Propranolol therapy for ventricular arrhythmias 2 months after acute myocardial infarction

Treatment of premature ventricular complexes with propranolol was studied in 32 patients 2 months after an uncomplicated acute myocardial infarction. All patients had more than 30 premature ventricular complexes/hour averaged over 24 hours, with bigeminy, couplets, multifocal complexes or ventricular tachycardia. Twenty-four hour ambulatory electrocardiographic monitoring and treadmill testing were performed during a control, a treatment and a second control period. The average dosage of propranolol was 160 mg daily. Treadmill testing and ambulatory electrocardiographic monitoring showed a significant decrease in complexity and frequency of premature ventricular complexes with propranolol treatment when the two control periods were compared (p < 0.01 for frequency). During treatment with propranolol 56 percent of patients had 70 percent or greater suppression and 13 (41 percent) had 90 percent or greater suppression of premature ventricular complexes; the median percent reduction was 80 percent. The frequency of premature ventricular complexes also decreased from the first to the second control period (p < 0.05). No patient died suddenly in the 6 month follow-up period.It is concluded that propranolol effectively suppresses premature ventricular complexes after acute myocardial infarction, reducing both frequency and complexity. No sudden death occurred in this high risk population with complex ventricular arrhythmias. Premature ventricular complexes did not tend to increase with time early after acute myocardial infarction in the patients treated with propranolol. Ambulatory electrocardiographic monitoring should be considered for routine evaluation of patients 3 to 8 weeks after acute myocardial infarction and should be followed by antiarrhythmic therapy when complex premature ventricular complexes are noted.     

Exercise testing early after myocardial infarction: Predictive value for subsequent unstable angina and death

Recently, modified treadmill exercise testing before hospital discharge has been reported to be safe in patients after uncomplicated myocardial infarction. Accordingly, the frequency of treadmill exercise-induced abnormalities and their prognostic value were evaluated in 130 patients with uncomplicated myocardlal infarction. Seventy-eight patients (60 percent) had one or more treadmill exercise-induced abnormalities; 42 had S-T segment depression, 35 had angina and 17 had an inadequate blood pressure response. During the mean follow-up period of 11 months, 27 patients experienced unstable angina, 12 had a recurrent myocardlal infarction and 10 died of cardiac causes. Compared with patients with no exercise-induced abnormality, patients with S-T segment depression, angina pectoris or an inadequate blood pressure response had a significantly greater (p < 0.001) incidence of all cardiac events during the follow-up period. Furthermore, unstable angina pectoris was significantly more frequent (p <0.005) in patients with S-T segment depression or angina pectoris. Finally, when the patients with ischemic treadmill abnormalities were combined with the patients exhibiting an inadequate blood pressure response, they had a statistically greater (p < 0.005) incidence of cardiac death than that of patients with no treadmill abnormalities. Therefore, these three abnormalities during modified treadmill exercise testing before hospital discharge identify patients with uncomplicated myocardial infarction who are at risk for a future cardiac event.     

Value of noninvasive techniques for predicting early complications in patients with clinical class II acute myocardial infarction

Twenty-six consecutive patients with acute clinical class II myocardial infarction were prospectively evaluated to assess the ability of two-dimensional echocardiography and gated equilibrium radionuclide angiography to predict early morbidity and mortality. Within 48 hours of the onset of symptoms, right heart catheterization, two-dimensional echocardiography and radionuclide angiography were performed. Serious in-hospital complications developed in 7 patients (27%, Group I), while the remaining 19 patients (Group II) had no complications. Mean left ventricular stroke work index was the only hemodynamic variable that differed significantly between Group I and Group II (28 +/- 8 [standard deviation] vs. 39 +/- 13 g-m/m2, respectively, p less than 0.02). Also, Group I compared with Group II had a significantly lower mean left ventricular ejection fraction by two-dimensional echocardiography (26 +/- 5 vs. 51 +/- 10%, p less than 0.001) or by radionuclide angiography (29 +/- 9 vs. 46 +/- 12%, p less than 0.001). Similarly, Group I had a higher average wall motion index than Group II by both techniques (2.2 +/- 0.2 vs. 1.7 +/- 0.3, p less than 0.001 by two-dimensional echocardiography, and 2.1 +/- 0.3 vs. 1.7 +/- 0.3, p less than 0.001 by radionuclide angiography). Selected stepwise multiple regression analysis demonstrated that left ventricular ejection fraction or wall motion index, by two-dimensional echocardiography or radionuclide angiography, had additional value to a history of prior myocardial infarction for predicting in-hospital complications in patients with class II infarction.(ABSTRACT TRUNCATED AT 250 WORDS)     

