Experimental infarct sizing using computer processing and a three-dimensional model.

A method for noninvasive sizing of myocardial infarction, in which data from technetium-99m stannous pyrophosphate scintigrams and a three-dimensional model were used, was tested on experimental, acute anterior infarcts in dogs. The results indicate that the method does size experimental anterior infarcts accurately, but further testing will be necessary to assess the capabilities of the technique for sizing other types of infarcts.

Pathophysiology of technetium-99m stannous pyrophosphate and thallium-201 scintigraphy of acute anterior myocardial infarcts in dogs.

In 17 dogs with acute myocardial infarcts produced by ligation of the proximal left anterior descending coronary artery, a comparative study was made of myocardial scintigrams obtained with technetium-99m stannous pyrophosphate (99mTc-PYP) and thallium-201 (201T1), tissue levels of 99mTc-PYP and 201T1 uptake, histopathologic alterations, and regional myocardial perfusion measured with radioactive microspheres. 9 of the 10 hearts examined histologically had transmural infarcts with outer peripheral, inner peripheral, and central zones characterized by distinctive histopathologic features. A progressive reduction in myocardial blood flow was demonstrated between normal myocardium and the centers of the infarcts, and correlated well with progressive reduction in 201T1 upatke in the same regions. Marked 99mTc-PYP concentration occurred in areas with partial to homogeneous myocardial necrosis and residual perfusion located in the outer peripheral regions of the infarcts. The latter areas also were characterized by the presence of muscle cell calcification. The patterns of distribution of 99mTc-PYP and 201T1 explained the filling defects on 201T1 myocardial scintigrams and the doughnut patterns on 99mTc-PYP myocardial scintigrams in dogs with transmural infarcts. One dog with a subendocardial infarct had a small homogeneous area of activity on the 99mTc-PYP myocardial scintigram, and showed marked uptake of 99mTc-PYP in subendocardial areas of extensive necrosis and calcification still receiving some coronary perfusion. Thus, the data indicate that the status of regional myocardial perfusion is a key determinant for the occurrence of distinctive patterns of myocardial necrosis and for the scintigraphic detection of acute myocardial infarcts with 99mTc-PYP and 201T1.

Sites and mechanisms of localization of technetium-99m phosphorus radiopharmaceuticals in acute myocardial infarcts and other tissues.

This study was performed to elucidate the localization at the cellular level of technetium-99m phosphorus ((99m)Tc-P) radiopharmaceuticals in acute myocardial infarcts and the mechanisms responsible for (99m)Tc-P uptake in acute myocardial infarcts and other tissues. In 20 dogs with proximal left anterior descending coronary arterial ligation for 1-3 days, elevated calcium levels were measured at all sites of increased (99m)Tc-P uptake (acute myocardial infarcts, necrotic thoracotomy muscle, lactating breast, and normal bone); however, a consistent linear relationship between (99m)Tc-P and calcium levels was not observed. A strong correlation (r = 0.95 and 0.99, n = 2 dogs) was demonstrated between levels of (3)H-diphosphonate and (99m)Tc-P in infarcted myocardium. Autoradiographic studies with (3)H-diphosphonate revealed extensive labeling in the infarct periphery which contained necrotic muscle cells with features of severe calcium overloading, including widespread hypercontraction as well as more selective formation of mitochondrial calcific deposits. Autoradiography also demonstrated labeling of a small population of damaged border zone muscle cells which exhibited prominent accumulation of lipid droplets and focal, early mitochondrial calcification. Cell fractionation studies revealed major localization of both (99m)Tc-P and calcium in the soluble supernate and membrane-debris fractions of infarcted myocardium and less than 2% of total (99m)Tc-P and calcium in the mitochondrial fractions; however, electron microscopic examination showed that mitochondria with calcific deposits were not preserved in the mitochondrial fractions. In vitro studies evaluating the role of serum protein binding on tissue uptake of (99m)Tc-P agents demonstrated that, in spite of significant complexing with serum proteins, serum (99m)Tc-P activity retained the ability to adsorp to calcium hydroxyapatite and amorphous calcium phosphate. In vivo studies showed that concentration of human serum albumin (labeled with iodine-131) in infarcted myocardium reached a maximum of only 3.8 times normal after a circulation time of 96 h, whereas (99m)Tc-P uptake was at least 10 times normal after a circulation time as short as 1 h. It is concluded that: (a) (99m)Tc-P uptake in acutely infarcted myocardium, and possibly other types of soft tissue damage, is limited to necrotic and severely injured cells; (b) concentration of (99m)Tc-P results from selective adsorption of (99m)Tc-P with various forms of tissue calcium stores, including amorphous calcium phosphate, crystalline hydroxyapatite, and calcium complexed with myofibrils and other macromolecules, possibly supplemented by calcium-independent complexing with organic macromolecules; and (c) lack of a linear relationship between (99m)Tc-P and tissue calcium levels mainly results from local differences in composition and physicochemical properties of tissue calcium stores and from local variations in levels of blood flow for delivery of (99m)Tc-P agents.

