Search

The variability of left ventricular ejection fraction, normalized mean ejection rate and regional wall motion was evaluated from first pass quantitative radionuclide angiocardiograms obtained with a computerized multicrystal scintillation camera. Three radionuclide studies separated by an average of 4.3 days were obtained in each of 20 patients. Ejection fraction and ejection rate obtained on the first, second and third studies did not differ significantly. The mean (± standard deviation) variability of sequential ejection fraction measurement was 4.4 ± 3.6 percent, and of sequential ejection rate was 0.56 ± 0.47 sec −1 . Variations in measurements were not related to fluctuations in heart rate or blood pressure. Variability in ejection rate was significantly greater in patients with normal function than in those with abnormal function. Regional wall motion analysis was constant in 19 of 20 patients. Thus, sequential quantitative radionuclide angiocardiography allows reproducible serial assessment of left ventricular performance that can be performed with a low level of intrinsic variability.

The effects in vivo of physiologic increases in insulin and amino acids on myocardial amino acid balance were evaluated in conscious dogs. Arterial and coronary sinus concentrations of amino acids and coronary blood flow were measured during a 30-min basal and a 100-min experimental period employing three protocols: euglycemic insulin clamp (plasma insulin equaled 70 +/- 11 microU/ml, n = 6); euglycemic insulin clamp during amino acid infusion (plasma insulin equaled 89 +/- 12 microU/ml, n = 6); and suppression of insulin with somatostatin during amino acid infusion (plasma insulin equaled 15 +/- 4 microU/ml, n = 6). Basally, only leucine and isoleucine were removed significantly by myocardium (net branched chain amino acid [BCAA] uptake equaled 0.5 +/- 0.2 mumol/min), while glycine, alanine, and glutamine were released. Glutamine demonstrated the highest net myocardial production (1.6 +/- 0.2 mumol/min). No net exchange was seen for valine, phenylalanine, tyrosine, cysteine, methionine, glutamate, asparagine, serine, threonine, taurine, and aspartate. In group I, hyperinsulinemia caused a decline of all plasma amino acids except alanine; alanine balance switched from release to an uptake of 0.6 +/- 0.4 mumol/min (P less than 0.05), while the myocardial balance of other amino acids was unchanged. In group II, amino acid concentrations rose, and were accompanied by a marked rise in myocardial BCAA uptake (0.4 +/- 0.1-2.6 +/- 0.3 mumol/min, P less than 0.001). Uptake of alanine was again stimulated (0.9 +/- 0.3 mumol/min, P less than 0.01), while glutamine production was unchanged (1.3 +/- 0.4 vs. 1.6 +/- 0.3 mumol/min). In group III, there was a 4-5-fold increase in the plasma concentration of the infused amino acids, accompanied by marked stimulation in uptake of only BCAA (6.8 +/- 0.7 mumol/min). Myocardial glutamine production was unchanged (1.9 +/- 0.4-1.3 +/- 0.7 mumol/min). Within the three experimental groups there were highly significant linear correlations between myocardial uptake and arterial concentration of leucine, isoleucine, valine, and total BCAA (r = 0.98, 0.98, 0.92, and 0.97, respectively); P less than 0.001 for each). In vivo, BCAA are the principal amino acids taken up by the myocardium basally and during amino acid infusion. Plasma BCAA concentration and not insulin determines the rate of myocardial BCAA uptake. Insulin stimulates myocardial alanine uptake. Neither insulin nor amino acid infusion alters myocardial glutamine release.

This study was designed to determine whether alterations in systemic oxygen transport induced by the use of vasodilators for pulmonary hypertension would simultaneously affect oxygen uptake in patients with chronic obstructive pulmonary disease (COPD). Six stable patients with moderate to severe COPD were studied during resting conditons, nitroprusside infusion, a second control period, and after administration of hydralazine. Systemic oxygen transport fell with nitroprusside infusion (523 ± 94 to 418 ± 78 ml/min/m2, p < 0.05). With this there was a fall in oxygen uptake (135 ± 11 to 119 ± 12 ml/min/m2, p < 0.05), but only a minimal increase in oxygen extraction. In contrast, systemic oxygen transport was augmented in all patients when hydralazine was administered (444 ± 121 to 840 ± 157 ml/min/m2, p < 0.05). There was also a net increase in oxygen uptake in these patients (122 ± 19 to 148 ± 21 ml/min/m2, p < 0.05). We postulate that these clinically stable patients have a resting oxygen uptake that may b...

A multicenter study of rest and exercise thallium-201 myocardial imaging in 190 patients from five centers was performed. Exercise images were obtained after graded treadmill or bicycle stress with use of five different gamma camera models and were interpreted by the originating investigator without knowledge of other clinical data. Of 42 patients with less than 50 percent coronary stenosis, 4 (10 percent) had a resting image defect, 1 (2 percent) a new exercise defect and 5 (12 percent) either a resting or an exercise image defect, or both. Of 148 patients with coronary stenosis of 50 percent or greater, 64, (45 percent) had an image defect in the study at rest, 90 (61 percent) had new or increased defects after exercise, and 115 (78 percent) had resting or exercise defects, or both. New exercise image defects were more common than exercise S-T depression (90 of 148 [61 percent] versus 62 of 148[42 percent]; P less than 0.01). In a second group of 111 patients with acute myocardial infarction studied at three centers, 90 patients (81 percent) had image defects compared with 71 (64 percent) two had new electrocardiographic Q waves (P less than 0.01). Smaller infractions, as assessed with serum enzyme values, and diaphragmatic infarctions were less commonly detected than larger or anterior infarctions. These findings suggest that myocardial imaging complements the electrocardiographic identification of acute myocardial infarction of exericse-induced myocardial ischemia.

Sudden unexplained death is a common cause of late mortality after aortic valve replacement. To evaluate the occurrence of ventricular arrhythmia in patients with aortic valve replacement, two 24 hour ambulatory electrocardiographic recordings were obtained in 45 such patients (mean age 55 years) who had undergone replacement an average of 3.3 years previously. In 43 patients, ventricular arrhythmia was detected; it was rare (mean premature ventricular complex frequency less than 1 15 min) in 18 patients (40 percent), moderately frequent (mean frequency 1− 10 15 min) in 14 patients (31 percent) and frequent (mean frequency more than 10 15 min) in 11 patients (24 percent). Multiformity was noted in 40 (89 percent), bigeminy in 27 (60 percent), couplets in 27 (60 percent) and ventricular tachycardia in 16 (36 percent) of the 45 patients studied. The occurrence of ventricular arrhythmia was not related to the predominant hemodynamic lesion or to the presence of coronary artery disease as determined at the time of preoperative cardiac catheterization. Radionuclide left ventricular ejection fraction, determined at the time of electrocardiographic monitoring in 39 patients, demonstrated normal left ventricular function (ejection fraction greater than 50 percent) in 27 patients (60 percent), moderately depressed function (ejection fraction 36 to 50 percent) in 8 (21 percent) and severe dysfunction in 4 (10 percent). When patients with abnormal versus normal left ventricular performance were compared, the mean premature ventricular complex frequency was 21 ± 26 15 min versus 5 ± 11 15 min ( p ; couplets occurred in 10 (83 percent) of 12 versus 13 (48 percent) of 27 patients (p

