Samuel E. Lewis

Value of Radionuclide Ventriculography in the Immediate Characterization of Patients With Acute Myocardial Infarction

Abstract The ability of admission radionuclide ventriculography to discriminate among various clinical subsets was evaluated in patients with acute myocardial infarction. One hundred patients with acute myocardial infarction were evaluated within 8 ± 3.1 hours (mean ± standard deviation) after the onset of chest pain. Forty-one patients were in Killip functional class I, 52 in class II and 7 in class III. The mean radionuclide left ventricular ejection fraction was significantly lower in patients with higher Killip classification because of significant elevation of mean left ventricular end-systolic volume rather than significantly altered mean end-diastolic volume. Killip classification frequently failed to correlate with ejection fraction in individual cases. Admission chest X-ray findings were categorized according to the presence of findings suggestive of impaired left ventricular function. Mean left ventricular ejection fraction was significantly lower in patients with abnormal than in patients with normal chest X-ray findings because of significant elevations in both mean end-diastolic and end-systolic volumes. The chest X-ray findings frequently failed to correlate with ejection fraction in individual cases. Stepwise linear regression analysis was employed to analyze the ability of historical, physical, electrocardiographic and chest X-ray findings to predict radionuclide left ventricular ejection fraction. The most predictive variables in order of decreasing significance were anterior myocardial infarction, abnormal chest X-ray findings, rales to two thirds of the posterior thorax, previous myocardial infarction, transmural myocardial infarction and heart rate greater than 100 beats/min. However, even these six optimal predictive variables could explain only 42 percent of the observed variability in left ventricular ejection fraction. Thus, early radionuclide ventriculography adds significantly to the discriminant power of clinical and radiographic characterization of ventricular function in patients with acute myocardial infarction.

Direct measurement of cardiac output by gated equilibrium blood pool scintigraphy: Validation of scintigraphic volume measurements by a nongeometric technique

Abstract A nongeometric technique for the determination of left ventricular volumes from the count data derived from gated equilibrium blood pool scans was previously described and validated by the demonstration of an excellent correlation between the derived data and angiographically determined left ventricular volumes. To provide a further prospective evaluation of this method and to validate its ability to determine stroke volume and cardiac output by a technique that is itself independent of geometric assumptions, simultaneous measurements of cardiac output by the thermodilution technique and gated scintigraphy were performed in 21 patients without valve regurgitation or intracardiac shunts. To substantiate the reliability of scintigraphic measurements at high levels of cardiac output, seven patients had multiple measurements of cardiac output at rest and during an infusion of isoproterenol. There was an excellent correlation between thermodilution and scintigraphic values for cardiac output (scan cardiac output = 0.99 thermodilution cardiac output − 0.005 liters/min; n = 31, standard error of the estimate [SEE]= 0.175 liters/min, r = 0.97) as well as between thermodilution and scintigraphic stroke volumes (scan stroke volume = 1.03 thermodilution stroke volume − 2.8 ml; n = 31, SEE = 2.5 ml, r = 0.95). In addition, the relation between scintigraphic and angiographic measurements of left ventricular volumes continued to be excellent: In 15 patients with technically adequate angiograms, scintigraphic left ventricular volume = 0.90 angiographic left ventricular volume + 7 ml (n = 30, SEE = 10 ml, r = 0.91). Thus, this study further validates the nongeometric method of measuring left ventricular volumes with gated scintigraphy and demonstrates its ability to measure left ventricular stroke volume and cardiac output reliably.

Symptomatic, electrocardiographic, metabolic, and hemodynamic alterations during pacing-induced myocardial ischemia