Nuclear magnetic resonance imaging in Marfan's syndrome.

Detection and evaluation of aortic root and other cardiovascular abnormalities in patients with Marfan's syndrome are important in determining appropriate therapy and preventing premature mortality. To evaluate the role of nuclear magnetic resonance imaging (NMR) in this syndrome, 10 patients were evaluated using a 0.35 tesla commercial nuclear magnetic resonance imaging system. Findings from these studies were compared with data from other noninvasive tests as well as surgical follow-up. Results from these examinations indicate that NMR-derived measurements of aortic root diameter agree closely with echocardiographic measurements. In addition, NMR provides more complete anatomic detail than does echocardiography and can be utilized to assess and follow up virtually all patients with this syndrome.

Gadolinium-DTPA-enhanced nuclear magnetic resonance imaging of reperfused myocardium: identification of the myocardial bed at risk.

Gadolinium-diethylenetriamine pentaacetic acid (Gd-DTPA)-enhanced nuclear magnetic resonance (NMR) imaging can be useful in the identification of reperfused myocardium. However, the effects of dose and the time of administration and the relation of the extent of the region of enhancement to the myocardial bed at risk have not been evaluated. In this study, dogs were given Gd-DTPA (0.1 mM/kg body weight [n = 21] or 0.34 mM/kg [n = 7]) or saline solution (n = 5) after various periods of occlusion and reperfusion. Twenty-five dogs were killed after 1 or 2 h of reperfusion and the excised hearts were imaged. Images were analyzed for presence, intensity and extent of a region of increased signal. All images in dogs given Gd-DTPA had easily identifiable regions of increased signal in the distribution of the reperfused myocardial bed. Analysis of the extent of these regions in spin-echo images of excised hearts when Gd-DTPA was administered after 5 min of reperfusion demonstrated a correlation coefficient of 0.72 with the bed at risk as determined postmortem with a dye perfusion technique. These images consistently overestimated the infarct size. Signal intensity of the reperfused myocardium increased to a maximum of 1.67 times control (p less than 0.05) in spin-lattice relaxation time (T1)-weighted sequences as the dose of Gd-DTPA increased. This was due to a higher concentration of Gd-DTPA in the reperfused myocardium with resultant shortening of the T1 relaxation time. When Gd-DTPA was given after 90 min of reperfusion, NMR images did not identify the bed at risk.(ABSTRACT TRUNCATED AT 250 WORDS)

Iodine-123 phenylpentadecanoic acid and single photon emission computed tomography in identifying left ventricular regional metabolic abnormalities in patients with coronary heart disease: comparison with thallium-201 myocardial tomography.

