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Early tomographic myocardial perfusion imaging with technetium-99m sestamibi was performed during inferior wall acute myocardial infarction to determine the relation between the amount and location of myocardium at risk and the presence or absence or anterior ST depression. The total size of the acute perfusion defect and its lateral and septal borders were measured in 29 consecutive patients who were admitted with > 30 minutes of chest pain and acute inferior ST elevation on their initial electrocardiogram. The 22 patients with anterior ST depression had significantly more left ventricular myocardium at risk than the 19 patients who did not have anterior ST depression (23 +/- 2% of the left ventricle vs 15 +/- 1%, p = 0.008). All 8 patients with > 25% of the left ventricle at risk had anterior ST depression. Patients with anterior ST depression had a significantly greater lateral extent of the acute perfusion defect (49 degrees +/- 8 degrees from the midinferior wall vs 23 degrees +/- 7 degrees, p = 0.002). There was no difference in the septal border of the perfusion defect between patients with and without anterior ST depression (-44 degrees +/- 4 degrees vs -46 degrees +/- 7 degrees, p = NS). No patient had a measurable anterior perfusion defect. Although there is considerable overlap between groups with and without anterior ST depression, anterior ST depression is a simple and readily available indicator of myocardium at risk in inferior wall acute myocardial infarction.

To determine whether an increased QRS duration in the absence of bundle branch block (BBB) on the presenting electrocardiogram of patients with acute myocardial infarction (AMI) is associated with decreased survival, we retrospectively reviewed 781 consecutive patients admitted to the coronary care unit of our institution with AMI without BBB between 1988 and 1998. In patients with ST elevation AMI (n = 412), the groups with QRS durationor =100 ms and100 ms had similar survival. Conversely, in patients with non-ST elevation AMI (n = 369), in-hospital, 1-, 3-, and 5-year survival was 84.4%, 75.6%, 66.7%, and 52.2%, respectively, in the group with QRSor =100 ms compared with 95.4%, 89.2%, 83.8%, and 74.3%, respectively, in the group with QRS100 ms (p0.01, log-rank test). In patients with non-ST elevation AMI, those with QRS durationor =100 ms were more likely to be men, to have had a prior AMI that healed, to be in Killip class II, III, or IV, and to have lower ejection fraction than patients with QRS duration100 ms. After adjusting for age, sex, prior AMI or stroke, heart rate, and Killip class on admission, QRS durationor =100 ms was independently associated with in-hospital and overall mortality in patients with non-ST elevation AMI. QRS durationor =100 ms in the absence of BBB is an independent predictor of increased mortality in patients with non-ST elevation AMI.

The relation between left ventricular (LV) filling variables measured by gated blood pool radionuclide ventriculography and clinical symptoms and survival was examined in 93 patients who had decreased LV systolic function. The diastolic data were not significantly associated with clinical symptoms. Time to peak filling rate, peak filling rate and ejection fraction were associated independently with survival free of cardiac death (chi-square = 7.74, S.91 and 3.92, respectively, by stepwise Cox regression analysis). A short time to peak filling rate or increased peak filling rate was associated with decreased survival, whereas the opposite indicated a good prognosis. One-year Kaplan-Meier survival was 73 and 98% when time to peak filling rate was below or above the median value of 167 ms, respectively, 82 and 90% when peak filling rate was above or below the median value of 1.67 end-diastolic volumes per second, respectively, and 76 and 95% when LV ejection fraction was below or above the median value of 0.35, respectively. Thus, filling variables (time to peak filling rate and peak filling rate) measured by radionuclide ventriculography may be valuable in predicting survival in patients with decreased LV systolic function.

