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The ability of predischarge quantitative exercise thallium-201 (201T1) scintigraphy to predict future cardiac events was evaluated prospectively in 140 consecutive patients with uncomplicated acute myocardial infarction; the results were compared with those of submaximal exercise treadmill testing and coronary angiography. High risk was assigned if scintigraphy detected 201T1 defects in more than one discrete vascular region, redistribution, or increased lung uptake, if exercise testing caused ST segment depression greater than or equal to 1 mm or angina or if angiography revealed multivessel disease. Low risk was designated if scintigraphy detected a single-region defect, no redistribution, or no increase in lung uptake, if exercise testing caused no ST segment depression or angina, or if angiography revealed single-vessel disease or no disease. By 15 +/- 12 months, 50 patients had experienced a cardiac event; seven died (five suddenly), nine suffered recurrent myocardial infarction, and 34 developed severe class III or IV angina pectoris. Compared with that of patients at low risk, the cumulative probability of a cardiac event was greater in high-risk patients identified by scintigraphy (p less than .001), exercise testing (p = .011), or angiography (p = .007). Scintigraphy predicted low-risk status better than exercise testing (p = .01) or angiography (p = .05). Each predicted mortality with equal accuracy. However, scintigraphy was more sensitive in detecting patients who experienced reinfarction or who developed class III or IV angina. When all 50 patients with events were combined, scintigraphy identified 47 high-risk patients (94%), whereas exercise-induced ST segment depression or angina detected only 28 (56%) (p less than .001). The presence of multivessel disease as assessed by angiography identified nine more patients with events than exercise testing (p = .06). However, the overall sensitivity of angiography was lower than that of scintigraphy (71% vs 94%; p less than .01) because three patients who experienced reinfarction and 10 who developed class III or IV angina had single-vessel disease. Importantly, 12 (92%) of these 13 patients with single-vessel disease who had an event exhibited redistribution on scintigraphy. These results indicate that (1) submaximal exercise 201T1 scintigraphy can distinguish high- and low-risk groups after uncomplicated acute myocardial infarction before hospital discharge; (2) 201T1 defects in more than one discrete vascular region, presence of delayed redistribution, or increased lung thallium uptake are more sensitive predictors of subsequent cardiac events than ST segment depression, angina, or extent of angiographic disease; and (3) low-risk patients are best identified by a single-region 201T1 defect without redistribution and no increased lung uptake.

The ability of quantitative thallium-201 scintigraphy to predict the extent and location of coronary artery disease before hospital discharge after acute myocardial infarction was evaluated in 52 patients. All patients underwent coronary angiography and serial thallium-201 imaging either at rest (10 patients) or after submaximal exercise stress (42 patients; target heart rate 120 beats/min). Two or three vessel disease was designated if abnormal thallium-201 uptake or washout patterns, or both, were seen in two or three vascular segments, respectively. Of 156 vessels analyzed in the 52 patients, 91 stenoses of 70 percent or greater were found by angiography. Seventy-four (81 percent) of these were predicted by scintigraphy. The specificity of scintigraphy for identifying vessel stenoses was 92 percent. Sensitivity for detecting and localizing stenoses supplying an infarct zone was 96 percent compared with 62 percent for stenoses supplying myocardium remote from the acute infarct. Perfusion abnormalities were more frequently seen in the distribution of vessels with severe (90 percent or greater) stenoses than in those with moderate (70 to 90 percent) stenoses (87 versus 53 percent, p less than 0.01). Scintigraphy detected a greater proportion of left anterior descending and right coronary arterial stenoses than circumflex stenoses (91 and 87 versus 63 percent, respectively, p less than 0.006). In the 42 patients who underwent submaximal exercise testing, multivariate analysis of 23 clinical and laboratory variables identified multiple thallium-201 defects as the best predictor of multivessel disease. The predictive accuracy of exercise-induced S-T segment depression was only 45 percent compared with 88 percent (p less than 0.05) for thallium-201 scintigraphy. Thus, 2 weeks after myocardial infarction, exercise thallium-201 scintigraphy is useful for predicting the extent and location of coronary artery disease, particularly stenoses in the left anterior descending and right coronary arteries. Moreover, thallium-201 imaging at rest is reliable in assessing the extent of coronary disease in hospitalized patients who cannot undergo exercise testing because of unstable angina, uncompensated heart failure, poorly controlled arrhythmias or physical limitations.

Three patients with true posterior myocardial infarctions and ventricular septal defects were treated by posterior infarctectomy, closure of the defect, and appropriate combinations of mitral valve replacement and coronary grafting. Aortic balloon pumping was not used. The technique of infarctectomy and ventricular septal defect closure is illustrated. Two of the 3 patients have excellent long-term results.

