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Circulation. 1995;92:334-341

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(Circulation. 1995;92:334-341.)
© 1995 American Heart Association, Inc.

Articles

Infarct Size After Acute Myocardial Infarction Measured by Quantitative Tomographic 99mTc Sestamibi Imaging Predicts Subsequent Mortality

Todd D. Miller, MD; Timothy F. Christian, MD; Mona R. Hopfenspirger, RN; David O. Hodge, MS; Bernard J. Gersh, MB, ChB, DPhil; Raymond J. Gibbons, MD

From the Divisions of Cardiovascular Diseases and Internal Medicine (T.D.M., T.F.C., M.R.H., B.J.G., R.J.G.) and Statistics and Health Sciences Research (D.O.H.), Mayo Clinic, Rochester, Minn; and the Cardiology Division (B.J.G.), Georgetown University Medical Center, Washington, DC.

Correspondence to Todd D. Miller, MD, East 16-A, Mayo Clinic, 200 First St SW, Rochester, MN 55905.


*    Abstract
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 *Abstract
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Background 99mTc sestamibi is a recently developed radioisotope that has been used to measure myocardium at risk and infarct size. The relation between these measurements and subsequent patient outcome has not yet been demonstrated.

Methods and Results Two hundred seventy-four consecutive patients with acute myocardial infarction underwent tomographic 99mTc sestamibi imaging on arrival at the hospital (to measure myocardium at risk before reperfusion therapy) and at hospital discharge (to measure the amount of salvaged myocardium and final infarct size). Defect size on the sestamibi images was quantified using a threshold value of 60% of peak counts from the circumferential count profile curves generated for five representative slices of the left ventricle. Patients were followed after hospital discharge to evaluate the association between final infarct size and subsequent mortality. The median defect size measured was 27% of the left ventricle at presentation to the hospital (range, 0% to 77%) and was 12% of the left ventricle at hospital discharge (range, 0% to 68%). Almost one half of the patients had a final infarct size of <=10%. The median amount of myocardium salvaged was 9% (range, -31% to 75%). During a median duration of follow-up of 12 months, there were 10 deaths (7 cardiac and 3 noncardiac) and 1 resuscitated out-of-hospital cardiac arrest. There was a significant association between infarct size and overall mortality ({chi}2=8.66, P=.003) and cardiac mortality ({chi}2=11.89, P<.001). Two-year mortality was 7% for patients whose infarct size was >=12% versus 0% for patients whose infarct size was <12%. There also was a significant association between myocardium at risk and cardiac mortality ({chi}2=6.87, P=.009). There was no association between myocardium at risk and overall mortality or between amount of myocardium salvaged and either overall mortality or cardiac mortality.

Conclusions Larger infarct size measured by 99mTc sestamibi imaging after acute myocardial infarction is associated with increased mortality risk during short-term follow-up.


Key Words: 99mTc sestamibi • imaging • myocardial infarction • mortality • prognosis


*    Introduction
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Imaging by 99mTc sestamibi in the setting of acute myocardial infarction can be useful for a number of reasons. Imaging performed on arrival at the hospital can identify the amount of myocardium at risk.1 2 3 4 5 6 7 8 9 Subsequent imaging after reperfusion therapy can measure final infarct size.1 2 3 4 5 6 7 8 9 10 The difference between these two measurements is the amount of myocardium salvaged. The amount of myocardium salvaged and final infarct size are sensitive end points that can be used to compare the effectiveness of different treatment strategies in myocardial infarction.11

Infarct size measured by 99mTc sestamibi imaging has been validated in a phantom model12 and shows a close correlation with directly measured infarct size in pathology specimens from both laboratory animals13 14 and humans.15 99mTc sestamibi infarct size also shows a close correlation with other physiological measurements of infarct size in humans, including left ventricular ejection fraction,1 4 6 7 left ventricular end-systolic volume index,7 extent of regional wall motion abnormality,1 6 201Tl infarct size,2 10 and myocardial enzyme release.4 It is reasonable to assume that infarct size measured by this technique is related to patient outcome, but this assumption has not yet been proved. The validity of using 99mTc sestamibi imaging to measure the efficacy of different treatment strategies in acute myocardial infarction depends on this assumption.