Mechanism of inferior electrocardiographic ST-segment depression during acute anterior myocardial infarction in a baboon model

Controversy exists concerning the mechanism of electrocardiographic (ECG) ST-segment depression in leads remote from an area of acute myocardial infarction. Thus, 13 baboons were studied during ligation of the distal third of the left anterior descending coronary artery. The morphologic pattern of the ECG limb leads in the supine baboons resembled that of an asthenic human and did not change when the chest was opened. The visually apparent infarct area of the distal anterior wall was confirmed by epicardial ECG mapping 30 minutes after ligation, and by tissue creatine kinase and histologic study at 24 hours. All 13 baboons had ST depression in leads III and aVF of 0.1 to 1.2 mV at 30 minutes, and 11 of 13 had similar changes in lead II. Also, all 13 baboons had ST elevation in lead aVL (n = 10) or aVR (n = 11), suggesting that the ST vector from the infarct area was directed away from the inferior leads. In no baboon did inferoposterior wall ventricular epicardial mapping show evidence of myocardial ischemia, and mean creatine kinase content from the infarct sites was markedly lower than that from posteroinferior sites (12.7 +/- 2.8 vs 20.6 +/- 2.1 IU/mg protein, p less than 0.01). In addition, the inferoposterior myocardium was normal histologically. In conclusion, acute myocardial infarction often results in reciprocal ST depression at sites distant from the area of acute necrosis and need not represent "ischemia at a distance."     

Serial measurements of left ventricular ejection fraction by radionuclide angiography early and late after myocardial infarction

The left ventricular ejection fraction was determined serially with radioisotope angiography in 63 patients with acute myocardial infarction. After the peripheral injection of a bolus of technetium-99m, precordial radioactivity was recorded with a gamma scintillation camera and the ejection fraction calculated from the high frequency left ventricular time-activity curve. Since this technique requires no assumptions with respect to left ventricular geometry, it is particularly useful in patients with segmental left ventricular dysfunction. Serial measurements during the first 5 days after hospital admission were made in 50 patients, 30 of whom were studied during the subsequent 2 to 39 months (mean 19.9 months). Late follow-up serial studies were also performed in an additional 13 patients who had only one measurement of the left ventricular ejection fraction during the early postinfarction period.Early after infarction, the left ventricular ejection fraction was normal (more than 0.52) in only 15 of the 63 patients, and averaged 0.52 ± 0.05 (standard deviation) in the 27 patients with an uncomplicated infarct. The ejection fraction was reduced in 24 patients with mild to moderate left ventricular failure (0.40 ± 0.05, P < 0.0001) and in the 12 patients with overt pulmonary edema (0.33 ± 0.07, P < 0.0001). In 35 patients the ejection fraction correlated with the mean pulmonary arterial wedge pressure (r = 0.72). In 15 patients with normal left ventricular wall motion by heart motion videotracking, the ejection fraction was significantly higher (0.53 ± 0.08) than in the 26 patients with regional left ventricular dysfunction (0.41 ± 0.10, P < 0.0001). During the early postinfarction period, the left ventricular ejection fraction improved in 55 percent of patients and remained unchanged or decreased in 45 percent. A further increase in the ejection fraction was noted in 61 percent of patients during the late follow-up period. Patients with an initially low or decreasing ejection fraction had a significantly greater incidence of early mortality and left ventricular dysfunction (P < 0.02) than those whose ejection fraction was normal or improved to normal early after infarction. These data indicate that the ejection fraction is a sensitive indicator of left ventricular function after acute myocardial infarction and that serial measurements are helpful in predicting early mortality and morbidity.     

Submaximal exercise testing after acute myocardial infarction: myocardial scintigraphic and electrocardiographic observations.