The prospectively assessed time course of changes in ventricular repolarization during acute myocardial infarction (AMI) is reported in 32 patients admitted 2.0 +/- 1.8 (SD) hours after AMI onset. The initial corrected QT interval (QTc) upon hospitalization was longer (0.52 +/- 0.07 seconds) in the 14 patients developing ventricular tachycardia (VT) within the first 48 hours as compared to QTc (0.47 +/- 0.03 seconds) in the eight patients with frequent ventricular premature beats (VPBs) and to QTc (0.46 +/- 0.03 seconds) in the 10 patients with infrequent VPBs (p less than 0.001; analysis of variance). By the fifth day after AMI onset, the QTc shortened significantly only in the VT group, suggesting a greater initial abnormality of repolarization in these patients. All 32 patients had coronary angiography, radionuclide ventriculography, and myocardial perfusion scintigraphy before hospital discharge. Significant discriminating factors related to early phase VT in AMI included initially longer QT and QTc intervals, faster heart rate, higher peak serum levels of creatine kinase, acute anterior infarction, angiographically documented proximal stenosis of the left anterior descending coronary artery, and scintigraphic evidence of hypoperfusion of the interventricular septum. Prior infarction, angina pectoris, hypertension, multivessel coronary artery disease, and depressed left ventricular ejection fraction did not provide discrimination among the three different ventricular arrhythmia AMI groups. We conclude that (1) the QT interval is frequently prolonged early in AMI, (2) the initial transiently prolonged ventricular repolarization facilitates and predicts complex ventricular tachyarrhythmias within the first 48 hours of AMI, (3) jeopardized blood supply to the interventricular septum frequently coexists, and (4) therapeutic enhancement of rapid recovery of the ventricular repolarization process merits investigation for prevention of VT in AMI.

The clinical significance of early ST segment elevation in patients with non-Q wave infarction is unknown. Therefore, 150 consecutive patients with creatine kinase isoenzyme-confirmed acute uncomplicated myocardial infarction who had ST segment elevation of 1 mm or more in at least two contiguous leads on the admission electrocardiogram were analyzed. None received thrombolytic therapy or acute coronary angioplasty. Predischarge angiography, radionuclide ventriculography and exercise thallium-201 scintigraphy were performed 10 +/- 3 days after myocardial infarction. Based on serial electrocardiograms (on days 1, 2, 3 and 10), all 150 infarcts were classified as Q wave (n = 115 [77%]) or non-Q wave (n = 35 [23%]). Although patients with Q wave infarction exhibited greater ST elevation, the amount observed in the non-Q wave group was appreciable, as reflected by the number of leads with ST elevation (3.8 +/- 1.8 versus 3.1 +/- 1.2, p = 0.007) and the sum of the ST elevation (9.6 +/- 7.4 versus 6.2 +/- 6.2 mm, p = 0.016). When compared with the Q wave group, patients with non-Q wave infarction had a shorter time to peak creatine kinase (23.0 +/- 9.1 versus 15.8 +/- 7.9 hours, p = 0.0001), a higher infarct vessel patency rate (24 versus 57%, p = 0.001), lower peak creatine kinase values based on 4 hour sampling (1,372 +/- 964 versus 664 +/- 924 IU/liter, p = 0.0002) and a higher left ventricular ejection fraction (46 +/- 12% versus 54 +/- 9%, p = 0.0003).(ABSTRACT TRUNCATED AT 250 WORDS)

To determine whether Tl-201 scintigraphy performed at rest during the late hospital phase of inferior myocardial infarction can predict subsequent coronary events, 25 patients with historical, enzymatic, and electrocardiographic criteria of transmural inferior infarction underwent serial imaging with computer quantification 7-35 days after admission. All 25 patients had inferior defects, and 13 (52%) also had anterior defects implying stenosis of the left anterior descending coronary artery. The patients were divided into those with inferior and anterior perfusion defects (Group 1) and those with inferior defects alone (Group 2). In Group 1, three patients had persistent defects in the anterior wall and ten had initial defects with redistribution. New or recurrent coronary events--which included new onset or progression of angina pectoris, sudden death, reinfarction, and congestive heart failure--were recorded over an average 7.2 months of followup (range 3-9 mo) for all patients. Ten of 13 (77%) patients in Group 1 had 17 coronary events and four of 12 (33%) patients in Group 2 had six coronary events (p < 0.02). Nine patients in Group 1 and three in Group 2 developed angina (p < 0.03). The apparently increased prevalence in Group 1 of sudden death (8% against 0%), reinfarction (8% against 0%), and congestive heart failure (46% against 25%) was not statistically significant. Thus resting Tl-201 scintigraphy with computer quantification is a highly sensitive method to detect inferior myocardial infarction even in the late hospital phase. Moreover, it appears to identify those patients with inferior infarction at high risk for subsequent coronary events, presumably due to stenosis of the left anterior descending coronary artery.