The primary purpose of the present study was to determine whether larger infarct size measured by 99mTc sestamibi imaging at hospital discharge predicts subsequent mortality. Secondary objectives were to assess whether myocardium at risk and amount of myocardium salvaged are associated with outcome.


*    Methods
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Study Design and Patient Entry Criteria
A consecutive series of 406 patients was enrolled in several different prospective studies evaluating the use of 99mTc sestamibi imaging in acute myocardial infarction between February 1988 and February 1993. From this series, patients were included in the present study if they fulfilled the criteria of documented myocardial infarction by the presence of chest pain at least 30 minutes in duration and elevated creatine kinase–MB isoenzyme levels measured within 24 hours of chest pain and 99mTc sestamibi imaging performed acutely on presentation to the hospital and at hospital discharge. Two hundred seventy-four patients met the entry criteria. The majority of these patients were also enrolled in other ongoing studies examining reperfusion therapy in acute myocardial infarction, including 6 patients in the Thrombolysis in Myocardial Infarction (TIMI) trial,16 55 patients in the Global Utilization of Streptokinase and Tissue Plasminogen Activator (GUSTO) trial,17 and 101 patients in a Mayo Clinic study comparing immediate angioplasty with thrombolytic therapy.11 Of the 129 patients who did not meet the study entry criteria, 7 were injected with 99mTc sestamibi after receiving reperfusion therapy, 29 were injected but either were never imaged or were unable to complete the acute images because of unstable clinical courses, and 93 had acute images but not predischarge images (23 died in the hospital, 24 had emergency coronary artery bypass graft surgery and did not undergo delayed imaging before discharge, and 46 treated with medical therapy and/or coronary angioplasty did not undergo delayed imaging at the discretion of the patients or their primary cardiologists).

99mTc Sestamibi Imaging
Image acquisition, processing, and interpretation have been reported in detail previously.1 12 In brief, all patients received an intravenous injection of 20 to 30 mCi of 99mTc sestamibi on presentation to the hospital before reperfusion therapy. Tomographic imaging was performed 1 to 6 hours later. Because 99mTc sestamibi does not undergo significant redistribution,18 19 imaging can be delayed until reperfusion therapy is completed and still accurately reflect myocardium at risk before the administration of reperfusion therapy. Imaging was repeated at hospital discharge 7±8 days after admission.

Images were acquired using a rotating gamma camera with an all-purpose collimator. Processing and reconstruction were performed using standard back-projection algorithms and a Ramp-Hanning filter. Circumferential count profiles were generated for five representative short-axis slices of the left ventricle extending from apex to base. Infarct size was quantified using a threshold value of 60% of peak counts. The defect size was expressed as a percentage of the left ventricle. Infarct size measured by this technique has been validated in a phantom model,12 in animal models of permanent occlusion13 and reperfusion,14 and in explanted human hearts at the time of cardiac transplantation.15 The limit for detection of infarction by this technique has been shown to be 3% of the left ventricle.1 12 Infarct size measured by 99mTc sestamibi imaging has also been demonstrated to correlate closely with other physiological parameters that have been used to measure infarct size in humans, including indexes of global and regional left ventricular systolic function,1 4 6 7 201Tl infarct size,2 10 and myocardial enzyme release.4