Atrial pacing has been used to assess the physiologic impact of coronary artery disease (CAD). Several variables have served as markers of pacing-induced myocardial ischemia, but their specificities and sensitivities are unknown. Accordingly, in 28 patients, incremental atrial pacing was performed. Of the 28, 10 had no CAD. The left ventricular ejection fraction (LVEF) (by gated equilibrium blood pool scintigraphy) increased in this group (0.60 +/- 0.11 [mean +/- standard deviation] before pacing to 0.67 +/- 0.13 at peak-pacing, p = 0.002). In no patient did left ventricular end-diastolic pressure increase by greater than 5 mm Hg. No patient had lactate production, and 2 (20%) had electrocardiographic S-T segment depression greater than or equal to 0.1 mV. Four (40%) had chest pain with atrial pacing. In the remaining 18 patients with CAD, atrial pacing caused a decrease in LVEF greater than or equal to 0.05 (0.46 +/- 0.10 to 0.33 +/- 0.09, p less than 0.001) and new segmental wall motion abnormalities in all, indicating pacing-induced myocardial ischemia. Only 8 (44%) had an increase in left ventricular end-diastolic pressure of greater than 5 mm Hg, and only 9 (50%) had lactate production. Ten (56%) had ischemic electrocardiographic changes, and 12 (67%) had chest pain. Thus, the electrocardiographic, metabolic, and hemodynamic alterations that may accompany pacing-induced ischemia are specific but relatively insensitive markers of ischemia. In contrast, chest pain during atrial pacing is a nonspecific occurrence, appearing with similar frequency in normal subjects and patients with CAD and pacing-induced ischemia.

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) less than or equal to 0.40 in 8 patients, by LVEF less than 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 greater than 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 less than or equal to 0.40, in 20 by LVEF less than 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 greater than 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.

Is anterior ST depression with acute transmural inferior infarction due to posterior infarction?: A vectorcardiographic and scintigraphic study

The hypothesis that anterior ST segment depression represents concomitant posterior infarction was tested in 49 patients admitted with a first transmural inferior myocardial infarction. Anterior ST depression was defined as 0.1 mV or more ST depression in leads V1, V2 or V3 on an electrocardiogram recorded within 18 hours of infarction. Serial vectorcardiograms and technetium pyrophosphate scans were obtained. Eighty percent of the patients (39 of 49) had anterior ST depression. Of these 39 patients, 34% fulfilled vectorcardiographic criteria for posterior infarction, and 60% had pyrophosphate scanning evidence of posterior infarction. Early anterior ST depression was neither highly sensitive (84%) nor specific (20%) for the detection of posterior infarction as defined by pyrophosphate imaging. Of patients with persistent anterior ST depression (greater than 72 hours), 87% had posterior infarction detected by pyrophosphate scan. In patients with inferior myocardial infarction, vectorcardiographic evidence of posterior infarction correlated poorly with pyrophosphate imaging data. Right ventricular infarction was present on pyrophosphate imaging in 40% of patients with pyrophosphate changes of posterior infarction but without vectorcardiographic evidence of posterior infarction. It is concluded that: 1) the majority of patients with acute inferior myocardial infarction have anterior ST segment depression; 2) early anterior ST segment depression in such patients is not a specific marker for posterior infarction; and 3) standard vectorcardiographic criteria for transmural posterior infarction may be inaccurate in patients with concomitant transmural inferior myocardial infarction or right ventricular infarction, or both.

Early detection of left ventricular dysfunction in chronic aortic regurgitation as assessed by contrast angiography, echocardiography, and rest and exercise scintigraphy