The relation between global and regional left ventricular function and electrocardiographic signs of ischemia at rest and during submaximal supine exercise was studied in 27 patients 2 to 3 weeks after acute myocardial infarction. Dynamic myocardial scintigraphy was performed at rest and during submaximal exercise utilizing an in vivo method of labeling red blood cells with technetium-99m pertechnetate. Gated radionuclide blood pool scintigrams were obtained in a modified left anterior oblique, and in some patients also in the right anterior oblique projection, to measure left ventricular ejection fraction and segmental wall motion. Electrocardiographic monitoring of heart rate and rhythm was provided during the exercise. The submaximal exercise test was terminated when the patient's heart rate reached 125 beats/min or if angina, malignant ventricular ectopy or electrocardiographic evidence of myocardial ischemia developed before this rate was reached. The data demonstrate that patients with a recent anterior myocardial infarct, in contrast to patients with a recent inferior or nontransmural infarct, manifest a significant reduction in left ventricular ejection fraction with submaximal exercise. Of the eight patients with an anterior infarct, seven had segmental wall motion abnormalities at rest. Four of these eight manifested more severe abnormalities with submaximal exercise; three had abnormalities at rest that did not change with exercise. Four of the eight had a positive electrocardiographic response during exercise (two were taking digoxin). Of these four, only two had more marked wall motion abnormalities with effort. Of the 13 patients with an inferior infarct, 11 had apparently normal wall motion in the modified left anterior oblique projection at rest, including 2 who manifested segmental wall motion abnormalities with submaximal exercise; the 2 remaining patients had wall motion abnormalities at rest that, on exercise, became more marked in one and were unchanged in one. Four of the 13 had a positive electrocardiographic response with exercise (one was taking digoxin); only one of these had a detectably more severe wall motion abnormality with exercise. Of the six patients with a nontransmural infarct, four had no identifiable wall motion abnormalities at rest; in one of these, an abnormality developed with exercise. The remaining two patients had wall motion abnormalities at rest; in one, a positive electrocardiographic ischemic response developed with exercise. Patients with an anterior infarct appear to have a different functional ventricular response to submaximal exercise at the time of hospital discharge than patients with an inferior or nontransmural infarct. To identify ischemic responses with submaximal exercise in these patients one should ideally use both electrocardiographic monitoring and dynamic myocardial scintigraphy.     

Mortality in patients undergoing coronary artery bypass surgery after myocardial infarction

Data on 1,700 patients who underwent coronary artery bypass surgery without additional cardiovascular procedures at the Texas Heart Institute were analyzed, relating the interval between myocardial infarction and operation to early mortality (within 30 days after operation). Patients who underwent coronary artery bypass surgery after a recent infarction (within 2 months before operation) had a higher rate of early mortality (14.5 percent) than patients who had an old infarction (6.9 percent) or no previous infarction (4.1 percent). The interval between recent infarction and operation was most significant. Mortality in patients who underwent operation within the first 7 days after acute infarction (38.1 percent) was more than six times greater than in patients who were operated on 31 to 60 days after infarction (5.8 percent). Mortality of those operated on 8 to 30 days after infarction was 16.4 percent. Elective coronary artery bypass surgery after recent infarction is best accomplished after the first 30 days, when there is no increased risk to the patient. Emergency coronary artery bypass after complicated acute myocardial infarction may be a lifesaving procedure, but it is associated with increased early mortality and should be reserved for those whose condition has not responded to aggressive medical therapy.     

Short- and long-term influence of beta-adrenergic antagonists after acute myocardial infarction

After coronary arterial occlusion, catecholamines are released from storage depots in the left ventricle and injured myocardial cells are exposed to relatively high concentrations of catecholamines during the evolutionary period in which cell injury is becoming progressively more severe. In addition, in experimental animal models, there is a substantial increase in beta-adrenergic receptor density without any alteration in affinity within 1 hour of permanent coronary arterial occlusion. Recent data suggest that alpha-adrenergic receptor density increases within 30 to 60 minutes after coronary arterial occlusion in experimental animal models. The administration of catecholamines during the early phases of evolving myocardial injury can result in heightened adrenergic biochemical responses in severely injured compared with normally perfused tissue in the hearts of experimental animals. Thus, there is adequate rationale for anticipating that beta-adrenergic antagonists would protect ischemic myocardium and potentially reduce the incidence of life-threatening arrhythmias in individuals with evolving acute myocardial infarction (AMI). Studies in animal models demonstrate that the administration of beta-adrenergic antagonists in the first few minutes after coronary artery occlusion may reduce the ultimate extent of myocardial necrosis. Clinical data from several different trials in which beta-adrenergic antagonists were administered to (1) protect ischemic myocardium and preserve ventricular function and (2) reduce the severity of serious ventricular arrhythmias in patients with AMI are reviewed. The effects of longer-term administration of beta-adrenergic antagonists in patients after AMI in prolonging life and reducing risk of reinfarction are presented.     