Attenuation of counts from overlying soft tissue (diaphragm and breast) occurs with all cardiac radioisotopes and theoretically might cause defects below the 60% threshold, which would erroneously be labeled as infarction using this technique. To address this issue, we quantitated the resting 99mTc sestamibi images from a consecutive series of 100 patients undergoing exercise sestamibi studies in our laboratory. These patients were selected on the basis of having a normal resting ECG and no clinical history of myocardial infarction. The majority of these patients were referred for 99mTc sestamibi imaging rather than 201Tl imaging because they were overweight. Mean body weight was 89±19 kg. Eighty-one patients had normal images by the use of the 60% threshold quantitative program. Eight patients had trivial defects measuring between 1% and 3% of the left ventricle. Thus, 89% of patients had normal images or trivial defects. The remaining 11 patients had inferior wall defects that measured between 4% and 21% of the left ventricle. Seven of these 11 patients underwent further cardiac evaluation, all of whom had either a significant stenosis in the artery supplying the defect and/or a wall motion abnormality on echocardiography in the same territory. These 7 patients included the 4 patients with defects of >10% of the left ventricle. Thus, tissue attenuation played a minor role in this series of patients, many of whom were obese, and would be expected to cause defects even less frequently in nonobese patients.

Coronary Angiography and Resting Radionuclide Angiographic Ejection Fraction
Two hundred forty-nine patients underwent coronary angiography before hospital discharge. Selective coronary angiography was performed in multiple views and graded subjectively by an experienced angiographer according to Coronary Artery Surgery Study criteria.20 A 6-week ejection fraction was measured in 124 patients according to previously published techniques.21

Follow-up Procedures
All follow-up information was collected using a combination of chart review or contact with patients or their physicians by mailed questionnaire or telephone. Significant events were defined as death from any cause and resuscitated cardiac arrest. Recurrent myocardial infarction and coronary angioplasty and bypass surgery performed after hospital discharge were also recorded but not counted as events. All events were verified by hospital records and/or death certificates. Deaths were categorized as cardiac or noncardiac on the basis of the data collected without knowledge of the 99mTc sestamibi imaging results. Follow-up was 100% complete at a median duration of 12 months in those patients alive at follow-up.

Statistical Analysis
The associations between patient outcome and predischarge infarct size, myocardium at risk, and myocardial salvage were analyzed using the proportional hazards general linear model (Cox) procedure.22 The outcome end points analyzed included overall mortality and cardiac mortality. Successfully resuscitated cardiac arrest was counted as a cardiac death. For the end point of overall mortality, patients were considered under analysis until death or last follow-up. No patients were censored. For the end point of cardiac mortality, two analyses were performed. In the first analysis, patients were followed to the time of cardiac death or last follow-up. Intervening revascularizations were ignored. The only patients censored from this analysis were those with noncardiac deaths. In the second analysis, patients who underwent revascularization before dying were also censored at the time of the procedure. Mortality curves were generated using the Kaplan-Meier method.23 For all analyses, a value of P<.05 was considered significant.


*    Results
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Study Group
Table 1Down shows demographic characteristics and coronary anatomy for the 274 patients. Only a minority of patients had a history of prior myocardial infarction or had previously undergone revascularization. Most patients presented with ST-segment elevation on the initial ECG and were treated with reperfusion therapy (defined as thrombolysis and/or revascularization performed within 24 hours of presentation to the hospital). Of the 249 patients who underwent coronary angiography before hospital discharge, 20% had three-vessel coronary artery disease. One hundred twenty-four patients had left ventricular ejection fraction measured at 6 weeks after hospital discharge. Median ejection fraction was 50% (range, 19% to 75%).


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  		Table 1. Clinical Characteristics and Coronary Anatomy of the 274 Study Patients

Results of Sestamibi Imaging
Myocardium at risk, infarct size, and amount of myocardium salvaged are presented in Table 2Down. The median initial defect size measured at hospital admission (myocardium at risk) was 27%. The median final defect size measured at hospital discharge (infarct size) was 12%. The median amount of myocardium salvaged was 9%. Fig 1Down is a histogram showing the percentages of patients grouped by infarct size measured on the predischarge 99mTc sestamibi images. The individual patients who had events are also indicated on this figure (see below). Of note, almost one fourth of the study group had infarct size measured at 0%, and another one fourth of the patients had infarct size measured at <=10% of the left ventricle. Thirty-three percent of patients had an infarct size of >20% of the left ventricle. Thirty-six patients (13% of the study group) had a final infarct size of >40%.