Iodine-123 phenylpentadecanoic acid (IPPA) is a synthetic long chain fatty acid with myocardial kinetics similar to palmitate. Two hypotheses were tested in this study. The first hypothesis was that IPPA imaging with single photon emission computed tomography (SPECT) is useful in the identification of patients with coronary artery disease. Fourteen normal volunteers (aged 27 +/- 2 years) and 33 patients (aged 54 +/- 11 years) with stable symptomatic coronary artery disease and at least one major coronary artery with luminal diameter narrowing greater than or equal to 70% were studied with symptom-limited maximal exercise testing. The IPPA (6 to 8 mCi) was injected 1 min before the termination of exercise, and tomographic imaging was performed beginning at 9 min and repeated at 40 min after the injection of IPPA. Nine of the normal volunteers and 13 of the patients had a second examination performed at rest on another day. Using the limits of normal as 2 SD from the normal mean values, 27 of the 33 patients with coronary artery disease demonstrated abnormalities in either the initial distribution or the clearance of IPPA, or both. Nineteen of the 33 patients had a maximal variation of activity distribution of greater than or equal to 25% on the 9 min IPPA images. Twenty-two of the 33 patients had a maximal variation in IPPA washout greater than 17% and 17 had a washout rate less than or equal to 2%. There was good agreement between the location of significant coronary artery stenoses and abnormalities in the initial distribution and clearance of IPPA. The second hypothesis tested was that IPPA imaging is as or more sensitive and, therefore, complementary to thallium-201 imaging in the identification of exercise-induced ischemia in patients. Twenty-five of the 33 patients underwent both thallium-201 and IPPA tomographic imaging after symptom-limited maximal exercise testing. The amount of exercise performed by each patient during both studies was similar. Twenty-one of the 25 patients had abnormal IPPA tomographic studies, whereas 18 had abnormal thallium-201 tomographic studies (p = NS). The results of this study suggest the following conclusions: 1) iodine-123 phenylpentadecanoic acid imaging using single photon emission computed tomography and exercise provides a sensitive and relatively noninvasive method for identifying abnormalities in myocardial metabolism associated with significant coronary artery stenoses, and 2) iodine-123 phenylpentadecanoic acid is at least as sensitive as thallium-201 for this purpose using tomographic imaging and exercise testing.

In vivo nuclear magnetic resonance imaging of myocardial perfusion using the paramagnetic contrast agent manganese gluconate.

Previous nuclear magnetic resonance (NMR) imaging studies have indicated that coronary occlusion does not produce sufficient changes in standard tissue relaxation times to allow the detection of acute ischemia. To identify acute myocardial perfusion abnormalities, the use of the paramagnetic agent manganese gluconate combined with calcium gluconate (MnGlu/CaGlu) was investigated in canine models of acute coronary artery occlusion. In vitro studies showed that MnGlu/CaGlu was a more efficient relaxing agent than gadolinium-DTPA (relaxivity of 7.8 versus 5.1 s-1 mM-1) and demonstrated affinity for normal myocardium. The distribution of MnGlu/CaGlu as measured by manganese-54 tracer studies was proportional to myocardial blood flow in both normal and ischemic tissue. Hearts excised from dogs after coronary artery occlusion and administration of 0.035 mM/kg MnGlu/CaGlu were imaged ex vivo using a relatively spin-lattice relaxation time (T1)-weighted gradient reversal technique (repetition time [TR] 50 ms and echo time [TE] 9 ms). These images showed increased signal intensity in the normally perfused myocardium with a mean signal intensity ratio of hypoperfused to normal myocardium of 0.55 +/- 0.12 (mean +/- SD). In vivo images obtained in nine dogs after coronary artery occlusion and administration of the same dose of MnGlu/CaGlu demonstrated the region of hypoperfused myocardium in six dogs with a signal intensity ratio of hypoperfused to normal myocardium of 0.64 +/- 0.23 (p less than 0.05 versus control). When a higher dose of 0.1 mM/kg MnGlu/CaGlu was utilized and in vivo imaging was performed using a relatively spin-spin relaxation time (T2)-weighted (TR gated, TE 60 ms) spin-echo sequence in six dogs, the signal intensity of normal myocardium was decreased.(ABSTRACT TRUNCATED AT 250 WORDS)

Assessment of myocardial systolic wall thickening using nuclear magnetic resonance imaging.