Abstract The best method for detecting early left ventricular (LV) dysfunction in patients with chronic aortic regurgitation is uncertain. Variables used previously to identify LV dysfunction have included (1) angiographic measurements to identify an LV end-systolic volume index (LVESVI) ≥60 ml/m 2 , (2) echocardiographic measurements to identify LV end-systolic dimension (LVESD) ≥5.5 cm or LV fractional shortening ≤25%, and (3) depressed LV ejection fraction (EF) at rest and/or an LVEF or LVESVI that deteriorates with exercise as detected by myocardial scintigraphic measurements. The hypothesis was tested that radionuclide ventriculography with exercise allows earlier detection of important LV dysfunction in patients with aortic regurgitation than the other variables. In 15 consecutive asymptomatic or only minimally symptomatic patients (8 men and 7 women, mean age 44 years) with isolated 2 to 4+ aortic regurgitation (1) rest and exercise-gated radionuclide ventriculography, (2) M-mode echocardiography, and (3) LV angiography were performed. No other cause of LV dysfunction was apparent in 13 patients; 1 patient had moderate systemic arterial hypertension and 1 had 50% luminal diameter narrowing of the proximal left anterior descending coronary artery. Ten patients did not have an increase in LVEF >0.05 EF units at peak exercise (0.58 ± 0.11 to 0.50 ± 0.12, mean ± standard deviation [SD]) (Group 2), whereas 5 had a normal LVEF response to exercise (0.63 ± 0.08 to 0.69 ± 0.07) (Group 1). Eight of the 10 patients with abnormal LVEF responses to exercise had a decrease in LVEF >10% during exercise. The same 8 patients also had an increase in LVESVI with exercise, whereas the 5 patients with normal LVEF responses to exercise had normal or blunted LVESVI responses to exercise. Only 4 of the 10 patients with exercise-induced LV dysfunction had an angiographic LVESVI ≥60 ml/m 2 , and only 1 had an echocardiographically determined LVESD ≥5.5 cm. Serial follow-up rest and exercise scintigraphic and echocardiographic measurements were made in 8 of the patients a mean of 9.4 months after the initial measurements; 3 patients were in Group 1 and 5 in Group 2. The 5 patients in Group 2 again demonstated abnormal LV function during exercise stress, and 2 of the 3 patients in Group 1 then demonstrated an abnormal LV functional response during exercise. Therefore, it is concluded that (1) exercise radionuclide ventriculography identifies LV dysfunction earlier than traditionally used assessments, (2) LV dysfunction appears to persist in patients that demonstrate it and develop in others that did not have it originally, and (3) echocardiographic dilatation of the LVESD to 5.5 cm appears to be a late and relatively unusual occurrence.

Effect of chronic oral digoxin therapy on ventricular function at rest and peak exercise in patients with ischemic heart disease

The effect of chronic digoxin therapy on left ventricular ejection fraction, left ventricular volumes and cardiac output was assessed using multigated blood pool imaging both at rest and during supine exercise in 14 patients with known ischemic heart disease. Digoxin had no significant effect on ejection fraction at rest or at peak exercise. Neither exercise nor digoxin therapy had a significant influence on stroke volume index. Cardiac index was also not significantly influenced by digoxin either at rest (3.1 ± 1.15 without digoxin versus 2.9 ± 1.03 liters/min per m2 during digoxin therapy) or at peak exercise (5.1 ± 2.08 versus 5.1 ± 2.04 liters/min per m2, respectively), although the increase in heart rate resulted in a significant increase in cardiac index with exercise in each state (p <0.01). End-diastolic and end-systolic volume indexes both tended to be smaller at rest after digoxin therapy than before, but this difference was not significant. In the eight patients with an ejection fraction at rest of less than 0.50 (range 0.15 to 0.47), both end-diastolic and end-systolic volume indexes increased significantly with exercise (p <0.05) irrespective of therapy with digoxin. Conversely, in the six patients with a well preserved (greater than 0.50) ejection fraction at rest, digoxin prevented the exerciseinduced increase in end-diastolic and end-systolic volume indexes, and at peak exercise end-systolic volume index was significantly smaller during digoxin therapy than before it (p <0.05). It is concluded that chronic digoxin therapy in patients with stable ischemic heart disease (1) does not have a significant deleterious functional effect on the nonfailing heart, and (2) does not result in a significant change in left ventricular function at rest, but that it (3) does provide improved ventricular function at peak exercise in patients with well preserved left ventricular function at rest.

Measurement of infarct size in acute canine myocardial infarction by single-photon emission computed tomography with technetium-99m pyrophosphate

