Threshold values for preserved viability with a noninvasive measurement of collateral blood flow during acute myocardial infarction treated by direct coronary angioplasty.

BACKGROUND: Quantitative measures of myocardial perfusion defect severity from acute (99m)Tc-sestamibi tomographic images (nadir) have correlated closely with collateral and residual antegrade blood flow during acute myocardial infarction. The purpose of this study was to determine whether a viability threshold could be identified from this measure in patients with acute myocardial infarction treated in a homogeneous manner with successful reperfusion therapy. METHOD AND RESULTS: The study group consisted of 61 patients with acute myocardial infarction with a risk area of >6% LV treated with primary angioplasty between 120 and 240 minutes after symptom onset. All patients were injected with 20 to 30 mCi of (99m)Tc-sestamibi before primary angioplasty and imaged after the procedure. Acute myocardium at risk (MAR) and subsequent infarct size (IS) were quantified by a threshold program. Severity (nadir) from the acute image was the lowest ratio of minimal/maximum counts from 5 short-axis slices. Infarct location was anterior in 22 and inferior in 39 patients. MAR was 33+/-15% LV and IS was 13+/-15% LV: 23 patients had no infarction despite MAR similar to those with infarction. Receiver-operator characteristic curve analysis identified a nadir value of 0.26 as providing the best separation of patients with and without infarction (sensitivity, 74%; specificity, 74%). This nadir threshold varied by infarct location: anterior defect, 0.21; inferior defect, 0.31. The sensitivity and specificity for absent infarction for these values were anterior, 69% and 67%, and inferior, 88% and 84%, respectively. CONCLUSIONS: In a time frame in which the presence of residual blood flow is important, the severity of the acute (99m)Tc-sestamibi defect can be used to predict whether infarction will develop despite successful reperfusion.

Prospective identification of myocardial stunning using technetium-99m sestamibi-based measurements of infarct size.

OBJECTIVES: We sought to prospectively identify patients with stunning and hyperkinesia at hospital discharge on the basis of mismatches between left ventricular (LV) function and infarct size as assessed by technetium-99m (Tc-99m) sestamibi perfusion tomographic imaging. BACKGROUND: Mechanical indexes of LV function may not accurately reflect myocardial damage after acute myocardial infarction (MI) because of myocardial stunning and compensatory hyperkinesia in noninfarct-related territories. Myocardial perfusion techniques are unaffected by these variables. METHODS: Eighty-four patients with acute MI underwent hospital admission and discharge Tc-99m-sestamibi tomographic imaging. Global LV ejection fraction (LVEF) was measured at hospital discharge and 6 weeks later. The perfusion defect size was quantified and expressed as a percentage of the LV. The discharge perfusion defect, which is a measure of infarct size, was used to predict the 6-week LVEF for each patient based on a previously reported regression equation. Patients were classified into one of three groups depending on whether their LVEF at hospital discharge fell within, above or below one standard error (6.8 LVEF points) of the predicted 6-week LVEF. RESULTS: There were 48 patients classified as having a "match" between function and infarct size; these patients demonstrated no significant change in LVEF at 6 weeks. There were 21 patients (25%) classified as "mismatch stunned" who had discharge LVEFs lower than those predicted by infarct size. These patients demonstrated a significant improvement in mean LVEF at 6 weeks (mean [+/-SD] discharge LVEF 0.41 +/- 0.08, 6-week LVEF 0.47 +/- 0.10; p = 0.003). Fifteen patients (18%) were classified as "mismatch-hyperkinetic." The mean LVEF for these patients significantly declined at 6 weeks (discharge LVEF 0.64 +/- 0.06, 6-week LVEF 0.58 +/- 0.09; p = 0.002). There was a marked increase in LVEF within the infarct zone (8 +/- 15 LVEF points; p = 0.03) for patients predicted to have stunning and a marked decline in LVEF outside the infarct zone (9 +/- 15 LVEF points; p = 0.06) in patients predicted to have hyperkinesia. Both discharge LVEF (p < 0.0001) and group classification (p = 0.005) were independent predictors of LVEF 6 weeks later. CONCLUSIONS: Perfusion imaging with Tc-99m-sestamibi can identify post-MI patients at hospital discharge in whom LV function is discordant with the measured infarct size. Patients with stunning have late increases in LVEF; patients with hyperkinesia have late decreases. This methodology, performed at discharge, is predictive of late changes in LV function.

Effect of infarct location on myocardial salvage assessed by technetium-99m isonitrile.