A quantitative nuclear magnetic resonance (NMR) imaging method of evaluating regional left ventricular function was compared with histochemical evidence of infarction in dogs and functional measurements in patients. Short-axis images of the heart were obtained at end-diastole and at 100 ms intervals thereafter. Regional diastolic left ventricular wall thickness and maximal percent systolic wall thickening were measured at the level of the papillary muscles in each of six segments. In six normal dogs, the mean end-diastolic wall thickness was 9 +/- 1.6 mm, and the mean maximal percent thickening was 61 +/- 11%. In eight dogs with a 4 day old infarct, maximal percent thickening was 5 +/- 8% (p less than 0.001) in the infarcted segments. In 10 normal human volunteers, the mean end-diastolic wall thickness was 10.1 +/- 1 mm, and the mean maximal percent systolic wall thickening was 60 +/- 18%. Reduced maximal percent systolic wall thickening was defined as a value greater than or equal to 2 SD below the mean value obtained in normal volunteers. Seven patients with regional wall motion abnormalities were independently assessed by NMR imaging and biplane ventriculography. With a sensitivity of 94% and a specificity of 80%, NMR imaging demonstrated reduced maximal percent systolic wall thickening in the same segments identified as akinetic or dyskinetic by biplane ventriculography. Thus, abnormalities of regional systolic wall thickening are accurately identified with this quantitative imaging technique.

Measurement of myocardial infarction fraction using single photon emission computed tomography.

Although infarct size correlates generally with prognosis after acute myocardial infarction, an absolute measure of infarct size may have differing prognostic significance depending on absolute left ventricular mass. To test the hypothesis that single photon emission computed tomography can accurately measure myocardial infarct size as a percent of total left ventricular mass ("infarction fraction"), thallium-201 and technetium-99m pyrophosphate tomograms were acquired in 21 dogs 24 to 48 hours after fixed occlusion of the left anterior descending or circumflex coronary artery. Pathologic infarct weight was measured as the myocardial mass that showed no staining with triphenyltetrazolium chloride. Scintigraphic infarct mass by technetium-99m pyrophosphate was calculated from the total number of left ventricular volume elements (voxels) demonstrating technetium-99m pyrophosphate uptake X voxel dimension [( 0.476 cm]3) X specific gravity of myocardium (1.05 g/cm3). Scintigraphic left ventricular mass was calculated in a similar fashion using an overlay of the thallium-201 and technetium-99m pyrophosphate scans. The "infarction fraction" was calculated as: infarction fraction = infarct mass/left ventricular mass. There was good correlation between single photon emission computed tomography and pathologic measurements of infarct mass (technetium-99m pyrophosphate mass = 1.01 X pathologic infarct mass + 0.96; r = 0.98), left ventricular mass (single photon emission computed tomographic left ventricular mass = 0.60 X pathologic left ventricular mass + 37.4; r = 0.86) and "infarction fraction" (single photon emission computed tomographic infarction fraction = 1.09 X pathologic infarction fraction - 1.7; r = 0.94).(ABSTRACT TRUNCATED AT 250 WORDS)

In vivo measurement of myocardial mass using nuclear magnetic resonance imaging.

To examine the accuracy of nuclear magnetic resonance imaging in measuring left ventricular mass, measurements of left ventricular mass made using this technique were compared with left ventricular weight in 10 mongrel dogs. Left ventricular myocardial volume was measured from five short-axis end-diastolic images that spanned the left ventricle. Left ventricular mass was calculated from left ventricular myocardial volume and compared with the left ventricular weight determined after formalin immersion-fixation. Linear regression analysis yielded the following relation in grams: left ventricular mass determined using nuclear magnetic resonance imaging = (0.94) (left ventricular weight) + 9.1 (r = 0.98, SEE = 6.1 g). The small overestimation of left ventricular weight by nuclear magnetic resonance imaging was judged to be secondary to both difficulty with proper border definition and partial volume effects. Hence, this imaging technique can be used to obtain accurate measurements of left ventricular mass in dogs in vivo.

Tests of fibrin metabolism in recurrent venous thromboembolism.