Left ventricular A wave amplitude in patients after myocardial infarction

The relations between left ventricular (LV) A wave amplitude and left ventricular dimensions, compliance, systolic function, and the size of abnormally contracting segments (ACS) of the left ventricle were examined in 42 patients studied within 1 year after acute myocardial infarction. Left ventricular A wave amplitude was measured from left ventricular pressure tracings both from zero (A₀) and from pre-A wave pressures (A_PAP). Left ventricular compliance was calculated from left ventricular volumes obtained from biplane angiograms and the left ventricular pressure recorded immediately before angiograms. Left ventricular compliance was evaluated by three formulas: $\text{ΔV}\text{ΔP}$ (angiographic stroke volume/left ventricular end-diastolic pressure (LVEDP) minus lowest early diastolic pressure); $\text{ΔV}\text{LV}$ end-systolic $\text{volume}\text{ΔP}$; and $\text{dV}\text{dP}{}_{\mathrm{ED}}\text{× 1/EDV/m}{}^2$. Percent ACS was measured as the akinetic or dyskinetic length along the end-diastolic perimeter on biplane left ventricular angiograms expressed as a percentage of the total left ventricular diastolic perimeter.A_O had a direct quadratic relation with A_PAP (r² = 0.72), and A₀ had high inverse quadratic correlations with $\text{ΔV}\text{ΔP}$ (r² = 0.59), $\text{δV}\text{ESV}$/δP (r² = 0.63), and dV/dPED × 1/EDV/m² (r² = 0.72). A₀ correlated directly with LVEDP (r² = 0.76), end-diastolic volume (r² = 0.32), LV mass (r² = 0.22) and percent ACS (r² = 0.36), and inversely with ejection fraction (r² = 0.43).Seven of the 42 patients were studied by dextran infusion. Diastolic volume change (ΔV_Ind.-Dil.) calculated from indicator-dilution cardiac output values, left ventricular diastolic pressure change (ΔP), and A₀ were obtained before infusion and after each 200 ml infusion. Values for diastolic pressure-volume slope ($\text{ΔP}\text{ΔV}{}_{\mathrm{Ind.-Dil.}}$ ) and A₀ increased with dextran infusion in all seven patients. The $\text{ΔP}\text{ΔV}{}_{\mathrm{Ind.-Dil.}}$ slopes had a significant direct linear relation with corresponding left ventricular A wave amplitudes. Thus, the slope of the diastolic pressure-volume curve for any ventricle, as reflected by the compliance values, is a major determinant of the increase in left ventricular A wave amplitude for a particular volume of dextran infused.In summary, increased left ventricular A wave amplitudes in patients after myocardial infarction signify a decrease in both left ventricular diastolic compliance and systolic function.     

Improved survival after 5 years in 1,144 patients after coronary bypass surgery.

To determine the influence of coronary bypass surgery on late survival, 1,144 consecutive patients were contacted 60 to 76 months after operation. There were 1,000 men (87.4 percent). The mean age was 50.1 years (range 24 to 75). Operation was performed for angina pectoris with coronary lesions of more than 70 percent reduction in luminal diameter in 1,101 patients (96.2 percent). Forty-three patients (3.8 percent) had congestive heart failure without angina and 240 (21.0 percent) had both heart failure and angina. Unstable angina was present in 149 patients (13 percent). Previous myocardial infarction had occurred in 675 patients (59 percent). Single vessel disease was present in 226 patients (19.8 percent), double vessel disease in 442 (38.6 percent), triple vessel disease in 376 patients (32.9 percent) and greater than 50 percent stenosis of the left main coronary artery in 100 patients (8.7 percent). The overall operative mortality rate was 4.6 percent (52 patients). With exclusion of patients with left main coronary artery disease, this rate was 3.8 percent (40 of 1,044) and the overall crude 5 year survival rate was 89.1 percent (930 of 1,044). The survival rates of men and women were comparable. Left ventricular function was classified as good if end-diastolic pressure was less than 15 mm Hg and the left ventriculogram revealed no aneurysmal or akinetic area. Among men, the respective survival rates for each subgroup and for those with good left ventricular function within that subgroup were as follows: one vessel disease, 92.9 percent (169 of 182) and 94.9 percent (130 of 137); two vessel disease, 90.3 percent (352 of 390) and 94.3 percent (248 of 263); three vessel disease, 85.7 percent (293 of 342) and 90.9 percent (189 of 208); left main coronary artery disease, 81.4 percent (70 of 86) and 90.6 percent (48 of 53). The graft patency rate in 157 patients was 86.4 percent (247 of 286 grafts), and 149 patients (94.9 percent) had at least one patent graft.Late survival of all patients with reasonably good preoperative left ventricular function was normal compared with the expected number of survivors based on the general U.S. population experience of 1973. Thus, the survival rates of surgically treated patients with reasonable preoperative left ventricular function, regardless of anatomic lesions, are restored to survival rates comparable with those of the general population. With poor ventricular function, survival is impaired but is still superior to that reported with medical treatment only.     