To investigate the influence of infarct location on myocardial salvage, technetium-99m isonitrile was injected into 43 patients with a first myocardial infarction before early reperfusion therapy. Primary coronary angioplasty was performed in 22 patients and successful intravenous thrombolytic therapy was given to 15 patients, both within 6 h of the onset of chest pain. Patency of the infarct-related artery was confirmed by angiography in all 37 patients. In the remaining six patients (three with and three without early thrombolytic therapy) the infarct-related artery remained occluded. Single photon emission computed tomography was performed within 6 h of the administration of technetium-99m isonitrile and repeated at the time of hospital discharge. Radionuclide ejection fraction at discharge was significantly lower for patients with anterior infarction (0.41 +/- 0.12) than for those with inferior infarction (0.56 +/- 0.09, p less than 0.001). Early perfusion defect size, a measure of myocardium at risk, was greater in patients with anterior than in those with inferior infarction (52 +/- 9% vs. 18 +/- 10% of the left ventricle, p = 0.0001) as was final defect size (30 +/- 20% vs. 9 +/- 8%, p less than 0.01). The change in myocardial perfusion, an estimate of myocardial salvage, was also greater in patients with anterior infarction (24 +/- 16% vs. 10 +/- 7%, p less than 0.01). However, the proportion of jeopardized myocardium salvaged (salvage index) was not significantly different between patients with anterior or inferior infarction (0.49 +/- 0.34 vs. 0.59 +/- 0.35, p = NS).(ABSTRACT TRUNCATED AT 250 WORDS)

Severity and response of chest pain during thrombolytic therapy for acute myocardial infarction: a useful indicator of myocardial salvage and infarct size.

OBJECTIVES: The purpose of this study was to determine noninvasively whether chest pain severity is predictive of the amount of myocardium at risk and whether the response of pain during thrombolysis is associated with myocardial salvage during acute myocardial infarction. BACKGROUND: The perception of chest pain and response to reperfusion therapy during acute myocardial infarction may provide important information for treatment benefit. Previous studies have been limited by the inability to measure myocardium at risk and myocardial salvage. METHODS: Sixty-two patients with acute myocardial infarction received an injection of technetium-99m sestamibi before thrombolysis and again at hospital discharge. Tomographic imaging was performed 1 to 6 h later. Myocardium at risk, infarct size and absolute myocardial salvage were derived from these images using previously described techniques and were expressed as a percent of the left ventricle. Salvage index was calculated by dividing myocardial salvage by the myocardium at risk. Chest pain severity was graded before thrombolysis as none, mild, moderate or severe. Chest pain response during thrombolytic therapy was graded as none, partial or completely resolved. RESULTS: There was no association between chest pain severity and myocardium at risk, but there was a weak trend toward greater myocardial salvage and salvage index (p = 0.09 and p = 0.12, respectively) for patients with more severe symptoms. Patients without chest pain at the start of thrombolysis still demonstrated significant salvage (11 +/- 11% of the left ventricle, p = 0.009). There was a significant association between chest pain response to therapy and both myocardial salvage (p = 0.03) and salvage index (p = 0.01). By multivariate analysis, chest pain severity and response of chest pain during thrombolysis were significant independent predictors of myocardial salvage, salvage index and infarct size. Thrombolysis was most effective in the 20 patients (32%) with moderate or severe chest pain and complete resolution of symptoms during thrombolysis (salvage of 79% to 89% of the area at risk). In the remaining 32 patients with chest pain, salvage of the area at risk was only 32%. CONCLUSIONS: These findings suggest that the assessment of chest pain before and after thrombolytic therapy is a readily available, useful indicator of the efficacy of the therapy.

Prognostic value of exercise thallium-201 imaging performed within 2 years of coronary artery bypass graft surgery.

OBJECTIVES: We sought to determine the prognostic capabilities of exercise thallium (Tl)-201 tomographic imaging performed relatively early (within 2 years) after coronary artery bypass graft surgery (CABG). BACKGROUND: Exercise testing is commonly performed after CABG, but few data exist demonstrating its prognostic value in this setting. METHODS: Four hundred eleven patients were followed up for a median duration of 5.8 years. Eleven prospectively chosen clinical, exercise and Tl-201 variables were tested for their associations with outcome end points by means of proportional hazards regression models. RESULTS: During follow-up there were 60 deaths from any cause, 53 initial cardiac deaths or nonfatal myocardial infarctions (MIs) and 22 late (>3 months after the Tl-201 study) revascularization procedures. The number of abnormal Tl-201 segments on the postexercise image was the only variable in the multivariate analyses to show a significant association with all three outcome end points: chi-square 7.3, p = 0.007 for overall mortality; chi-square 8.1, p = 0.004 for cardiac death or MI; chi-square 7.8, p = 0.005 for any cardiac event. Other independent predictors of outcome were exercise duration (chi-square 10.7, p = 0.001) and age (chi-square 3.9, p = 0.049) for overall mortality and exercise angina score (chi-square 8.7, p = 0.003) for cardiac death or MI. The 5-year survival rate free of cardiac death or MI was 93% for patients without angina and a normal image or small postexercise perfusion defect versus 71% for patients with angina and a medium or large defect. CONCLUSIONS: Exercise Tl-201 imaging performed within 2 years of CABG can stratify patients into low and high risk subgroups.