We analyzed the ordering and impact of the first 171 fee-for-service cardiovascular nuclear medicine procedures at one hospital. The ordering physicians said 72% of the study results were useful and 28% contributed to changes in patient management. Experienced cardiology reviewers, however, felt that only 65% of studies were appropriately ordered, that 97% of appropriately ordered studies provided potentially useful information, and that 12% of all studies made important contributions to appropriate changes in patient management. The revieweres were most likely to rate exercise thallium procedures and procedures ordered by physicians from distant hospitals as being appropriately ordered and having important clinical impact. We conclude that (1) ordering physicians and revieweres may disagree substantially in their estimates of the impact of a diagnostic test; and (2) although a test may yield important information in appropriate patients, its total clinical impact will depend on how often it is suitably ordered and used.

First pass radionuclide angiocardiography under conditions of rest and exercise was utilized to evaluate a group of 16 postoperative patients who had undergone total surgical correction of tetralogy of Fallot. Functional data were related to thallium-201 myocardial imaging at rest, a noninvasive means of detecting right ventricular hypertrophy. All 16 patients were asymptomatic and 15 demonstrated normal right ventricular ejection fraction (equal to or greater than 45 percent) at rest. However, 13 patients manifested abnormal right ventricular ejection fraction responses to exercise (normal response is an absolute increment in an ejection fraction of 5 or greater percent). For the entire group, right ventricular ejection fraction at rest was 55 ± 2 percent, whereas at exercise it was 52 ± 2 percent (p = not significant). In contrast, left ventricular ejection fraction responses were normal in all patients. Thallium-201 imaging revealed substantial right ventricular uptake consistent with residual right ventricular hypertrophy, which was quantifiable in all patients. Thus, abnormalities in right ventricular performance during exercise may be detected readily by this radionuclide approach in these postoperative patients despite their asymptomatic clinical status and generally normal right ventricular performance at rest.

Infarct site, extent, and the degree of associated asynergy are major determinants of the hemodynamic consequences of myocardial infarction. Although conventional electrocardiography and vectorcardiography are routinely employed in assessing the location and size of infarction, they are relatively nonspecific. The newer techniques of high-frequency electrocardiography and isopotential mapping offer promise but have yet to undergo systematic evaluation. A rough measure of the extent of infarction is obtained from serum enzyme measurements. However, they furnish no information with regard to localization. The region of infarction may be detected by precordial scanning following the intravenous or intracoronary injection of a radioisotope. The infarct may be revealed as an area of decreased perfusion (cold spot) or as an area to which a specific radioactive label is bound (hot spot). With the availability of newer radionuclides such as 43 potassium and the use of computer techniques, a more precise means of localizing and quantifying myocardial infarction may become available. Optimal definition of asynergy is obtained with contrast angiography. However, the risk of this procedure has limited its use, to date, in acute myocardial infarction. Apex- and kinetocardiography, chest X-ray, and fluoroscopy often suggest regional ventricular dysfunction, but these techniques are not sufficiently specific. Newer noninvasive methods for objectively evaluating regional ventricular dysfunction are ECG-gated cardiac scintiphotography and radarkymography. With ECG-gated scintiphotography, end-diastolic and end-systolic cardiac isotope images are obtained following intravenous injection of 99m technetium-albumin. From these images, assessment of asynergy and extent and location of infarct can be made. With radarkymography, heart-wall motion is assessed and quantitated by tracking segments of the cardiac silhouette visualized on a cinefluorogram. These techniques are ideally suited to the acutely ill patient. Echocardiography is another noninvasive technique with potential application to the study of asynergy. However, at present, only posterior-wall motion can be measured. At the time of surgery regions of infarction may be localized by means of chemical indicators (fluoroscein), isotope techniques, or epicardial electrocardiographic mapping. Recently much has been learned about the hemodynamics of myocardial infarction. Through the use of the techniques described, further insight into regional ventricular abnormality and extent and localization of myocardial infarction could be obtained. With this information better approaches to therapy and prognosis could be developed. Many students of the coronary circulation must have noted that the ventricular zone affected by ligating a large coronary branch not only appears cyanotic and dilated, but that it seems to alter in its mode of contraction. The detailed and sequential changes in contraction are not easily followed by the unaided eye and so far have not been recorded myographically. The reasons for this were the lack of an adequate and suitable myograph and a technique for the application of one to a limited ventricular surface so that records obtained represent, at least reasonably well, changes in muscle length and not predominantly artifacts due to position changes, thrusts and vibrations of the vigorously beating ventricle. 1

A radioactive tracer method for the measurement of left ventricular ejection fraction in man without cardiac catheterization is described. The tracer (99mtechnetium-labeled albumin) is injected intravenously. Images of the heart at end-systole and end-diastole are obtained using a scintillation camera and an electronic gate triggered by the patient's electrocardiogram. Each image is composed of 300,000 counts, representing a summation of 200 to 400 heartbeats at end-systole and end-diastole. An outline of the left ventricular free wall is drawn from each gated image. The position of the aortic and mitral valve planes is determined using a radionuclide angiogram obtained at the time of tracer injection. Left ventricular ejection fraction is calculated from the area and length of the long axis of the ventricular outline at end-systole and end-diastole. Determinations of ejection fraction in 20 patients using this tracer method were correlated with measurements obtained by contrast cineangiography with the following results: ejection fraction r = +0.92, P < 0.001; end-diastolic volume r = −0.76, P < 0.001; and end-systolic volume r = −0.75, P < 0.001.

Ten hospitalized patients performed two exercise tests per day on five consecutive days to determine the efficacy and duration of action of three sublingual long-acting nitrate preparations: isosorbide dinitrate, pentaerythritol trinitrate, and erythrityl tetranitrate. The duration of exercise to the point of ischemia, manifest as typical anginal pain and/or 1.0 mm ST-segment depression, was determined 45 min and 100 min after each long-acting nitrate was administered. These results were compared with the duration of exercise after placebo and two minutes after nitroglycerin administration. The mean durations of exercise in two tests after placebo were 62.5 sec and 58.4 sec (not significant) and the mean durations of exercise after nitroglycerin administration were 90.5 sec and 88.4 sec, both different from placebo ( P < .001). There was no difference from placebo found 55 min after taking nitroglycerin. The mean durations of exercise 45 min after erythrityl tetranitrate, isosorbide dinitrate and pentaerythritol trinitrate were 89.1, 87.5, and 87.5 sec respectively and all were different from placebo ( P < .01). Mean durations of exercise 100 min after erythrityl tetranitrate, isosorbide dinitrate, and pentaerythritol trinitrate were 76.4, 75.5, and 69.7 sec and none were significantly different from placebo. This study indicates that each long-acting nitrate is effective for at least 45 min and suggests that they should not be given on a fixed dosage schedule but rather should be taken prophylactically whenever an angina-provoking situation is anticipated.