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  		Table 2. Results of 99mTc Sestamibi Imaging



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  		Figure 1. Bar graph of distribution of infarct size grouped by 10% increments of the left ventricle (LV). The individual patients with events during follow-up are also shown according to type of event and infarct size.

Events During Follow-up
Eleven patients had subsequent events, including 10 deaths and 1 resuscitated out-of-hospital cardiac arrest. Three of the 10 deaths were noncardiac (prostate cancer, stroke, and multisystem failure with disseminated intravascular coagulation). Of the 7 cardiac deaths, 5 were initial cardiac events after the index infarction and 2 occurred after intervening revascularization procedures (1 occurred 33 months after bypass surgery, and 1 perioperative death occurred at the time of bypass surgery). Table 3Down describes characteristics of the individual patients who had events. As shown in Table 3Down and Fig 1Up, no patient with an infarct size of <20% had a cardiac event. Six of the 8 cardiac deaths occurred in patients whose infarct size was more than the 75th percentile of 26%.


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  		Table 3. Characteristics of Individual Patients With Events During Follow-up

In addition to the 11 patients with events noted above, during follow-up 8 patients had recurrent myocardial infarctions and 51 patients underwent at least one revascularization procedure after hospital discharge (33 patients within 3 months).

Association Between Infarct Size and Mortality
There was a significant association between infarct size and overall mortality ({chi}2=8.66, P=.003). The association was stronger between infarct size and cardiac mortality ({chi}2=11.89, P<.001 if all 8 cardiac events were included as end points; {chi}2=11.91, P<.001 if the 2 patients who underwent revascularization before dying were censored at the time of revascularization from analysis). Fig 2Down shows overall mortality curves for the entire population and for the population divided into two groups on the basis of median infarct size. For the entire population, 2-year mortality was very low—3%. For patients with infarct size of >=12%, 2-year mortality was 7%; in contrast, all patients with infarct size of <12% were alive at 2 years.



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  		Figure 2. Plot of mortality curves for the entire study population and for the population divided into two groups on the basis of median infarct size. Numbers in parentheses at the bottom of the figure indicate the patients from each group available for analysis at the given points in time.

There also was a significant association between myocardium at risk and cardiac mortality ({chi}2=6.87, P=.009 if revascularizations were ignored; {chi}2=6.06, P=.014 if revascularizations were censored). There was no association between myocardium at risk and overall mortality ({chi}2=2.62, P=NS) or between myocardial salvage and either overall mortality ({chi}2=1.03, P=NS) or cardiac mortality ({chi}2=0.51, P=NS).


*    Discussion
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*Discussion
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Measurements of global left ventricular function such as ejection fraction and end-systolic volume index traditionally have been shown to be the strongest prognostic indicators after acute myocardial infarction.24 25 These measurements reflect not only infarct size but also myocardial stunning, compensatory hyperkinesia, and loading conditions. There is a discrepancy between the effects of therapy on left ventricular function and patient survival.26 A method of accurately measuring infarct size independent of other variables that affect left ventricular function could be useful for research and clinical purposes. In the prethrombolytic era, defect size by 201Tl measured early27 28 29 and later30 31 32 in the hospital course was predictive of mortality. In patients treated with thrombolytic therapy, Cerqueira et al33 reported that larger 201Tl infarct size measured at 8 weeks after acute infarction was associated with worse survival. The data from the present study are in agreement with data from these earlier prognostic studies that used 201Tl to measure infarct size.

Low Mortality Rate
The low 2-year overall mortality rate in the present study of 3% is consistent with other studies of patients with myocardial infarction who have been treated with thrombolytic therapy.34 35 There are multiple reasons for this favorable outcome. First, reperfusion therapy increases myocardial salvage, modifies ventricular remodeling, and usually results in an open infarct-related artery, all of which may improve survival.36 37 Second, clinical and anatomic characteristics (low prevalence of severely reduced global left ventricular function and three-vessel disease) place these patients at low risk.16 38 39 Third, a high percentage of these patients are treated with revascularization, which should limit residual ischemia and improve outcome. Fourth, many patients are treated with ß-blockers and angiotensin-converting enzyme inhibitors, which are of proven benefit.40 41

It generally is more difficult to predict patient outcome in low-risk populations. For example, treadmill42 and thallium43 exercise testing after myocardial infarction were useful for prognostic purposes in the prethrombolytic era (when event rates were higher) but are less predictive in patients who have been treated with thrombolysis (with low subsequent event rates).34 44 45 The significant association between discharge infarct size and outcome in this low-risk population further underscores the prognostic value of the measurement of infarct size.