Mismatch of left ventricular function and infarct size demonstrated by technetium-99m isonitrile imaging after reperfusion therapy for acute myocardial infarction: identification of myocardial stunning and hyperkinesia.

Quantitation of perfusion defect size using tomographic imaging with technetium-99m-hexakis-2-methoxy isobutyl isonitrile was performed at the time of hospital discharge in 32 patients with a first myocardial infarction who underwent successful coronary reperfusion within 8 h of the onset of chest pain. Reperfusion was accomplished with thrombolysis or primary coronary angioplasty. Radionuclide angiography was performed at discharge and 6 weeks later. There was a close correlation between perfusion defect size and values for ejection fraction and regional wall motion both at discharge (r = -0.80 and -0.75, respectively) and 6 weeks later (r = -0.81 and -0.81, respectively). There was no overall group difference in ejection fraction between the value at discharge and at 6 weeks; however, five patients had a significant increase (greater than or equal to 0.08) and six had a significant decrease (greater than or equal to 0.08) in ejection fraction. In patients with a significant increase at 6 weeks, ejection fraction was significantly lower at discharge than the value predicted from perfusion defect size (0.37 +/- 0.09 measured versus 0.47 +/- 0.13 predicted, p less than 0.05) and it improved at 6 weeks to near predicted values (0.51 +/- 0.07). In patients with a significant decrease at 6 weeks, ejection fraction was significantly higher at discharge than the value predicted from perfusion defect size (0.60 +/- 0.10 measured versus 0.50 +/- 0.10 predicted, p less than 0.05) and it decreased at 6 weeks to near predicted levels (0.51 +/- 0.09). Left ventricular ejection fraction at the time of hospital discharge is a potentially misleading index of the efficacy of reperfusion therapy for myocardial infarction. In a significant minority (34%) of patients this index does not accurately reflect perfusion defect size, apparently because of the effects of myocardial stunning and compensatory hyperkinesia.

Myocardium at risk and infarct size after thrombolytic therapy for acute myocardial infarction: implications for the design of randomized trials of acute intervention.

OBJECTIVES: The purpose of this study was to estimate the effect of an improved reperfusion therapy for acute myocardial infarction on myocardial salvage and ventricular function for anterior and inferior infarctions and to ascertain the sample size required to detect such an effect. BACKGROUND: There are significant differences in myocardium at risk between anterior and inferior infarctions that affect the benefit of reperfusion therapy. METHODS: We studied 58 patients with acute myocardial infarction (24 anterior, 34 inferior) treated with intravenous recombinant tissue-type plasminogen activator and angioplasty when necessary. Tomographic imaging with technetium-99m sestamibi was performed to measure myocardium at risk, final infarct size and myocardial salvage and to estimate the beneficial effects of an improved therapy. RESULTS: A new therapy that was 30% more effective than existing therapy (with respect to salvage) would increase salvage (and reduce mean infarct size) by 5.2% of the left ventricle and increase late ejection fraction by only 0.012 (95% confidence interval [CI] 0.009 to 0.015) in inferior infarction and by 0.038 (95% CI 0.027 to 0.047) in anterior infarction. If anterior and inferior infarctions occurred with equal frequency, a sample size of 140 patients in each treatment group would be required to detect such a change with 80% power. In a trial of interior infarctions alone, a sample size of 236 patients in each treatment group would be required compared with only 98 patients in a trial of anterior infarctions alone. CONCLUSIONS: The anticipated mean benefit from an improved reperfusion therapy in individual patients with inferior infarction is very small and of questionable clinical significance. The anticipated benefit in anterior infarction is greater and easier to detect. Future randomized trials should be stratified for infarct location and should consider the greater absolute benefit of treatment in anterior infarction.

Severe exercise-induced ischemia does not identify high risk patients with normal left ventricular function and one- or two-vessel coronary artery disease.