SummaryFollowing amputation of approximately 70% of a rat's liver, there ensues a period of active nucleic acid synthesis followed by a wave of cell division. Surface alterations occur during the preparation for mitosis which result in an increase of electro-phoretic mobility and it has been suggested that cell division is dependent upon surface charge. The present study demonstrates that the assumption of increased electrostatic charge during the preparation for cell division is not the result of newly synthesized protein and in accord with previous work indicates that cell division is independent of surface charge. However, it was suggested that the total surface charge of interphase cells is related to the constant synthesis of surface proteins.

Technetium-99m isonitrile is a new myocardial perfusion imaging agent that accumulates according to the distribution of myocardial blood flow. However, unlike thallium-201, it does not redistribute over time. This imaging agent was used with serial quantitative planar imaging to assess the initial risk area of infarction, its change over time and the relation to infarct-related artery patency in 30 patients with a first acute myocardial infarction. Twenty-three of 30 patients were treated with recombinant tissue-type plasminogen activator (rt-PA) within 4 h after the onset of chest pain. Seven patients were treated in the conventional manner without thrombolytic therapy. Technetium-99m isonitrile was injected before or at the initiation of thrombolytic therapy, and imaging was performed several hours later. These initial images demonstrated the area at risk. Repeat imaging was performed 18 to 48 h later and at 6 to 14 days after the onset of myocardial infarction to visualize the ultimate extent of infarction. The initial area at risk varied greatly (range defect integral 2 to 61) both in patients treated with rt-PA and in those who received conventional treatment. For the total group, the initial imaging defect decreased in size in 20 patients and was unchanged or larger in 10 patients. Patients with a patent infarct-related artery had a significantly greater decrease in defect size than did patients with persistent coronary occlusion (-51 +/- 38% versus -1 +/- 26%, p = 0.0001). All patients with a decrease in defect size greater than 30% had a patent infarct-related artery. In 12 patients who also had predischarge quantitative exercise thallium-201 imaging, good agreement existed between the extent and severity of myocardial perfusion defect on the last technetium-99m isonitrile study before discharge and that noted on delayed thallium-201 imaging. It is concluded that serial planar technetium-99m isonitrile myocardial imaging in patients with acute myocardial infarction undergoing thrombolytic therapy offers a new quantitative noninvasive approach for assessment of the initial risk zone as well as the success of reperfusion.

Sequential first pass radionuclide angiocardiography can be performed in rapid succession using gold-195m because of its low radiation dose and short half-life (30.5 seconds). In 25 patients with known or suspected coronary artery disease, first pass studies with gold-195m were obtained using a computerized multicrystal gamma camera at rest (n = 29), at the end of each 3 minute stage of exercise (n = 25) and immediately after exercise (n = 23). In 13 patients, assessment of left ventricular function during exercise with gold-195m was combined with thallium-201 stress scintigraphy. Left ventricular ejection fraction at rest assessed with technetium-99m and gold-195m correlated well (r = 0.93). In addition, repeat left ventricular ejection fractions at rest with gold-195m correlated closely (r = 0.96). Comparing peak exercise left ventricular ejection fraction with ejection fraction at rest, abnormal left ventricular reserve was found in 20 of 25 patients. Various abnormal patterns of left ventricular ejection fraction response were noted, showing the diagnostic potential of serial exercise angiocardiography. Thallium-201 myocardial images, obtained on a single crystal gamma camera after multiple gold-195m injections, were all of good diagnostic quality and were abnormal in 10 of 13 patients. Thus, multiple high count rate first pass studies can be obtained with gold- 195m during and after exercise, allowing serial study Of physiologic changes in left ventricular function during exercise. Thallium-201 myocardial imaging can be performed using the same exercise test, providing direct comparison of myocardial function and perfusion.

Low osmolar contrast agents produce less adverse electrophysiologic and hemodynamic alterations during cardiac catheterization. The nonionic agents probably reduce the risk of provoking myocardial ischemia during coronary arteriography or ventriculography. Patients also report less subjective sensation of discomfort during administration of low osmolar agents for cardiovascular procedures. However, nonionic agents have not been proved to reduce the incidence of several serious complications of cardiac catheterization, including acute renal failure and anaphylactoid reaction. Although evidence is inconclusive, there may be an increased risk of thromboembolic complications during cardiac catheterization when certain low osmolar nonionic agents are administered. Nonionic contrast agents have not been definitely proved to reduce the risk of death after cardiac catheterization.

Restenosis after balloon angioplasty may be mediated through platelet deposition at the site of arterial dilatation. The purpose of this study was to determine whether platelet deposition at the site of dilatation could be detected using indium-111 platelet scintigraphy. Fifteen patients, aged 60 ± 9 years, with iliac or femoral (n = 12), renal artery (n = 2) or distal aortic (n = 1) stenoses were studied. All patients received intravenous heparin at the time of dilatation. Labeled platelets containing 471 ± 65 μCi indium-111 were injected 0.25 to 4 hours after dilatation and 1 to 24 hours after imaging. In 11 of 12 patients with iliac and femoral dilatations, focal uptake was demonstrated at the angioplasty site. In 4 patients (2 patients with renal, 1 patient with iliofemoral, and 1 with distal aortic stenoses), uptake at the dilatation sites was not detected. This preliminary study indicates that despite intravenous heparin, platelets accumulate at sites of balloon dilatation. Platelet scintigraphy may be useful in predicting sites of future narrowing after angioplasty and may be used to test the efficacy of antiplatelet therapy in retarding restenosis.

We studied a patient with an anomalous left coronary artery arising from the pulmonary artery by using conventional angiographic and myocardial imaging techniques. Myocardial imaging with radioactive 201thallium confirmed the significance of resting Q waves, and the defect in anterior perfusion coupled with the presence of thallium in the pulmonary outflow tract during exercise underscored the dynamic nature of the ischemic response to exercise in this syndrome.

The intrinsic variability and accuracy of left ventricular ejection fraction determined by multiple gated cardiac blood pool imaging was evaluated in 83 patients. Ejection fraction by gated studies correlated well with data from first pass radionuclide angiocardiography (r = 0.94) and from contrast angiography (r = 0.84). Intra- and interobserver variabilities of absolute ejection fraction were minimal (mean +/- standard deviation 1.4 +/- 1.2 and 1.6 +/- 1.5 percent, respectively) and were not different for normal (ejection fraction 55 percent or greater) and abnormal patients. Ejection fraction was determined twice in 70 patients: on the same day at intervals separated by 1 to 2 hours (41 patients) and on 2 different days (29 patients). Ejection fraction ranged from 18 to 91 percent and was normal in 37 patients. There was no difference in mean serial variabilities of absolute ejection fraction for all repeat studies performed on the same and separate days (3.3 +/- 3.1 versus 4.3 +/- 3.1 percent (not significantly different). The mean variability of absolute ejection fraction for repeat studies in normal patients was significantly greater than in abnormal patients (5.4 +/- 4.4 versus 2.1 +/- 2.0 percent, P less than 0.01). The incidence rate of absolute interstudy changes of 5 percent or more was significantly higher in normal than in abnormal patients (P less than 0.01). This differential variability should be considered in interpreting sequential changes in left ventricular ejection fraction. To be attributed to nonrandom physiologic alterations, the absolute change in ejection fraction should be 10 percent or more in normal patients and 5 percent or more in abnormal patients.