Uncomplicated acute myocardial infarction: long-term management

The components of long-term management of the patient recovered from uncomplicated myocardial infarction include identification and alteration of nonatherosclerotic factors that might increase the risk of early reinfarction or sudden coronary death, alteration of modifiable coronary atherosclerotic risk factors to prevent progression or induce regression of the atherosclerotic process, and optimal restoration and maintenance of residual cardiovascular function to help improve the quality of life of the patient.     

Permanent pacing in patients with transient trifascicular block during acute myocardial infarction

Patients with acute myocardial infarction and transient complete atrioventricular (A-V) block in association with right bundle branch block and left anterior hemiblock have a high incidence rate of late sudden death presumably due to recurrent A-V block. Over a 5 year period, 18 patients demonstrated right bundle branch block and left anterior hemiblock and had transient complete block during an acute myocardial infarction and survived to hospital discharge. Of six patients who did not have permanent pacing, five died suddenly (one was lost to follow-up) with a mean survival time of 2.4 months after hospital discharge. Twelve subsequent patients received permanent demand pacemakers and had a significantly improved prognosis with a mean survival time of 18 months (P < 0.001). Six patients were still alive at an average follow-up time of 20 months. Prophylactic permanent pacing significantly improves the prognosis after acute myocardial infarction in this select subgroup of patients.     

Serial myocardial scintigraphy after a single dose of thallium-201 in men after acute myocardial infarction

Serial myocardial scintigraphy after a single dose of thallium-201 in the period immediately after myocardial infarction may demonstrate redistribution of thallium-201 into perfusion defects that were evident in the initial scan. This study tested the hypothesis that evaluation of this redistribution, available within hours of infarction, could provide a more accurate estimate of the eventual perfusion defect than a single thallium-201 Image obtained immediately after infarction. The study group comprised 14 patients with a diagnosis on admission of probable acute myocardial infarction. The patients received thallium-201 a mean of 1.3 hours after admission to the coronary care unit. Imaging began 10 minutes after the thallium injection and was repeated 4 to 8 hours later.Eight patients with acute myocardial infarction had a definite reduction in one or more perfusion defects on serial scintigraphy, possibly indicating reperfusion of transiently Ischemic zones. Two patients with acute infarction had an increase in perfusion defects in a second study performed 6 hours after the initial scintigram. In the interval between scans, one patient had a cardiac arrest with clinical evidence of infarct extension after successful resuscitation; the other sustained a lateral extension of the infarct. One patient with acute aortic dissection had normal scans on both studies. All three patients with unstable angina had an abnormal initial scan; on repeat scan, the thallium-201 defect was unchanged in one patient, increased in one and decreased in the third. In the patients with myocardial infarction, repeat thallium-201 scans corresponded more nearly than the initial scans to the extent of technetilum-99m stannous pyrophosphate uptake by the heart.These data suggest that serial myocardial imaging with thallium-201 immediately after myocardial infarction can overcome some of the limitations of a single thallium-201 scintigram and may be useful in delineating ischemic from infarcted myocardium in the postinfarction period.     

Impaired parasympathetic responses in patients after myocardial infarction

To assess whether vagal and sympathetic responses are impaired 3 months after myocardial infarction, 27 patients, 15 age-matched control subjects and 13 young normal subjects underwent physiologic stress tests. In patients, facial immersion in water at 25 ° and 0 ° C provoked less slowing of heart rate than in age-matched control subjects. Young normal persons responded with the greatest reduction in heart rate. Response to facial immersion decreased linearly with age in normal subjects (Y = −0.97X + 86). Isometric handgrip or cold pressor test elicited brisk increases in blood pressure in almost all patients, but the vagal response to facial immersion correlated poorly with such pressor responses. Thus, in the patients studied 3 months after myocardial infarction, the parasympathetic response to facial immersion was significantly impaired whereas sympathetic pressor responses remained intact.     