OBJECTIVES: This study was conducted to determine whether severe exercise-induced ischemia identifies high risk patients with a normal left ventricular ejection fraction and one- or two-vessel coronary artery disease. BACKGROUND: Severe ischemia during exercise radionuclide angiography has been shown to identify high risk patients among certain other patient subsets. METHODS: Four hundred twenty patients with left ventricular ejection fraction > or = 50% and one- or two-vessel disease underwent exercise radionuclide angiography within 3 months of coronary angiography. Patients were treated initially with revascularization (n = 140) or medical therapy (n = 280) at the discretion of their physicians. Patients treated with revascularization were more likely to have angina by history, a positive exercise electrocardiogram, a lower exercise ejection fraction, two-vessel disease and proximal left anterior descending coronary artery disease. Two hundred sixty-four of the 280 patients given medical therapy who had complete follow-up data formed the study group. Outcome was compared between patients with (n = 56) and without (n = 208) severe exercise-induced ischemia, defined by previously published criteria (work load < or = 600 kg-m/min, ST segment depression > or = 1 mm and decrease in ejection fraction with exercise). RESULTS: During follow-up, there were 30 initial cardiac events (12 cardiac deaths and 18 nonfatal myocardial infarctions). There was no difference in the 5-year event-free survival rate: 91% in patients with and 87% in patients without severe ischemia (p = 0.89). There was no association between event-free survival and severe ischemia (chi 2 = 1.41, p = 0.24). The study had approximately 80% power at alpha = 0.05 to detect a 25% decrease in event-free survival in the group with severe ischemia. In addition, there was no association between severe ischemia and outcome if late revascularization was included as an event or if the total mortality rate (overall survival) was analyzed. CONCLUSIONS: Severe exercise-induced ischemia fails to identify a high risk subgroup among patients with normal left ventricular function and one- or two-vessel disease who are treated initially with medical therapy.

Relation of initial infarct size to extent of left ventricular remodeling in the year after acute myocardial infarction.

OBJECTIVES: This study attempted to determine the relation between infarct size after acute myocardial infarction and subsequent left ventricular remodeling using precise clinical measurements. BACKGROUND: Animal studies have demonstrated that the degree of left ventricular remodeling after myocardial infarction is linearly related to infarct size. Clinical studies have not clearly replicated these results because of imprecise measurements and failure to adjust for patency of the infarct-related artery. METHODS: Infarct size was measured from technetium-99m (Tc-99m) sestamibi perfusion images in 14 patients (12 with an anterior, 2 with an inferior infarction) by a threshold method previously described and expressed as percent of the left ventricle (32 +/- 17% left ventricle [mean +/- SD], range 6% to 58%). Absolute end-systolic volume, end-diastolic volume and ejection fraction were determined by electron beam computed tomographic images performed at discharge and at 6 weeks, 6 months and 1 year after myocardial infarction. All patients had documented infarct-related artery patency after reperfusion therapy. RESULTS: At hospital discharge, there was no correlation between infarct size and end-systolic and end-diastolic volumes or ejection fraction. There was significant left ventricular dilation in the study group over the next year. As remodeling progressed, there was closer correlation between infarct size and ejection fraction and end-systolic volume measures (infarct size vs. end-systolic volume, from r = 0.43 at discharge to r = 0.80 at 1 year; infarct size vs. ejection fraction, from r = -0.39 at discharge to r = -0.84 at 1 year). There was a strong inverse correlation between infarct size at discharge and subsequent changes over the next year in end-systolic volume (r = 0.63, p = 0.02) and ejection fraction (r = -0.66, p = 0.01). CONCLUSION: Infarct size as measured by Tc-99m sestamibi at hospital discharge after an index infarction is predictive of subsequent change in left ventricular volume and function in the year after myocardial infarction. Patients with a large infarct demonstrated the greatest degree of dilation in the setting of patency of the infarct-related artery.

Identification of severe coronary artery disease in patients with a single abnormal coronary territory on exercise thallium-201 imaging: the importance of clinical and exercise variables.