Myocardial ischemia has been associated with dispersion of ventricular refractory periods and this dispersion has been related to the ventricular arrhythmias seen with coronary occlusion. This study relates the degree of change in measured ventricular refractory period with the degree of regional myocardial blood flow abnormality after coronary occlusion. When regional myocardial blood flow is less than 70 percent of that of nonischemic areas, refractory periods are significantly (P < 0.001) shortened. The greatest change in refractory periods occurs in areas with a regional myocardial blood flow that is 21 to 40 percent of that of non-ischemic areas. Marked (less than 20 percent) and minimal (61 to 80 percent) reductions in regional myocardial blood flow are associated with less, but still significant, shortening of ventricular refractory periods. Thus dispersion of refractoriness can be related to the inhomogeneity of regional myocardial blood flow after acute coronary occlusion. Interventions designed to salvage ischemic myocardium by increasing regional myocardial blood flow may affect dispersion of ventricular refractory periods in complex and divergent ways.

The ventricular antiarrhythmic properties of oral digoxin were examined in 13 patients with chronic ventricular ectopy using serial 24-hour electrocardiographic monitoring. Mean premature ventricular complex frequency (per 1,000 normal beats) decreased from 56 +/- 47 during the placebo period to 40 +/- 27 (p = not significant [NS]) and 25 +/- 17 (p less than 0.05) during daily administration of digoxin, 0.25 and 0.375 mg. Digoxin had no significant effect on the qualitative occurrence of complex ventricular arrhythmia patterns (multiformity, bigeminy, couplets, ventricular tachycardia). Radionuclide left ventricular (LV) ejection fraction was measured during the placebo period. Seven patients had normal (ejection fraction greater than 50%) and 6 abnormal global LV performance. In the normal group, the mean premature ventricular complex frequency decreased from 69 +/- 58 to 20 +/- 18 (p less than 0.05) and the mean couplet frequency decreased from 0.59 +/- 0.85 to 0.07 +/- 0.06 (p less than 0.04) during the placebo and 0.375 mg digoxin dosing periods, respectively. In contrast, no significant changes in either variable occurred after digoxin in subjects with depressed LV function. This study indicates that oral digoxin is moderately effective in suppressing premature ventricular complexes, and that its effects are greatest in patients with normal overall LV performance.

Balloon inflation performed during percutaneous transluminal coronary angioplasty causes transient total occlusion of the coronary artery and thus provides a model for evaluation of the regional myocardial responses to transient ischemia. Twenty patients with normal left ventricular function undergoing angioplasty of isolated stenosis of the proximal left anterior descending coronary artery were studied. In group A (14 patients) analysis of one inflation-deflation sequence per patient was performed. Group B (six patients) had multiple (greater than 5) inflations; the first and last sequences were analyzed. Assessment included continuous two-dimensional echocardiography with computerized quantitative analysis of regional left ventricular wall motion, and continuous 12 lead electrocardiographic recordings. The mean duration of inflation in group A was 62 +/- 6 seconds (mean +/- SD). The onset of regional left ventricular dysfunction was 12 +/- 5 seconds after inflation. Profound dysfunction was noted in all patients. After 60 seconds of balloon occlusion of the coronary artery, 29% of patients had severe hypokinesia of the ischemic region and 71% had akinesia or dyskinesia. With deflation there was prompt recovery of regional function, with full recovery at 43 +/- 17 seconds. Comparison of data from first and last inflations in group B revealed no significant differences in time to onset of dysfunction, magnitude of dysfunction or time to complete recovery of function. The onset of ischemic electrocardiographic changes lagged behind the onset of wall motion abnormalities, with only 64% of patients showing evidence of ischemia on 12 lead electrocardiograms at 20 seconds of inflation. After 60 seconds, 86% had ischemia detectable by electrocardiography. Thus, balloon inflation during coronary angioplasty leads to profound but reversible regional left ventricular dysfunction. Repeated occlusions of the coronary artery during angioplasty do not have a cumulative ischemic effect. It may be hazardous to apply these findings to patients who have underlying major left ventricular dysfunction and in whom the reversibility of dysfunction and lack of cumulative ischemic effect may not be assured.

The dual radionuclide myocardial distributions of imaging agents potassium-43 (43K) and technetium-99m stannous pyrophosphate (99mTc-PYP) were studied in a 24-hour closed chest canine infarct preparation. In multiple myocardial biopsies in 20 dogs, tissue levels of both radionuclides were compared to either an index of tissue viability (myocardial creatine phosphokinase [CPK] depletion), or to estimates of regional myocardial blood flow as measured by the microsphere technique. Myocardial 43K uptake in the ischemic and infarcted zone correlated well with both CPK depletion (r = 0.73) and microsphere estimates of relative blood flow. The correlation with microspheres was excellent in the transmural sample (r = 0.93) as well as endocardial (r = 0.97) and epicardial (r = 0.86) portions. On the other hand, 99mTc-PYP myocardial uptake did not correlate with the extent of CPK depletion. Maximal uptake was frequently noted in border zones with only moderate CPK depletion, while lesser degrees of 99mTc-PYP uptake were noted in the central infarct zone where CPK activity was lowest. The relationship of 99mTc-PYP uptake to microsphere regional flow estimates demonstrated that 99mTc-PYP uptake was maximal at flows of 0.3 to 0.4 of normal. At lower flows, 99mTc-PYP uptake fell toward normal levels. A similar relationship was noted between the distributions of 99mTc-PYP and 43K. In relatively high flow border segments (larger than or equal to 0.80 of normal), abnormal 99mTc-PYP uptake of five to six times normal persisted. The transmural distribution of 99mTc-PYP demonstrated that in low flow regions 99mTc-PYP uptake was primarily epicardial, while in the higher flow ischemic periphery of the infarct endocardial uptake predominated. Thus, while there is a direct correlation between cationic 43K myocardial uptake and regional myocardial viability and blood flow, no such direct relationship exists for 99mTc-PYP. This is in part based on the necessity for delivery of the radioactive tracer to the infarct zone.