The long-term outcome and the significance of residual ischemic myocardium, as assessed by predischarge exercise thallium scintigraphy and vessel patency, were studied in 97 patients with single vessel coronary artery disease by angiography 12 +/- 4 days after uncomplicated myocardial infarction. During a mean follow-up period of 39 +/- 17 months, no patients died, 6 (6%) had a recurrent nonfatal infarction and 25 (26%) experienced rapidly progressive angina requiring hospitalization. Although neither exercise-induced angina nor ST segment depression was predictive of a recurrent cardiac event, the mean number of infarct zone scan segments showing thallium redistribution (1.0 +/- 1.0 versus 0.5 +/- 0.8, p = 0.01) and the percent of patients with infarct zone redistribution (61 versus 39%, p = 0.05) were greater in those patients who experienced a late ischemic event. Kaplan-Meier analysis demonstrated a lower event-free survival rate in patients with redistribution (n = 45) than in those without redistribution (n = 52) (p = 0.019). Although no patient received immediate thrombolytic therapy, the infarct-related vessel was angiographically patent in 40 patients (41%). Vessel patency did not influence event-free survival, although a patent vessel, as compared with an occluded vessel, was associated with a greater prevalence of non-Q wave infarction (58 versus 21%, p less than 0.001), fewer persistent infarct zone thallium defects (1.2 +/- 1.1 versus 2.0 +/- 1.2, p = 0.001), more reversible infarct zone thallium defects (1.0 +/- 1.0 versus 0.5 +/- 0.9, p = 0.02) and a trend toward a higher left ventricular ejection fraction (53 +/- 10% versus 49 +/- 12%, p = 0.07). In summary, uncomplicated myocardial infarction in patients with single vessel coronary artery disease is associated with a very low incidence of subsequent death and reinfarction. The presence of infarct zone thallium redistribution, compared with its absence, is predictive of a higher cardiac event rate. These data should be considered when recommending prophylactic percutaneous transluminal angioplasty after uncomplicated myocardial infarction in asymptomatic patients with single vessel coronary disease. On the basis of these results, future randomized trials designed to evaluate the therapeutic efficacy of revascularization in asymptomatic postinfarction patients with single vessel disease should limit enrollment to those patients with residual ischemia located within the infarct zone.

The cause and associated pathophysiology of precordial ST-segment depression (ST decreases) during acute inferior myocardial infarction (IMI) are controversial. To investigate this problem, electrocardiographic findings in 48 consecutive patients with acute IMI were prospectively compared with results of coronary angiography, submaximal exercise thallium-201 (201TI) scintigraphy and multigated blood pool imaging, all obtained 2 weeks after IMI, and with clinical follow-up at 3 months. Patients were classified according to the admission ECG obtained 3.3 +/- 3.1 hours after the onset of chest pain. Twenty-one patients (group A) had no or less than 1.0 mm ST decreases, and 27 (group B) had greater than or equal to 1.0 mm ST decreases in two or more precordial (V1-6) leads. Patients in group B had more prolonged chest pain after admission to the coronary care unit than those in group A (2.8 +/- 3.0 vs 1.2 +/- 1.1 hours, p less than 0.03), greater summed ST-segment elevation in leads II, III, aVF (6.7 +/- 4.7 vs 3.3 +/- 4.5 mm, p less than 0.02), higher plasma peak creatine kinase levels (1133 +/- 781 vs 653 +/- 482 IU/l, p less than 0.01), a higher prevalence of "true posterior" infarction by ECG criteria (26% vs 5%, p less than 0.05), a lower radionuclide ejection fraction (46 +/- 9% vs 54 +/- 6%, p less than 0.001), more extensive infarct-related asynergy (p less than 0.001) and 201TI perfusion abnormalities (p less than 0.01), more complications during hospitalization (p less than 0.03), and more cardiac events at 3 months (p less than 0.02). There were no significant differences between group A and group B in the extent of underlying coronary disease, prevalence of left anterior descending coronary artery disease, exercise-induced ST decreases or angina, and 201TI defects or wall motion abnormalities in anterior or septal segments. Thus, patients with acute IMI who have associated precordial ST decreases have greater global and regional left ventricular dysfunction due to more extensive inferior or inferoposterior wall infarction, rather than concomitant anteroseptal ischemic injury.