OBJECTIVES: The aim of this study was to determine which clinical, exercise and thallium variables can aid in the identification of three-vessel or left main coronary artery disease (3VLMD) in patients with one abnormal coronary territory (either a reversible or fixed defect) on exercise thallium testing and to test the prognostic value of these variables. BACKGROUND: Although the sensitivity of detection of coronary artery disease by thallium-201 imaging is high, the actual detection of 3VLMD by thallium tomographic images alone is not optimal. METHODS: A multivariate model for prediction of 3VLMD was developed from several clinical, exercise and thallium-201 variables in a training population of 264 patients who had one abnormal coronary artery territory on exercise thallium testing and had undergone coronary angiography. Using this model, patients were stratified into risk groups for prediction of 3VLMD. A separate validation cohort of 474 consecutive patients who were treated initially with medical therapy and who had one abnormal coronary territory were divided into identical risk groupings by the variables derived from the training population, and they were followed for a median of 7.0 years to evaluate the prognostic value of this model. RESULTS: The prevalence of 3VLMD was 26% in the training population despite one abnormal thallium coronary territory. Four clinical and exercise variables--diabetes, hypertension, magnitude of ST segment depression, and exercise rate-pressure product-were found to be independent predictors of 3VLMD. In the training population, the prevalence of 3VLMD in low-, intermediate- and high-risk groups was 15%, 22% and 51%, respectively. When the multivariate model was applied to the validation population, the eight-year overall survival rates in the low-, intermediate- and high-risk groups were 89%, 73% and 75%, respectively (p < 0.001). CONCLUSIONS: A substantial proportion of patients with one abnormal thallium coronary territory have 3VLMD with subsequent divergent outcomes based upon risk stratification by clinical and exercise variables. Consequently, the finding of only a single abnormal coronary territory by thallium-201 perfusion imaging does not necessarily confer a benign prognosis in the absence of consideration of nonimaging variables.

Time to therapy and salvage in myocardial infarction.

OBJECTIVES: This study sought to examine the influence of time to reperfusion on myocardial salvage. BACKGROUND: Major trials of reperfusion therapy for myocardial infarction (MI) have demonstrated improved outcome for patients achieving earlier reperfusion. However, some patients experience significant benefit despite delayed reperfusion. METHODS: Fifty-five patients with a first anterior MI underwent successful reperfusion therapy (angioplasty or thrombolysis). Technetium-99m (Tc-99m) sestamibi was injected before reperfusion therapy and again at hospital discharge to determine the myocardial salvage index for each patient. Residual flow to the infarct territory was assessed by the nadir of the Tc-99m sestamibi count-profile curve. RESULTS: The salvage index showed wide variability (range -0.04 to 1.0), and extreme values were seen in 34.5% of the group (<0.10 in 9%, >0.90 in 25%). A high salvage index was associated with reperfusion therapy before 2 h (p=0.02) or good residual blood flow (p < 0.01). For the 10 patients who received reperfusion therapy within 2 h, residual blood flow was not correlated with salvage (p=0.12). For the 45 patients treated after 2 h, residual blood flow correlated significantly with salvage (r=0.57, p < 0.0001). There was a significant interaction (p < 0.05) between residual blood flow and time to therapy, indicating that the effect of each variable on salvage depended on the value of the other. Multiple historic and hemodynamic variables were examined, but none demonstrated any association with residual flow or myocardial salvage. CONCLUSIONS: In patients with acute MI, successful reperfusion therapy within 2 h is associated with the greatest degree of myocardial salvage. For patients treated after 2 h, residual blood flow to the infarct-related territory appears to be the most important determinant of myocardial salvage.

Independent and incremental value of coronary artery calcium for predicting the extent of angiographic coronary artery disease: comparison with cardiac risk factors and radionuclide perfusion imaging.

OBJECTIVES: The study was done to test the ability to predict the extent of angiographically determined coronary artery disease (CAD) by quantification of coronary calcium using electron-beam computed tomography (EBCT) and to compare it with more conventional parameters for delineating the angiographic extent of CAD, that is, cardiovascular risk factors and radionuclide single-photon emission computed tomography (SPECT). BACKGROUND: The angiographic extent of CAD is a powerful predictor of subsequent events. Use of EBCT may be able to define it by virtue of its ability to determine plaque burden. METHODS: We examined 308 patients presenting with suspected but not previously known CAD who underwent selective coronary angiography. As measures of the angiographic extent of CAD, coronary artery greater even 20 (CAGE > or =20) and CAGE > or =50 scores represented the total number of coronary segments with > or =20% or > or =50% stenoses, respectively. The EBCT-derived total calcium scores were obtained in 291 patients, risk factors as defined by the National Cholesterol Education Program in 239 patients, and SPECT scans in 136 patients. RESULTS: Using multiple linear regression analysis, total calcium scores were better independent predictors of both CAGE > or =20 and CAGE > or =50 scores than either a SPECT-derived radionuclide perfusion score or the risk factors age, male gender and ratio of total/high-density lipoprotein (HDL) cholesterol. The association between EBCT and angiographic scores remained highly significant after excluding the influence of all interrelated risk factors and SPECT variables (r = 0.65; p < 0.001 for CAGE > or =20 scores, r = 0.50; p < 0.001 for CAGE > or =50 scores). CONCLUSIONS: Coronary calcium predicts the angiographic extent of CAD in symptomatic patients and provides independent and incremental information to the more conventional clinical parameters derived from SPECT or risk assessment.