The ability of cardiac scintigraphy with indium-111 (/sup 111/In)-labeled platelets to detect coronary artery thrombosis (CAT) was assessed in a canine model. Cardiac imaging and tissue distribution studies were performed shortly after administering /sup 111/In-labeled platelets to 12 dogs (group 1) with acute CAT. Four dogs (group 2) with acute CAT were studied 2 and 22 hours after administering /sup 111/In platelets. In addition, four dogs (group 3) with 24-hour-old CAT were similarly evaluated. In all group 1 animals, in vivo imaging 1 to 2 hours after /sup 111/In platelet administration revealed intense uptake in the region of thrombus-containing left anterior descending arteries that was readily discernible from background blood pool activity. Sequential imaging of the four group 2 animals over a 22-hour period revealed no change in the scintigraphic pattern of the thrombosed arteries. In contrast, /sup 111/In platelet imaging in the four group 3 animals with 24-hour-old CAT failed to reveal enhanced activity within the region of the thrombus-containing coronary artery. In the 12 group 1 animals, the CAT accumulated 69 +- 10 (mean +- SEM) times greater activity than present in blood and 651 +- 135 times greater activity than normal left ventricular myocardium. There was 24more » +- 7 times greater /sup 111/In activity in the damaged left anterior descending arteries compared with normal circumflex arteries. Similar uptake ratios were seen in group 2 animals. The 24-hour old thrombi from group 3 animals showed no enhanced /sup 111/In uptake. This study demonstrates that experimental acute CAT can be detected readily with /sup 111/In platelet cardiac scintigraphy.« less

In 1971, gated equilibrium radionuclide angiocardiography was developed [1, 2] and in the following year, an alternative technique, first-pass radionuclide angiocardiography was described [3]. Since their introduction ten years ago, these two radionuclide techniques for assessment of cardiac function have undergone substantial technical development and have progressed from the investigational stage to that of clinical application. Both techniques have advantages and limitations. In many instances, the approaches are complementary, and both can and should be performed in an individual patient. The decision as to which technique to utilize and when to combine them should be based upon available instrumentation, clinical setting, and type of patient being studied. In general, these nuclear studies provide important physiologic insights into both right and left ventricular function. They require only intravenous injection of minimal amounts of radioactive tracers, which do not perturb hemodynamics or other aspects of human physiology. Indices of global and regional left and right ventricular performance have been developed, providing a means of characterizing cardiac pump function under a number of conditions [4].

Right ventricular myocardial infarction has been reported to occur exclusively in association with inferlor left ventricular infarction. To determine the frequency of right ventricular myocardial infarction in association with anterior left ventricular myocardial infarction, all hearts with anterior myocardial infarction studied over a 3-year period were examined for evidence of right ventricular necrosis or scar. Of 97 hearts with anterior myocardial infarction, 13 (13%) had anterior right ventricular myocardial infarction. The right ventricular infarcts involved from 10% to 50% (mean 28%) of the circumference of the right ventricular free wall from base to apex. The associated left ventricular infarcts were all anteroseptal and large and involved from 36% to 67% (mean 50%) of the total area of the left ventricular free wall and septum. Nine of the 13 patients underwent equillbrium radionuclide angiography and six had demonstrable right ventricular regional and global dysfunction. Thus, right ventricular myocardial infarction does occur with anterior wall left ventricular infarction, and right ventricular dysfunction may be demonstrable by radionuclide angiography. Further investigation is needed to define the hemodynamic characteristics, clinical importance, and therapeutic implications of anterior right ventricular myocardial infarction.

The noninvasive measurement of left ventricular filling has relied predominantly on radionuclide-derived peak filling rate normalized to end-diastolic volume. Doppler echocardiography also has the ability to measure peak filling rate, but wide application of this technique has been limited by technical errors involved in quantitative echocardiographic determination of mitral anulus cross-sectional area and ventricular volumes. For Doppler echocardiography, normalization of peak filling rate to mitral stroke volume rather than end-diastolic volume permits the derivation of a diastolic filling index that is relatively free of errors caused by geometric assumptions, diameter measurements and sample volume positioning. This normalization process can be achieved by simply dividing early peak filling velocity by the time velocity integral of mitral inflov. To validate this new Doppler echocardiographic filling index, Doppler echocardiographic and radionuclide-derived peak filling rate, both normalized to mitral stroke volume, were compared in 30 patients; there was an excellent correlation (r = 0.91, SEE = 0.88). This variable was not influenced by the position of the sample volume in relation to the mitral apparatus in contrast to early filling velocity, which increased 37%, and early/late filling (E/A) ratio, which increased 43% as the sample volume was moved from the anulus to the tips of the mitral leaflets. In a cohort of 22 normal patients, the mean peak filling rate normalized to mitral stroke volume (SV) was 5.25 ± 1.47 SV/s. The mean peak filling rate for a subgroup of eight normal patients aged 57 to 89 years (mean 71 ± 9) was 3.9 ± 1 SV/s. In conclusion, normalization of peak filling rate to mitral stroke volume minimizes technical errors involved in measuring Doppler echocardiographic peak filling rate in the same fashion that normalization to end-diastolic volume minimizes technical errors involved in radionuclide angiographic measurement of peak filling rate. For this reason, peak filling rate normalized to mitral stroke volume may provide a more reliable and reproducible method for assessing left ventricular filling. Further studies are required to assess the clinical relevance of this new index.

Before commencing the randomized Thrombolysis in Myocardial Infarction phase II (TIMI II) study, 370 patients were administered intravenous recombinant tissue plasminogen activator (rt-PA) within 4 hours of onset of acute myocardial infarction (AMI) and assigned to 2-hour (immediate) percutaneous transluminal angioplasty (n = 33), 18- to 48-hour (delayed) angioplasty (n = 288) or no angioplasty (n = 49) in a nonrandomized, observational pilot study. Left ventricular ejection fraction at rest and during exercise was assessed by gated equilibrium radionuclide ventriculography at hospital discharge and again at 6 weeks. At hospital discharge, ejection fraction averaged 50% at rest and 56% at peak exercise. At 6-week follow-up, ejection fraction averaged 50% at rest and 53% at peak exercise. At 6-week follow-up, resting ejection fraction averaged 49% in the 2-hour angioplasty group, 49% in the 18- to 48-hour angioplasty group and 55% in the no-angioplasty group. Variables independently predicting “good functional outcome” at 6-week follow-up (survival with resting ejection fraction ≥50% and no decrease with exercise) in the 18- to 48-hour angioplasty group were fewer leads with ST-segment elevation ≥0.1 mV, younger age, rapid normalization during rt-PA infusion of ST segments or dramatic relief of chest pain, absence of arrhythmias within the first 24 hours of treatment initiation, no prior infarction and not a cigarette smoker at entry. Thus, the TIMI II pilot study demonstrates that most patients with AMI of ≤4-hour duration treated with rt-PA have good ventricular function after AMI. Although nonrandom group assignment prevented rigorous statistical comparison of the 3 treatment groups, no obvious disadvantage of the more conservative noangioplasty assignment was apparent.