Prognostic value of submaximal exercise radionuclide ventriculography after myocardial infarction

Submaximal exercise testing with radionuclide ventriculography (RVG) was performed in 117 patients before hospital discharge 17 +/- 7 days (+/- standard deviation) after an acute myocardial infarction (MI). The hypothesis tested in these studies was that submaximal exercise testing coupled to RVG allows the identification of patients at risk for future ischemic events in the subsequent 6 months, irrespective of MI location and type. The sites of MI were characterized as anterior transmural in 33, inferior transmural in 39, limited nontransmural in 18, extensive nontransmural in 24 and indeterminant in 3. During 6 months of follow-up, 9 patients died, 14 had recurrent MI, 18 had refractory angina pectoris, 16 had limiting angina and 17 had congestive heart failure. Discriminant function analysis ranked exercise changes in left ventricular (LV) ejection fraction and end-systolic volume the most important of all clinical, exercise and scintigraphic variables for predicting future cardiac events. The predictive accuracy of changes in LV ejection fraction and end-systolic volume were 93 and 91%, respectively, for the entire group, and were significantly more sensitive than any degree of ST-segment depression or elevation (p less than 0.001). These findings were generally independent of MI location and type. Thus, submaximal exercise RVG after MI is an accurate means of identifying patients at risk for major cardiac events in the 6 months after hospital discharge.     

Prognosis after recovery from first acute myocardial infarction: determinants of reinfarction and sudden death

Factors associated with total cardiac mortality, sudden cardiac death and reinfarction were studied in 325 male survivors aged younger than 60 years of age (mean 50) of a first myocardial infarction (MI). All patients had undergone exercise testing and cineangiocardiography 4 weeks after MI, 24% underwent coronary artery surgery and 30% received beta-blocking therapy. Patients were followed 1 to 6 years (mean 3.5). Total cardiac mortality was best predicted by the left ventricular (LV) ejection fraction (EF) and by a coronary prognostic index. In contrast, neither the severity of coronary arterial lesions measured with a scoring system nor the results of the exercise test gave significant prediction of mortality. Of the 2 major late sequelae of MI, reinfarction could not be predicted by any clinical or cineangiocardiographic variable. However, sudden death not associated with reinfarction was significantly more common (p less than 0.001) when EF was less than or equal to 40% than when it was greater than 40%. Comparison of patients with an EF less than or equal to 40% who did or did not die suddenly showed that LV dilation (high volumes at ventriculography) was an added risk factor, but the extent of coronary occlusions and stenoses was not. It is concluded that, at least for groups of patients treated with standard modern methods after MI, the main determinant of medium-term survival is the extent of LV damage. The state of the coronary arteries and the presence of ischemic myocardium during exercise are only of secondary importance for survival.     

Prognostic value of resting and submaximal exercise radionuclide ventriculography after acute myocardial infarction in high-risk patients with single and multivessel disease

In patients who survive the acute phase of myocardial infarction, those with multivessel coronary artery disease generally have a worse prognosis than those with single-vessel disease. However, some patients with significant multivessel stenoses have a good prognosis, whereas some with a significant single-vessel stenosis have a poor prognosis. Thus, although definition of coronary anatomy may be helpful, it is a not a fail-safe prognosticator. In this retrospective analysis, the association of abnormalities at rest and during submaximal exercise testing with radionuclide ventriculography after acute myocardial infarction with major cardiac complications (death, recurrent infarction, severe angina or congestive heart failure) in the ensuing 6 months was assessed in patients with single and multivessel disease. Coronary angiography and submaximal exercise testing with radionuclide ventriculography were performed within 3 months of each other in 42 patients. Eleven of the 16 patients with single-vessel coronary stenosis had major cardiac complications. The subsequent course of these 16 patients was correctly predicted by left ventricular ejection fraction (LVEF) ≤ 0.40 in 8 patients, by LVEF < 0.55 in 7 patients, by failure of LVEF to increase by 0.05 units in 13 patients, and by an increase in left ventricular end-systolic volume index (LVESVI) during exercise >5% above baseline in 11 patients. Of the 26 patients with multivessel coronary artery disease, 24 had major cardiac complications. The subsequent course of these 26 patients was correctly predicted in 13 by LVEF ≤ 0.40, in 20 by LVEF < 0.55, in 25 by a failure of LVEF to increase by 0.05 units during exercise, and in 20 by an increase in LVESVI by > 5% during exercise. Thus, submaximal exercise testing with radionuclide ventriculography may provide valuable prognostic information concerning the occurrence of major cardiac events after myocardial infarction not only in patients with multivessel disease, but also in those with single-vessel disease. Exercise-induced abnormalities of left ventricular function may have greater prognostic importance than the delineation of coronary arterial anatomy or the assessment of residual left ventricular function at rest.