Estimates of myocardium at risk and collateral flow in acute myocardial infarction using electrocardiographic indexes with comparison to radionuclide and angiographic measures.

OBJECTIVES: This study sought to determine the accuracy of the initial 12-lead electrocardiogram (ECG) in predicting final infarct size after direct coronary angioplasty for myocardial infarction and to examine which physiologic variables known to be determinants of outcome the ST segment changes most closely reflect. BACKGROUND: Myocardium at risk, collateral flow and time to reperfusion have been shown to be independent physiologic predictors of infarct size in animal and clinical models. However, such measurements may be difficult to perform on a routine basis in patients with myocardial infarction. The standard 12-lead ECG is inexpensive and readily available. METHODS: Sixty-seven patients with acute myocardial infarction, ST segment elevation and duration of chest pain < 12 h had an initial injection of technetium-99m sestamibi. Tomographic imaging was performed 1 to 8 h later (after direct coronary angioplasty), and the images were quantified to measure perfusion defect size (myocardium at risk) and severity (a measure of collateral flow). Contrast agent injection and tomographic acquisition were repeated at hospital discharge to measure infarct size. The ST segment elevation score was calculated for each patient according to infarct location and using previously described formulas. RESULTS: ST segment elevation score correlated closest with the radionuclide measure of collateral flow (r = -0.44, p < or = 0.0001), as well as an angiographic measure of collateral flow (r = -0.38, p = 0.05). Although ST segment elevation score correlated weakly with the magnitude of myocardium at risk by technetium-99m sestamibi, it was not as strong as infarct location alone in predicting myocardium at risk ([mean +/- SD] anterior 51 +/- 13% left ventricle vs. inferior 17 +/- 10% left ventricle, p < 0.0001). ST segment elevation score was weakly associated with final infarct size (r = 0.34, p = 0.005). A multivariate ECG model was constructed with infarct location as a surrogate for myocardium at risk, ST segment elevation score as a surrogate for estimated collateral flow, and elapsed time to reperfusion from onset of chest pain. All three variables were independently associated with infarct size. CONCLUSIONS: The initial standard 12-lead ECG can provide insight into myocardium at risk and, to a greater extent, collateral flow and can consequently provide some estimate of subsequent infarct size. However, the confidence limits for such predictors are wide.

Association between anterior ST depression and increased myocardial salvage following reperfusion therapy in patients with inferior myocardial infarction.

PURPOSE: To determine electrocardiographic features associated with myocardial salvage following reperfusion therapy in patients with inferior myocardial infarction. PATIENTS AND METHODS: Ninety-two consecutive patients with acute inferior myocardial infarction were treated with reperfusion therapy in a tertiary care center. Several features were measured on the presenting electrocardiogram, including the presence or absence of ST depression in the chest leads and the total magnitudes of ST elevation or depression, and were then evaluated for their association with myocardial salvage. Myocardial salvage (% of left ventricle) was the difference between myocardium at risk and final infarct size. Tomographic myocardial perfusion imaging with technetium-99m sestamibi was performed acutely to measure myocardium at risk and repeated prior to hospital discharge to measure final infarct size. RESULTS: The amount of myocardium at risk of infarction in the 92 patients was 19.1%+/-11.3% (range 1% to 68%), and the final infarct size was 10.6%+/-10.0% (range 0% to 45%). Thus, myocardial salvage in the 92 patients was 8.5%+/-8.4% (range -11% to 35%) of the left ventricle, or 0.51+/-0.38 (range 0.0 to 1.0) when expressed as a fraction of the myocardium at risk (salvage index). The presence or absence of anterior ST depression was the only one of seven electrocardiographic variables that was associated with myocardial salvage. Myocardial salvage was significantly greater in patients with anterior ST depression compared with those without it (10.6%+/-9.0% versus 5.9%+/-6.7%, P=0.025). Myocardium at risk was significantly greater in patients with anterior ST depression compared with those without the depression (22.8%+/-12.2% versus 14.6%+/-8.3%, P=0.0006), and infarct size tended to be larger (12.1%+/-10.4% versus 8.7%+/-9.4%, P=0.10). Myocardial salvage as a fraction of the myocardium at risk (salvage index) was similar between the two patient groups (0.52+/-0.37 versus 0.50+/-0.39, P=NS). CONCLUSION: The presence of anterior ST depression during inferior myocardial infarction identifies a group of patients with the potential for greater myocardial salvage with reperfusion therapy. Such patients derive greater absolute benefit from reperfusion therapy because they have a larger amount of myocardium at risk, although their response to therapy (salvage index) is not intrinsically different.