Distribution of Infarct Size, Myocardium at Risk, and Amount of Myocardium Salvaged and Association With Outcome
The distribution of infarct size was clearly skewed toward smaller infarcts in this study (Table 2Up and Fig 1Up). Two thirds of the study population had an infarct size of <=20% of the left ventricle, including almost one fourth of the population who had no detectable scintigraphic evidence of infarction. Previous studies from our laboratory have shown that an infarct size of 20% is approximately equal to an ejection fraction of 50%.6 The small residual infarct size clearly was a contributing factor to the low mortality rate in this population.

Thirty-six patients (13% of the study group) had a final infarct size of >40% of the left ventricle. Although patients who die in cardiac shock frequently have infarction involving more than 40% of the left ventricle,46 47 48 an earlier publication from our laboratory showed that patients with these large infarcts can survive the acute infarction.49 Medrano et al15 have provided additional convincing evidence that patients can survive large infarctions. In nine patients with "ischemic cardiomyopathy" undergoing cardiac transplantation, the directly measured area of scar in the explanted hearts was 40±11% of the left ventricle. The mean defect size measured by 99mTc sestamibi was 47±14% and correlated very closely (r=.95) with the pathological measurement. Sestamibi uptake in areas of scar alone was 29% of normal and in areas consisting of a mixture of scar and viable myocardium was 63% of normal. Using a method previously described,8 we determined the nadir of sestamibi uptake in 34 of the 36 patients with large defects. The mean nadir value was 21±11% of normal. Thus, these patients with large defects had severely reduced sestamibi uptake, consistent with fibrosis.

The median amount of myocardium at risk was 27%, and one fourth of the population had myocardium at risk of >47% of the left ventricle (Table 2Up). The association of myocardium at risk with cardiac mortality was not surprising since there is a correlation (r=.61) between myocardium at risk and infarct size.8 This association presumably would have been stronger if in-hospital mortality had been included as an end point for all patients who underwent acute imaging, since some of these patients died in the hospital. The median amount of myocardium salvaged was modest at 9%. Only one fourth of the patients had salvage of >20% (Table 2Up). Myocardial salvage should reflect future myocardium at risk if the infarct-related artery should reocclude. Our findings suggest that the extent of myocardial damage was a more important determinant of mortality after infarction than subsequent reocclusion.

Validation of the Predischarge 99mTc Sestamibi Defect Size for Measurement of Infarct Size
The sestamibi defect size reflects all areas of myocardium that have <60% of peak counts.12 Is it possible that 99mTc sestamibi defects that fall below the 60% threshold represent mildly or moderately hypoperfused normal myocardium at rest, attenuated normal myocardium, or hibernating rather than infarcted myocardium?

The true percent reduction in myocardial blood flow is greater than the percent reduction of myocardial sestamibi uptake. In one experimental study,50 the lowest point on scintigraphic 99mTc sestamibi count profile was 35% of normal when the actual tissue 99mTc sestamibi uptake was 18% of normal and the tissue microsphere uptake was 6% of normal. Thus, areas that have <60% of peak counts have far less than 60% of normal flow. The phantom validation of this technique demonstrated that the borders of an area of absent flow were best defined by using the 60% threshold.12 The nadir, representing the lowest point in the circumferential count profile, generally will be much lower. As noted above, for the study patients with final infarct size of >40% of the left ventricle, the nadir was 21±11% of peak counts. Thus, only severe defects are classified as infarcted by this technique. As a result, tissue attenuation does not appear to be a major limitation of this technique (see "Methods").