While previous studies have demonstrated that sequential radionuclide angiocardiography allows identification of patients at risk for development of congestive heart failure and prediction of the appropriate time for safe discontinuation of doxorubicin, these studies were based predominantly on patients with normal baseline left ventricular performance. This study addresses the use of doxorubicin in patients with abnormal left ventricular ejection fraction (less than 55%) prior to drug administration. Of 337 patients referred for evaluation of left ventricular performance prior to doxorubicin therapy during a 36-month period, 45 (13%) had abnormal baseline left ventricular performance determined by first-pass radionuclide angiocardiography. Sixteen patients had antecedent cardiovascular disease, and 16 patients had received thoracic radiation, while only four patients had both. Left ventricular ejection fraction in each of these subgroups was comparable. In 7 of 16 patients who only had a baseline determination of left ventricular function, doxorubicin was not administered because of a significant concern for the potential risk of doxorubicin cardiotoxicity. In the group of 29 patients followed sequentially over 3 to 15 months (mean, 6 months), there was no significant difference between baseline and final left ventricular ejection fraction (48 +/- 5 vs 47 +/- 9%, p = NS). Only in the 12 patients who received greater than or equal to 350 mg/m2 cumulative dose was there a small but significant fall in left ventricular ejection fraction (48 +/- 4 vs 43 +/- 8%, p less than 0.05). Only one patient developed congestive heart failure. This study demonstrates that doxorubicin can be administered safely to patients with abnormal baseline left ventricular performance using serial radionuclide studies as a means of monitoring therapy. Guidelines for doxorubicin therapy in these patients have been developed.

Left ventricular performance was evaluated at rest and during maximal upright bicycle exercise in 51 patients with chronic essential hypertension. Twenty-eight of these patients had no clinical or electrocardiographic evidence of coronary artery disease and comprise the primary study population. The remaining 23 patients had coronary artery disease and represent a comparison group. First-pass radionuclide angiocardiograms were obtained at rest and during maximal upright bicycle exercise, allowing evaluation of global left ventricular ejection fraction and regional wall motion. At the time of the radionuclide studies, all patients were hypertensive, defined as a diastolic blood pressure 90 mm Hg or greater and/or a systolic blood pressure 140 mm Hg or greater with the patient at rest and sitting. In the primary study group, the left ventricular functional response to upright bicycle exercise was normal in 26 of 28 patients. Left ventricular ejection fraction averaged (+/- standard error) 65 +/- 2 percent at rest and increased significantly to 76 +/- 2 percent with exercise (p less than 0.001). Regional wall motion was normal both at rest and during exercise in all patients. Seventeen patients had electrocardiographic evidence of left ventricular hypertrophy, and 14 were receiving propranolol therapy. The left ventricular functional response also was normal in these subgroups. In contrast to the nearly uniform normal left ventricular responses noted in the patients with hypertension alone, the group with concomitant coronary artery disease had a markedly higher incidence of abnormal left ventricular reserve (19 of 23 versus two of 28, p less than 0.001) during exercise. Thus, in most patients with essential hypertension but without concomitant coronary artery disease, left ventricular reserve during exercise was normal. Hypertension, even with left ventricular hypertrophy, should not be viewed as the cause for an abnormal left ventricular response to exercise in a patient undergoing diagnostic exercise radionuclide angiocardiography.

The feasibility of performing rapid sequential first pass radionuclide angiocardiography using a new short-lived radiotracer, gold-195m (195mAu) half-life 30.5 seconds) was evaluated. This radionuclide emits a 262 keV gamma ray and is the daughter of mercury-195 (195mHg) (half-life 41.6 hours). The prototype tabletop 195mHg/195mAu generator produced 20 to 25 mCi of 195mAu in 2 ml of eluate (yield of 40 percent). The breakthrough of 195mHg in the eluate was 0.02 percent of the amount of 195mHg in the generator. The eluate contained 20 microCi of 195mHg per study, resulting in an estimated human radiation dose of 0.007 rad/study to the whole body and 0.34 rad/study to the kidney. Four dogs each had 15 to 20 sequential first pass studies performed with 195mHg at 3 to 10 minute intervals using a computerized multicrystal gamma camera. During the left ventricular phase, 160,000 to 190,000 counts/s were acquired. The end-diastolic left ventricular region of interest contained 3,000 to 6,000 counts (background- and decay-corrected). Multiple reproducible values for left ventricular ejection fraction were obtained during stable conditions. The mean (+/- standard deviation) interstudy variability was 4 +/- 2 percent. During infusion of isoproterenol, rapid increase of left ventricular ejection fraction was demonstrated. Excellent agreement was observed between studies performed with technetium-99m diethylenetriaminepentaacetic acid (99mTc-DTPA) and 195mAu. The mean interstudy difference was 4 +/- 3 percent. Thus, sufficiently high yield and dose are obtained from the 195mHg/195mAu generator for reliable high count rate first pass determination of left ventricular ejection fraction. This new short-lived radiotracer makes possible rapid sequential assessments of ventricular function at greatly reduced patient exposure to radiation.

Using a combined hemodynamic and radionuclide technique, 20 patients with varied ventricular function were evaluated during positive end-expiratory pressure (PEEP) application. Left ventricular (LV) and right ventricular (RV) ejection fractions and cardiac output were measured, and ventricular volumes were derived. Seven patients (group 1) who had an increase in LV end-diastolic volume with PEEP and 13 patients (group 2) who had the more typical response, a decrease in LV end-diastolic volume with PEEP, were identified. Compared with group 2, group 1 patients had a higher incidence of coronary artery disease (5 of 7 vs 1 of 13, p less than 0.005) and lower cardiac output (3.9 +/- 1.6 vs 9.1 +/- 3.2 liters/min, p less than 0.005), LV ejection fraction (27 +/- 13 vs 51 +/- 21%, p less than 0.05), RV ejection fraction (15 +/- 6 vs 32 +/- 8%, p less than 0.005) and peak filling rate (1.32 +/- 0.43 vs 3.51 +/- 1.70 end-diastolic volumes/s, p less than 0.05). LV and RV volumes increased and peak filling rate decreased with PEEP in group 1, whereas in group 2 LV volume decreased and RV volume and peak filling rate remained unchanged. Using stepwise regression analysis, the change in LV volume with PEEP was related directly to baseline systemic vascular resistance and inversely to baseline blood pressure. Similarly, the change in peak filling rate with PEEP was inversely related to the change in RV end-diastolic volume. Thus, the hemodynamic response to PEEP is heterogeneous and may be related to LV ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)