Technetium-99m MIBI to assess coronary collateral flow during acute myocardial infarction in two closed-chest animal models.

UNLABELLED: Collateral flow is an independent determinant of infarct size in both animal and clinical studies of myocardial infarction. The purpose of this study was to quantitatively evaluate, in a closed-chest animal model, a noninvasive method of measuring coronary collateral flow over a wide spectrum of collateral flow rates from a tracer that can be injected during occlusion but measured after reperfusion. METHODS: Fourteen animals underwent 40 min of coronary occlusion using a closed-chest technique. Two closed-chest models representing different rates of collateral flow were used: canine and porcine. Coronary blood flow was measured by radiolabeled microspheres. Collateral blood within the risk zone was estimated from the severity of 99mTc-sestamibi tomographic perfusion defect. RESULTS: Collateral blood flow was significantly higher in the canine model than it was in the porcine model. There was close agreement (r = 0.90) between absolute collateral flow by microspheres and the severity of the tomographic perfusion defect. CONCLUSION: These results suggest that an accurate noninvasive estimate of collateral blood flow can be provided by an intravenous injection of 99mTc-sestamibi.

Serial tomographic imaging with technetium-99m-sestamibi for the assessment of infarct-related arterial patency following reperfusion therapy.

The purpose of this study was to determine the relationship of changes in the severity and extent of hypoperfusion on serial tomographic 99mTc-sestamibi images with patency of the infarct related artery during acute myocardial infarction. We studied 109 patients with acute myocardial infarction using tomographic 99mTc-sestamibi imaging acutely and at 18-48 hr later. Perfusion defect extent and defect area, an index of defect severity, were measured on both studies. Both defect extent and defect area were significantly (p = 0.0001) greater for anterior infarctions than for inferior and lateral infarctions. By two factor analysis of variance, the change in defect area varied significantly with both infarct location (p = 0.0001) and patency of the infarct-related artery (p = 0.002). The change in defect extent also varied significantly with both infarct location (p = 0.0001) and with patency of the infarct-related artery (p = 0.004). In patients with inferior myocardial infarction, a change in defect extent or defect area of greater than 4% or 0.017, respectively, had a positive predictive accuracy of 96% and 93%, respectively, for the identification of a patent infarct artery. Therefore, sequential changes on tomographic 99mTc-sestamibi images are of potential value for the noninvasive assessment of patency of the infarct-related artery.

Effects of scatter correction on the measurement of infarct size from SPECT cardiac phantom studies.

UNLABELLED: Thallium-201 and 99mTc-sestamibi images of the heart contain a significant amount of scattered events which degrade image quality. Newer generation gamma cameras exhibit enhanced energy resolution and hardware/software to perform scatter correction. The principal aim of this study was to evaluate the effects of these advances in instrumentation on the quantitation of defect size from tomographic images of the heart obtained from a cardiac phantom. METHODS: Tomographic images of a cardiac phantom containing no defect and defects of 5%-70% of total myocardial mass were acquired both with and without scatter correction for 201Tl and 99mTc studies. Data were acquired on a newer generation gamma camera with an energy resolution of 8.7% at 140 keV. From conventional short-axis slices of the heart, circumferential count profiles were generated from five representative slices. Defect size was computed from the fraction of radians that fell below a fixed threshold value in each of the five count profiles. The nadir value (min/max) of the count profiles in each study was used as an index of image contrast. RESULTS: For both 201Tl and 99mTc, threshold values between 55%-60% gave the best correlation (r > 0.99), with the lowest average absolute error in estimating defect size (< 2.1%). Scatter correction reduced the average absolute error to 0.8% for 99mTc and 1.4% for 201Tl, significantly reduced the nadir values for both isotopes (p < 0.0001 for both 201Tl and 99mTc and led to a marked improvement in image quality for both tracers. CONCLUSION: Scatter correction reduces the error associated with measurement of infarct size, increases image contrast and improves image quality for both 201Tl and 99mTc, as assessed in a phantom model.