Stunned myocardium, severe asynergy with partial volume effects, and hibernating myocardium may contribute to severe defects in some patients. The effects of stunning6 14 51 52 and partial volume53 on measured defect size have been shown to be small. Hibernation requires a decrease in resting blood flow, which should occur after thrombolysis only if there is a very high-grade residual stenosis, which often results in recurrent ischemia before discharge. Although predischarge coronary angiography was not performed uniformly in these patients, the aggressive management strategy by which they were treated did not leave many with closed or nearly closed arteries. Of the 249 patients (91% of the study population) who underwent coronary angiography during this hospitalization (see Table 1Up), 171 underwent revascularization before discharge, 169 of whom had successful revascularization of the infarct-related vessel. Of the remaining 79 patients who underwent coronary angiography but not revascularization, 19 had an occluded infarct-related artery, 37 did not have a high-grade stenosis (<=80% diameter narrowing) of the infarct-related artery, and 23 had a high-grade stenosis (>=90% diameter narrowing) of the infarct-related artery. In this last group of patients, 11 had TIMI grade 3 flow. Thus, 217 patients (87% of the patients with angiography) had a documented patent infarct-related artery with good flow, indicating that only a small number of patients could have had hibernating myocardium. Although stunning, partial volume effects, and hibernation likely did not have a meaningful impact on the study population as a whole, these factors nevertheless could have significantly affected the measured sestamibi defect size in some of the individual patients.

Two recent studies of patients undergoing exercise sestamibi imaging have reported that fixed sestamibi defects underestimate viability compared with positron emission tomography. In the study by Sawada et al,54 the severity of the defect was not a helpful discriminator of viability, as 47% of severe resting defects (uptake of <50% of normal) were viable by positron emission tomography. Dilsizian et al,55 however, reported that the severity of the defect was helpful. Although the large majority of mild to moderate fixed sestamibi defects (uptake, 51% to 85% of normal) were viable by positron emission tomography, only 20% to 25% of severe defects were viable. Both of these studies only compared sestamibi imaging with positron emission tomography rather than ventricular functional recovery after revascularization. Udelson et al56 have demonstrated that the 60% sestamibi threshold accurately separated segments with severe regional dysfunction at baseline that subsequently showed improved function over those without improved function after revascularization. Galli et al57 reported that sestamibi defect size and severity do improve over time after an anterior myocardial infarction. The improvement in their study was modest, however, with defect size decreasing from 32% at 5 weeks to 26% at 7 months.

The gold standard for measuring infarct size is to directly quantify the amount of scar in a pathology specimen. Animal models of permanent occlusion13 and reperfusion14 have shown that the 99mTc sestamibi defect size accurately measures infarct size. In a study of explanted human hearts from patients undergoing transplantation, Medrano et al15 reported that 99mTc sestamibi defect size modestly overestimated infarct size by a mean of 7% but correlated very closely (r=.95) with directly measured pathological scar. Thus, the available evidence suggests that the error in this technique due to hibernating myocardium is modest.

Advantages of 99mTc Sestamibi Over Other Measures of Infarct Size in Clinical Trials of Reperfusion Therapy
Serum creatine phosphokinase release,4 58 59 the ECG,60 61 201Tl imaging,2 10 27 28 29 30 31 32 33 and regional and global left ventricular function1 4 6 7 23 24 25 28 29 30 31 32 33 36 37 62 have been used to measure infarct size. The kinetics of creatine kinase release are complex, highly variable, and may not reliably predict successful reperfusion. The ECG does not appear to reliably measure infarct size in patients treated with reperfusion therapy.63 201Tl begins to redistribute immediately after injection, which would necessitate delaying the administration of reperfusion therapy to acquire images to measure myocardium at risk. Global and regional left ventricular function is influenced by myocardial stunning and compensatory hyperkinesia, particularly in patients treated with reperfusion therapy, and loading conditions, which are rapidly changing in the setting of acute infarction. These factors can affect the measurement of left ventricular function for several weeks after hospital discharge. In a previous study from our laboratory,6 there was no difference in mean ejection fraction measured at hospital discharge and at 6 weeks, but 34% of patients were found to have a significant change (>=8%) in ejection fraction measured at these 2 points in time. For these reasons, serial 99mTc sestamibi imaging is superior to these other methods for measuring myocardium at risk, myocardial salvage, and infarct size at hospital discharge.