We studied the temporal effects of various types of mental stress and physical exercise on the left ventricular ejection fraction (LVEF) in seven normal volunteers and nine patients with coronary artery disease. Three types of psychological stress were administered: mental arithmetic, the Stroop color word test, and a personally relevant speaking task. In the normal volunteers the LVEF response was either flat or increased (p less than 0.05) compared to the baseline value during the mental tasks and increased by a mean of 10 +/- 5% (p less than 0.05) during exercise. In contrast, in patients with coronary disease in whom LVEF did not increase greater than or equal to 5% during exercise, LVEF decreased significantly during the mental tasks (p less than 0.05 for arithmetic and Stroop tasks). Typically LVEF decreased quickly during mental stress with an immediate rebound after intervention. Decreases in LVEF during mental stress occurred without chest pain and were not associated with ECG changes. In patients with coronary disease in whom LVEF increased normally with exercise (LVEF increase greater than or equal to 5%), no significant changes in LVEF occurred during mental stress. The heart rate x systolic blood pressure double product during mental stress was significantly less than that achieved during exercise (p less than 0.05) in each normal subject and patient. Thus psychological stress can provoke acute decreases in LVEF in patients with coronary disease and exercise-inducible dysfunction. The silent nature of the mental stress-induced abnormalities and their occurrence at a lower physiologic workload compared to abnormalities during exercise parallel characteristics of transient ischemia noted during ambulatory monitoring.(ABSTRACT TRUNCATED AT 250 WORDS)

There is wide beat-to-beat variability in cycle length and left ventricular performance in patients with atrial fibrillation. In this study, left ventricular ejection fraction and relative left ventricular volumes were evaluated on a beat-to-beat basis with the computerized nuclear probe, an instrument with sufficiently high sensitivity to allow continuous evaluation of the radionuclide time-activity curve. Of 18 patients with atrial fibrillation, 5 had mitral stenosis, 6 had mitral regurgitation, and 7 had coronary artery disease. Fifty consecutive beats were analyzed in each patient. The mean left ventricular ejection fraction ranged from 17 to 51%. There was substantial beat-to-beat variation in cycle length and left ventricular ejection fraction in all patients, including those with marked left ventricular dysfunction. In 14 patients who also underwent multiple gated cardiac blood pool imaging, there was an excellent correlation between mean ejection fraction derived from the nuclear probe and gated ejection fraction obtained by gamma camera imaging (r = 0.90). Based on beat-to-beat analysis, left ventricular function was dependent on relative end-diastolic volume and multiple preceding cycle lengths, but not preceding end-systolic volumes. This study demonstrates that a single value for left ventricular ejection fraction does not adequately characterize left ventricular function in patients with atrial fibrillation. Furthermore, both the mean beat-to-beat and the gated ejection fraction may underestimate left ventricular performance at rest in such patients.

G OALS common to both the clinical and investigative study of coronary heart disease concern accurate detection and definition of the site and extent of acute myocardial infarction, myocardial scar, and reversible myocardial ischemia. Radionuclide myocardial imaging techniques offer the possibility of ultimately fulfilling at least a portion of these goals. The increasing prevalence of the various myocardial imaging approaches over the past 5 yr has been due in part to major advances in instrumentation, development of new radiopharmaceuticals, and application of computer technology to standard clinical nuclear imaging. Early recognition of the association between acute myocardial ischemia and infarction and abnormality in regional potassium metabolism led to investigation of the possibility of utilizing radioactive potassium or radioactive potassium analogs to define abnormalities in the diseased atherosclerotic heart. When these radioactive cations are administered intravenously, sufficient myocardial uptake occurs to allow external detection or imaging of a myocardial radioactivity distribution. This distribution displays zones of infarction or ischemia as “cold spots,” or regions of relatively decreased to

An obvious application of the rest-and-exercise myocardial-imaging approach would be the study of patients having undergone aortocoronary bypass surgery. The recent introduction of this surgical modality has significantly altered the therapeutic approach toward patients with coronary heart disease. Coronary revascularization procedures are now being performed in patients representing the entire spectrum of coronary disease, ranging from the situation of minimally symptomatic angina pectoris to cardiogenic shock. However, postoperative subjective improvement may not, in all cases, be due to increased myocardial perfusion. Reduction or elimination of symptoms in the individual patient may also result from perioperative infarction of ischemic muscle, partial denervation, or placebo effect. On the other hand, symptoms may persist in the presence of entirely patent bypass grafts. Dispute currently rages as to whether the procedure, even in the face of symptomatic improvement, will have a long-term effect on patient survival and prognosis. Definitive objective evaluation of the postoperative patient has required cardiac catheterization and contrast angiography, which by their very nature are limited in terms of sequential study. For this reason, a noninvasive means of evaluating graft patency and myocardial viability would have definite clinical and investigative value. To this end, we have applied rest and exercise 43K and 81Rb myocardial imaging to the study of the postoperative patient.

We evaluated the pathophysiologic correlates of right ventricular (RV) thallium-201 (/sup 201/Tl) visualization in three canine models: (1) acute RV pressure overload (RVPO) induced by acute constriction of the pulmonary artery; (2) acute RV volume overload (RVVO) induced by acute left-to-right atrial shunt; and (3) RV hypetrophy (RVH) induced by chronic constriction of the pulmonary artery. Thallium-201 myocardial images, RV and left ventricular (LV) /sup 201/Tl tissue accumulation and RV and LV myocardial blood flow (MBF) were compared with control measurements. In control dogs, the right ventricle was not visualized. In dogs with RVPO, RVVO, and RVH, the right ventricle was clearly visualized. In RVPO, and to a lesser degree in RVVO, RV/LV /sup 201/Tl uptake per gram tissue and RV/LV MBF per gram tissue were increased significantly compared with control, whereas in RVH, these values were not significantly different from control. However, total RV/LV /sup 201/Tl tissue uptake and total RV/LV MBF (RV/LV MBF x RV/LV mass) were not significantly different in RVPO and RVH, consistent with the similar degree of RV visualization on /sup 201/Tl images. Total RV/LV /sup 201/Tl tissue uptake correlated well with the degree of RVH (r = 0.91). However, quantitative analysis of computerized /supmore » 201/Tl images correlated less well (r = 0.77) with the degree of RVH. We conclude that RV visualization at rest in /sup 201/Tl images does not necessarily indicate RVH, but may be due to acutely increased RV work load. In acute RVPO, RV visualization is predominantly due to a marked increase of RV MBF per unit tissue, whereas in RVH this is predominantly due to an increase of RV mass.« less

Fifty-seven patients with acute myocardial infarction were observed for early postmyocardial infarction angina and associated transient ST-segment changes. Nine patients had postinfarction angina with transient ST-segment elevation (Group 1), seventeen patients had postinfarction angina with ST-segment depression or no ST-segment changes (Group 2), and 31 patients had no postinfarction angina (Group 3). The patients in Group 1 had a statistically significant increased incidence of early reinfarction and death, when compared with the other two groups, singly or combined. There was no significant difference in the incidence of reinfarction and death when Group 2 is compared with Group 3. Patients with transient ST-segment elevation associated with early postmyocardial infarction angina may be an appropriate group in whom to consider newer, more aggressive modes of postinfarction management.