The location and extent of myocardial infarction (MI) are important predictors of patient course. The current study tests the hypothesis that MI size could be measured accurately using rotating gamma camera single-photon emission computed tomography ( SPECT ) and technetium-99m pyrophosphate (PPi) and that the accuracy of these measurements was independent of MI location and transmural or nontransmural distribution. SPECT was performed in 38 dogs 48 hours after ligation of the left anterior descending coronary artery (14 dogs) or left circumflex coronary artery (LC) (24 dogs) at the mid-level or below. Projection images were corrected for center-of-rotation and field nonuniformity and processed with a 1-dimensional low-pass filter to diminish rib activity. Sixteen 0.5-cm-thick transverse sections, including the entire left ventricle, were reconstructed by filtered backprojection , low-pass filtered, contrast enhanced and processed with a 3-dimensional boundary enhancement operator. The boundary of PPi uptake in each slice was marked automatically using an algorithm that combined a directional derivative and a threshold, and required continuity of the boundary in 3 dimensions. The total number of volume elements that showed abnormal tracer uptake were summed, corrected to absolute volume, and multiplied by the specific weight of cardiac muscle. Scintigraphic MI weight was compared with pathologic MI weight. There was an excellent correlation between scintigraphic and pathologic MI weight. The poorer correlation for nontransmural compared with transmural MIs is most likely a function of size alone, since MIs that weighed less than 10 g (n = 12, range 1.3 to 9.5 g), both transmural and nontransmural, showed a similar correlation: S = 1.07 X P + 0.56 (r = 0.81, standard error of the slope = 0.245).(ABSTRACT TRUNCATED AT 250 WORDS)

Determination of left ventricular mass using single-photon emission computed tomography

To test the hypothesis that single-photon emission computed tomography (SPECT) could actually determine left ventricular LV mass in humans, SPECT measurements of LV mass were compared with LV mass determined by cineangiography in 12 patients with normal coronary arteries and LV function. Repeat SPECT determinations of LV mass were carried out in 5 patients. Projection images of the left ventricle were acquired after intravenous injection of thallium-201 (TI-201) using a rotating gamma camera. Transverse sections were reconstructed by filtered backprojection. The boundary of LV uptake of TI-201 in each transverse section was defined using a 3-dimensional threshold detector. Scintigraphic LV mass (total number of voxels demonstrating LV TI-201 uptake X voxel volume X specific gravity of myocardium) was compared with angiographic LV mass. There was good correlation between LV mass determined by SPECT and that determined by cineangiography. Mean angiographic LV mass was 208 +/- 45 g (+/- standard deviation). Mean SPECT LV mass was 204 +/- 42 g. Linear regression analysis revealed the following relation: SPECT LV mass = 0.76 X angiographic LV mass + 46.1 (r = 0.82, root-mean-square deviation from regression = 24.7). The SPECT values of LV mass varied an average of 10.4 +/- 4.6% (+/- standard deviation) in the 5 patients in whom 2 determinations were made. Thus, SPECT of TI-201 can accurately measure LV mass in humans.

Radioimmunoassay of serum creatine kinase B isoenzyme in the diagnosis of acute myocardial infarction: Correlation with technetium-99m stannous pyrophosphate myocardial scintigraphy

Abstract In 80 patients admitted to a coronary care unit within 24 hours of chest pain thought to be due to acute myocardial infarction, routine diagnostic tests (electrocardiograms, total serum creatine kinase) as well as 99m technetium stannous pyrophosphate, TcPYP myocardial scintigraphy and serial serum radioimmunoassay determinations of the B subunit of creatine kinase (CK-B), were performed. None of these patients had clinical evidence of acute cerebral injury. A definite decision regarding the presence of acute myocardial infarction could be made in 77 patients on the basis of the results of routine diagnostic tests. The calculated sensitivity, specificity and predictive value of an elevated serum CK-B level in the recognition of acute myocardial infarction were each 100 per cent. Serial TcPYP scintigraphy was 97 per cent sensitive and 70 per cent specific, and had a predictive value of 96 per cent for the recognition of acute myocardial infarction. Both serum CK-B analysis and TcPYP myocardial scintigraphy were helpful in the recognition of infarct extension, and serial studies with both techniques suggested the presence of asymptomatic extension of infarction in several patients. The predictive value of each of these techniques for the recognition of a myocardial infarct suggests that both may be of diagnostic assistance to the physician in clinical settings in which the history, electrocardiogram or total serum creatine kinase are for some reason not interpretable. These techniques may also prove complementary in furthering the ability to assess the extent of acute myocardial damage and the course of its progression.