch ([23, 24]). We also designated segments as having nontransmural and transmural infarction based solely on the severity of reduction of perfusion and metabolism in the absence of pathologic data determining the true transmural extent of necrosis.
This study did not provide any information on the relative merits of dobutamine stimulation and PET for predicting improvement in contractile function after revascularization. This topic may arguably be the most important to investigate, but the primary purpose of this study was to examine patterns of perfusion and metabolism in dysfunctional myocardium that responds to dobutamine. Our study demonstrated that dobutamine stimulation underestimates the number of segments with preserved FDG uptake. For prediction of functional recovery, the results of recent studies suggest that the sensitivity of dobutamine stimulation is similar to that reported for PET ([8, 9, 14, 15, 18, 21, 23, 25]).
Normal perfusion and metabolism occurred more frequently than mismatch, suggesting that myocardial stunning may be more common than hibernation in this study group with advanced coronary artery disease and left ventricular dysfunction. Improvement of wall motion at both low and peak doses of dobutamine was highly correlated with PET evidence of myocardial viability. Improvement of wall motion with dobutamine was more frequent in segments with normal perfusion compared with those with patterns of mismatch or nontransmural infarction. A biphasic response to dobutamine was indicative of segments with normal perfusion, suggesting transmural viability, and the presence of severe coronary artery disease. Positron emission tomography and echocardiography demonstrated fair agreement for detection of myocardial viability, with PET identifying more segments as viable compared with echocardiography.
We thank Patricia Brenneman and Ratnakar Amaravadi for their technical assistance.
☆ The study was supported in part by the Herman C. Krannert Fund, Indianapolis; the SCOR grant (HL-52323) in Sudden Cardiac Death; and Grants HL-06308 and HL-07182 from the National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland. This study was presented in part at the 67th Annual Scientific Sessions of the American Heart Association, Dallas, Texas, November 1994.
- fluorine-18 fluorodeoxyglucose
- positron emission tomography
- Received August 11, 1995.
- Revision received July 15, 1996.
- Accepted September 16, 1996.
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