To examine the sequential changes in left ventricular volume after thrombolytic therapy for acute myocardial infarction, gated radionuclide ventriculography was performed within 12 hours of thrombolysis and at 1 and 6 weeks in 34 consecutive patients who received intravenous thrombolytic therapy in the Thrombolysis in Myocardial Infarction Trial. Angiographic confirmation of immediate reperfusion (mean 5.6 hours after onset of symptoms) that persisted at 24 hours was noted in 24 patients; 10 patients were not reperfused. A small (9.5%), but significant (p = 0.05), increase in end-diastolic volume index was noted in the reperfused group between 1 and 6 weeks; however, a marked degree of dilatation (35%) was noted in the nonreperfused group (p = 0.01). The change in left ventricular volume between 1 and 6 weeks differed in the 2 groups for both end-diastolic volume index and end-systolic volume index (p = 0.01 and p = 0.02, respectively). By 6 weeks, both end-diastolic volume index and end-systolic volume index were greater in the nonreperfused group (p < 0.05). Between the acute and 6-week studies, definite increases in end-diastolic volume index (p < 0.05) and end-systolic volume index (p < 0.01) occurred commonly in the nonreperfused group but rarely in the reperfused group. Compared to the nonreperfused group, the reperfused group also had significantly higher ejection fractions at both 1 and 6 weeks (p < 0.05). The change in end-diastolic volume index between 1 and 6 weeks correlated significantly and inversely with the ejection fraction at 1 week (r = -0.60, p < 0.001). These results indicate that ventricular dilatation occurs between 1 and 6 weeks after myocardial infarction, is proportional to systolic dysfunction and may be largely prevented by successful thrombolytic reperfusion.

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.

Left ventricular (LV) filling at rest was studied by radionuclide ventriculography using alternate R-wave gating in 42 patients (29 men, 13 women) who had a low likelihood of cardiac disease. LV filling measurements differed little between men and women. Age was correlated positively with atrial filling duration (r = 0.55), atrial filling duration fraction (r = 0.52) and atrial filling fraction (r = 0.56) and negatively with rapid filling fraction (r = -0.58). Age was not correlated with peak filling rate, time to peak filling rate and first-half filling fraction. The heart rate at rest was significantly negatively correlated with rapid (r = -0.62), slow (r = -0.81) and atrial (r = -0.72) filling durations, but not with isovolumic duration. The heart rate at rest was weakly positively correlated with peak filling rate in end-diastolic volume per second (r = 0.36) and negatively correlated with first-half filling fraction (r = -0.35). Systolic pressure at rest influenced atrial filling duration. LV ejection fraction and end-diastolic volume index were not correlated significantly with LV filling in relatively normal subjects.

In 622 patients with known coronary artery anatomy, heart rate (HR).blood pressure (BP) product and left ventricular (LV) ejection fraction (EF) at maximal supine exercise measured by radionuclide ventriculography were used to estimate, by logistic regression analysis, the probabilities of absence of significant coronary artery disease (CAD), presence of significant CAD, presence of multivessel CAD and presence of 3-vessel CAD. Thus, for example, estimated probabilities of each of the aforementioned 4 categories of CAD are 0.39, 0.61, 0.32 and 0.12, respectively, for HR.BP product of 26,000 beats.mm Hg/min and LVEF of 0.6 at maximal exercise and 0.08, 0.92, 0.77 and 0.48, respectively, for HR.BP of 15,000 and LVEF of 0.4. The graphic presentations of these estimated probabilities form useful guidelines for interpreting the results of exercise radionuclide ventriculography. In addition, specific cutoff values at maximal exercise defined 2 groups: (HR.BP product greater than or equal to 21,000 beats.mm Hg/min and LVEF greater than or equal to 0.55) with a high (70%) likelihood of absence of significant CAD or 1-vessel CAD and a low (7%) likelihood of 3-vessel CAD, and (HR.BP product less than 21,000 and LVEF less than 0.55) with a high (72%) likelihood of multivessel CAD and a low (8%) likelihood of absence of CAD.

The significance of a decline in systolic blood pressure (BP) during supine exercise was examined in 820 patients who underwent both supine exercise gated equilibrium radionuclide ventriculography and coronary angiography. Twenty-seven patients, 3% of the study population, had a decrease in systolic BP at peak exercise of more than 10 mm Hg from the systolic BP at rest. Other indicators of ischemia--angina, ST-segment depression, a decrease in ejection fraction and wall motion abnormality during exercise--were present frequently but not uniformly in these patients. Although most patients had a decline in ejection fraction and a new wall motion abnormality with exercise, 4 patients had an increase in ejection fraction with exercise without any regional wall motion abnormalities. Coronary angiography in the 27 patients with systolic hypotension demonstrated severe coronary artery disease (CAD). Twenty-two patients (81%) had 3-vessel or left main CAD. Twenty of these 22 patients with 3-vessel CAD had at least 2 arteries with 90% or more diameter stenoses. Systolic hypotension during supine exercise radionuclide angiography is infrequent, usually associated with evidence of global and regional left ventricular dysfunction, and a marker of very severe CAD.