Technetium-99m stannous pyrophosphate (99mTc-PYP) cardiac scintigraphy was performed in 15 rabbits with experimental Streptococcus sanguis aortic valve infective endocarditis. The animals were imaged five to seven days after the administration of bacteria, and in each case abnormal accumulation of the tracer was visualized in the region of the aortic valve. Three types of cardiac scintigraphic patterns were demonstrated: focal, multifocal and extensive, each correlating well with the anatomical extent of the lesion as defined by gross pathology. Tissue distribution studies demonstrated a 30 +/- 5.3 (mean +/- SEM) fold excess of radionuclide uptake in the infective endocarditis lesion compared with that of normal myocardium. Imaging of excised hearts from four animals showed an excellent correlation with in vivo imaging as well as gross pathology. Five animals with nonbacterial thrombotic aortic valve endocarditis demonstrated similar scintigraphic and tissue distribution results. In contrast, four normal animals failed to demonstrate abnormal 99mTc-PYP cardiac scintigrams or tissue uptake. This study demonstrates that 99mTc-PYP cardiac scintigraphy is a sensitive technique to detect experimental aortic valve endocarditis.

Hemodynamic and angiographic observations are described in an adult patient with the contracted form of endocardial fibroelastosis. Of note were the findings of elevated diastolic pressures in the left and right side of the heart, decreased left ventricular compliance, mitral regurgitation and distortion of the usual left and right ventricular angiographic anatomy, presenting a picture indistinguishable from mat of a primary cardiac neoplasm. These findings are related to those described in children.

First-pass radionuclide angiocardiography allows noninvasive determination of right and left ventricular performance from a single study. Analysis is made from the high frequency components of the regional radionuclide time-activity curves. Both regional and global ventricular performance can be assessed at rest and during exercise. Sequential studies can be performed to evaluate therapeutic interventions. This technique has been applied in a broad spectrum of patients with cardiac and pulmonary disease and has been shown to have major clinical impact.

Although myocardial imaging with 43K and the rectilinear scanner has been shown to evaluate regional myocardial perfusion reliably, attempts to duplicate these results using a gamma camera have not been satisfactory, primarily due to collimator penetration by higher-energy gamma rays. Satisfactory images were obtained when the pinhole collimator was fitted with a small insert and additional lead shielding was placed between the collimator and the patient.

In 1909 Pleschl described an indirect method for measuring mixed venous carbon dioxide tension (\(P\bar{v}\) CO2). Application of this technique led to the development of non-invasive determination of cardiac output (CO) by carbon dioxide rebreathing (CO2RB). Clinical utilization of this method, however, has been limited because of technical considerations: expired gas must be collected and analyzed; and various calculations, including correction formulas, are necessary2,3.

The spontaneous changes in left ventricular ejection fraction (LVEF) during the first 24 hours of a first transmural infarction were assessed in 34 patients by serial gated cardiac blood pool imaging. Major therapeutic interventions with a view to limit infarct size were not used. Four determinations of LVEF were performed. Study 1 was performed as soon as possible after admission to the hospital. Studies 2 and 3 were performed 2 and 4 hours, respectively, after study 1. Twenty-four patients (70%) had study 1 within 6 hours after the onset of acute chest pain and 10 had it 6-12 hours after the onset of chest pain. Study 4 was performed 24 hours after the onset of chest pain. Compared with study 1, 19 of 34 patients (56%) had spontaneous changes in LVEF in at least one of the subsequent studies, exceeding the expected variability in stable patients. The changes ranged from a 32% increase to 14% absolute decrease. LVEF improved in 11 patients and deteriorated in eight. These spontaneous changes in left ventricular performance indicate that a single assessment of LVEF during the early hours of transmural myocardial infarction may not properly characterize cardiac performance in an individual patient and may not be the most appropriate reference against which to compare subsequent evolution of left ventricular function. These data may have implications for studies of the effects of early therapeutic interventions on LVEF.

The effect of incremental dosages of oral propranolol (mean peak dose of 165 +/- 13 mg/day) of left ventricular ejection fraction, ejection rate and regional wall motion was studied sequentially in 22 stable, resting patients with coronary artery disease using a geometry-independent first-pass radionuclide angiocardiographic technique. All patients improved clinically, in association with a fall in heart rate and therapeutic serum propranolol levels. No significant changes were noted in ejection fraction, ejection rate or regional wall motion. No patient developed a new regional wall motion disturbance. Thus, oral propranolol administered at clinically effective antianginal dosages in patients with stable coronary artery disease does not appear to have significant deleterious effects on resting left ventricular performance.

Changes in the capacitance vasculature influence venous return and cardiac performance, so an understanding of the effects of pathophysiologic states on the human capacitance vasculature is necessary to understand integrated cardiovascular function in man. Techniques available to assess the capacitance vasculature in man, however, have limitations. We performed radionuclide imaging of the calf or forearm in 51 patients whose erythrocytes had been labeled in vivo with technetium-99m, basing our approach on the principle that counts from the radiolabeled intravascular space are proportional to blood volume. Two-minute or 15 second count acquisitions were obtained from the calf in 42 patients. Counts obtained at rest demonstrated little variation. With veno-occlusion at 15 and 30 mm Hg, counts increased 8 +/- 1% (+/- SEM) (p less than 0.001) and 28 +/- 2% (p less than 0.001), respectively. After 0.4 mg of sublingual nitroglycerin, counts increased 9 +/- 1% (p less than 0.001). With leg elevation, counts decreased 34 +/- 4% (p less than 0.001). Response patterns were similar with 2-minute and 15-second acquisitions. In nine patients who underwent forearm imaging (2-minute acquisitions), counts increased 14 +/- 2% (p less than 0.001) and 26 +/- 4% (p less than 0.001) at 15- and 30-mm Hg veno-occlusion and 15 +/- 3% (p less than 0.001) after nitroglycerin. Volume displacements, recorded simultaneously with a fluid-filled plethysmograph about the contralateral forearm, correlated linearly in all nine patients. Thus, gamma camera imaging of the radiolabeled peripheral intravascular space provides a quantitative and reliable assessment of peripheral vascular capacity in man. The technique could be used in conjunction with gated cardiac imaging in order to assess the interactions of peripheral vascular capacity and ventricular performance.

Right and left ventricular pump performance was assessed at rest and during upright bicycle exercise in 30 patients with chronic obstructive pulmonary disease and in 25 normal control subjects. Right ventricular and left ventricular ejection fractions were ascertained noninvasively using first-pass quantitative radionuclide angiocardiography. The normal ventricular response to exercise was at least a 5% absolute increase in the ejection fraction of either ventricle. In patients the predominant cardiac abnormality involved performance of the right ventricle. Right ventricular ejection fraction was abnormal at rest in eight patients. Twenty-three patients demonstrated an abnormal right ventricular response to submaximal exercise. Airway obstruction and arterial hypoxemia were significantly more severe in patients with abnormal right ventricular exercise reserve than in those with normal reserve. Abnormal left ventricular performance was infrequent either at rest (four patients) or during exercise (six patients). Thus, this radionuclide technique allows noninvasive assessment of biventricular exercise reserve in chronic obstructive pulmonary disease.