Current studies that compare clinical outcomes of patients with acute myocardial infarction treated with different strategies of reperfusion therapy are difficult and expensive to perform. Because 30-day and 1-year mortality rates are very low in trials of patients treated with reperfusion therapy,16 17 33 34 35 64 65 66 67 thousands of patients must be enrolled to measure a difference in mortality between treatment strategies. From a practical standpoint, these "mega" trials cannot address every clinical question and should be performed on the basis of promising data from smaller pilot studies. Surrogate end points for mortality are needed in pilot studies of new reperfusion therapies and strategies; infarct size may be one such end point. In patients who are successfully treated and left with little if any infarction, infarct size is a highly reproducible measurement with less variability than the ejection fraction, permitting clinical pilot studies with fewer patients.68

Despite the limitations of left ventricular ejection fraction, this variable is a very strong prognostic indicator after myocardial infarction.24 Because predischarge ejection fraction was not uniformly measured in these patients, a direct comparison between ejection fraction and infarct size was not possible in the present study. Even if predischarge ejection fraction had been uniformly measured in all patients, this study did not contain enough patients to address this issue. In view of the strong correlation (r=.81) between infarct size measured at hospital discharge and ejection fraction measured at 6 weeks6 and the low mortality rate in these patients, demonstration that infarct size contains 25% more prognostic information than left ventricular ejection fraction would require a study population of 1500 patients.

Implications
In the present study, where the majority of patients presented with ST-segment elevation and were treated with reperfusion therapy, no patient with infarct size of <20% of the left ventricle had a cardiac death during follow-up. These results demonstrate that successful myocardial salvage, as indicated by small predischarge infarct size, is related to patient salvage.36 37


*    Acknowledgments
 
This study was supported in part by grants from the Burroughs Wellcome Company and E.I. duPont de Nemours and Company. We thank Lisa VandeWalker for secretarial preparation of this manuscript and Tammy Hudson for assistance with collection of follow-up data.

Received September 20, 1994; revision received January 4, 1995; accepted January 22, 1995.


*    References
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*References
 

  1. Gibbons RJ, Verani MS, Behrenbeck T, Pellikka PA, O'Connor MK, Mahmarian JJ, Chesebro JH, Wackers FJ. Feasibility of tomographic 99mTc-hexakis-2 methoxy-2 methylpropy-isonitrile imaging for the assessment of myocardial area at risk and the effect of treatment in acute myocardial infarction. Circulation. 1989;80:1277-1286. [Abstract/Free Full Text]
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  4. Behrenbeck T, Pellikka PA, Huber KC, Bresnahan JF, Gersh BJ, Gibbons RJ. Primary angioplasty in myocardial infarction: assessment of improved myocardial perfusion with technetium-99m-isonitrile. J Am Coll Cardiol. 1991;17:365-372. [Abstract]
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  8. Christian TF, Schwartz RS, Gibbons RJ. Determinants of infarct size in reperfusion therapy for acute myocardial infarction. Circulation. 1992;82:81-90.
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  10. Christian TF, O'Connor MK, Hopfenspirger MR, Gibbons RJ. Comparison of reinjection thallium-201 and resting technetium-99m sestamibi tomographic images for the quantification of infarct size after acute myocardial infarction. J Nucl Cardiol. 1994;1:17-28. [Medline] [Order article via Infotrieve]
  11. Gibbons RJ, Holmes DR, Reeder GS, Bailey KR, Hopfenspirger MR, Gersh BJ, for the Mayo Coronary Care Unit and Catheterization Laboratory Groups. Immediate angioplasty compared with the administration of a thrombolytic agent followed by conservative treatment for myocardial infarction. N Engl J Med. 1993;328:685-691. [Abstract/Free Full Text]
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