Relation of left ventricular volume and function over one year after acute myocardial infarction to infarct size determined by technetium-99m sestamibi.

Twenty patients with a first acute myocardial infarction (AMI) (15 anterior, 5 inferior) who received successful reperfusion therapy underwent tomographic imaging with technetium-99m (Tc-99m) sestamibi and radionuclide ventriculography at discharge, 6 weeks, and 1 year after AMI. Patency of the infarct-related artery after reperfusion (thrombolysis, 8 patients; coronary angioplasty, 12 patients) was confirmed by angiogrpahy in all patients. Tc-99m sestamibi perfusion defect at discharge (a measure of infarct size) was quantitated using previous methods and expressed as a percentage of the left ventricle (28 +/- 19%, range 0 to 59%). This perfusion defect size correlated closely with ejection fraction at discharge (r = -0.87), 6 weeks (r = -0.81) and at 1 year (r = -0.78, all p less than 0.0001). Perfusion defect size at discharge also correlated closely with end-systolic volume index at discharge (r = 0.71, p less than 0.0005), 6 weeks (r = 0.63, p less than 0.005) and at 1 year (r = 0.76, p less than 0.0001). Perfusion defect size at discharge did not correlate significantly with end-diastolic volume index at discharge or at 6 weeks, but did correlate at 1 year (r = 0.66, p less than 0.005). There was no significant group change in end-systolic or end-diastolic volume indexes from discharge to 1 year later, although 7 patients had definite individual changes in end-diastolic volume index (3 increased and 4 decreased). There was no relation between defect size and late changes in end-systolic volume index, but there was a weak correlation between defect size and late changes in end-diastolic volume index (r = 0.42, p = 0.07).(ABSTRACT TRUNCATED AT 250 WORDS)

Left ventricular systolic response to exercise in patients with systemic hypertension without left ventricular hypertrophy.

Supine exercise radionuclide angiography was performed in 367 men to assess left ventricular (LV) systolic response to exercise; 58 had systemic hypertension without LV hypertrophy on a resting electrocardiogram and 309 were normotensive. All patients met the following criteria defining a low pretest likelihood of coronary artery disease: age less than 50 years; normal electrocardiographic response to exercise; absence of typical or atypical chest pain; and exercise heart rate greater than 120 beats/min. Patients taking beta-receptor blockers were excluded. There were no significant differences between hypertensive and normotensive groups in peak exercise heart rate, workload or exercise duration. However, hypertensive patients had significantly higher peak exercise systolic blood pressures and peak exercise rate-pressure products. There were no differences between patients with and without hypertension in resting ejection fraction, peak exercise ejection fraction (hypertensive patients 0.71 +/- 0.01, normotensive patients 0.70 +/- 0.05) or change in ejection fraction at peak exercise (hypertensive patients 0.07 +/- 0.01, normotensive patients 0.07 +/- 0.04). Diastolic and systolic ventricular volumes tended to be smaller in the hypertensive patients, but the difference was not statistically significant. The change in systolic volume with exercise was similar in the 2 groups (hypertensive -10 +/- 3 ml/m2, normotensive -10 +/- 1 ml/m2). In the absence of electrocardiographic evidence of LV hypertrophy, systemic hypertension does not influence LV systolic response to exercise.

Prognosis with abnormal thallium images in the absence of significant coronary artery disease.

In the presence of coronary artery disease (CAD), thallium imaging has been reported to add prognostic information that is independent of coronary anatomy. To investigate the prognostic importance of thallium imaging in the absence of significant CAD, 87 patients (65 men, 22 women) with abnormal thallium images without significant CAD were followed for a median duration of 22 months (range 11 to 50). Tomographic thallium images obtained immediately and 4 hours after exercise were interpreted by 2 experienced observers who graded thallium uptake in 24 segments in 3 views (short axis, horizontal long axis, vertical long axis) on a 5-point scale (normal; mildly, moderately, or severely reduced; absent). All patients had an abnormal thallium study, defined as a reversible defect of at least mild severity or a fixed defect of at least moderate severity seen in > or = 2 views, or a combination of these, and a coronary angiogram with stenosis not > or = 70% in diameter narrowing. Eighty-two patients had at least 1 reversible segment, and 26 patients had defects in > or = 2 coronary artery distributions. During follow-up there were no deaths or myocardial infarctions. Coronary angioplasty and bypass surgery were performed in 2 patients. Three-year survival without myocardial infarction or revascularization was 97%. Patients with abnormal thallium images in the absence of significant CAD have an excellent short-term prognosis.