Fibrinogen/fibrin degradation products (FDP/fdp) and soluble fibrin complexes (SFC) were measured serially in 60 patients heparinized for pulmonary embolism or deep venous thrombosis. Eight patients had recurrent thromboembolism. In patients without recurrence, FDP/fdp and SFC tended to normalize within three to five days. In patients with recurrence, results of both tests were significantly higher on admission, and FDP/fdp values were significantly higher throughout ten days of therapy, than in patients without recurrence. The SFC values were not different between the two groups during the first six days of treatment, but again became significantly higher on the seventh day in patients with recurrence. There were no differences in clotting times, heparin dosage, or any other clinical features between patients with and without recurrence. Measurement of FDP/fdp and SFC can help identify patients at risk of recurrent thromboembolism if performed serially during treatment.

Infarct sizing with technetium-99m stannous pyrophosphate scintigraphy in dogs and man; relationship between scintigraphic and praecordial mapping estimates of infarct size in patients.

The present study was performed in order to evaluate the ability of technetium-99m stannous pyrophosphate (99mTc-PYP) myocardial scintigrams to size infarcts in experimental animals and man. In 10 dogs with proximal left anterior descending coronary artery occlusion and acute anterior myocardial infarcts, there was a significant correlation between scintigraphic infarct size and histological infarct weight (P less than 0.01). In 25 patients with acute anterior or anterolateral myocardial infarcts, there was a significant correlation between relatively large infarct size determined scintigraphically and the acute development of left ventricular failure. There was some overlap, however, in 99mTc-PYP scintigraphic infarct size between patients who did and did not develop left ventricular failure with infarction. Presumably this is explained by some patients having had earlier myocardial damage and thus developing left ventricular failure with relatively small new infarcts. There was also a statistically significant, but weak, correlation in patients between scintigraphic infarct size and precordial ST segment mapping including peak ST segment elevation (P less than 0.05) and the number of praecordial sites with ST segment elevation equal to or greater than 2 mm (P less than 0.01). The data suggest that 99mTc-PYP scintigrams and praecordial mapping measure some similar but some dissimilar aspects of infarct size in patients, and that 99mTc-PYP scintigraphy does size acute anterior and anterolateral infarcts in experimental animals and patients.

Heparin therapy in venous thromboembolism.

Patients with pulmonary embolism or deep venous thrombosis were randomly assigned to receive either intermittent or continuous intravenous heparin therapy. In patients with an enhanced risk of bleeding, major bleeding was significantly more common during the intermittent use of heparin; in patients without these risk factors, hemorrhage occurred with equal frequency during intermittent and continuous heparin therapy. Recurrent thromboembolism was seen significantly more often in patients receiving continuous heparin therapy. Controlling the dose of heparin with coagulation tests resulted in the administration of significantly larger daily doses of heparin with intermittent injections than with continuous infusion. Therefore, the bleeding complications of intermittent heparin therapy could have been due to the higher dose, and the recurrences associated with continuous heparin therapy may have resulted from lower doses rather than from differences in the method of administration. In a small trial, arbitrary lower doses of heparin given intermittently similar to the doses of heparin given continuously resulted in fewer bleeding complications and more recurrences. In patients without risk factors for bleeding, the intermittent administration of heparin in the higher dose is preferable because of fewer recurrences and no increase in hemorrhagic complications. In patients with a high risk of bleeding, conventional doses of heparin given continuously can reduce the rate of hemorrhagic complications but will result in more recurrences.

Thallium-201 myocardial perfusion studies in patients with the mitral valve prolapse syndrome.

To determine whether regional myocardial ischemia plays a role in patients with the mitral valve prolapse syndrome, we examined myocardial perfusion with exercise stress testing and thallium-201 myocardial scintigraphy. Twelve patients were studied, 11 women and one man aged 18 to 56 years, mean age 30 years. In all patients, mitral valve prolapse was documented by echocardiography or phonocardiography. Patients over 35 years of age underwent cardiac catheterization. Electrocardograms disclosed abnormalities during maximal exercise in eight of the 12 patients. In two patients, angina developed during exercise. Thallium-201 (201Tl) scintigrams were normal in the 11 patients with presumed or documented normal coronary arteries. One patient, in whom an apical defect was demonstrated on scintigraphy, had significant disease of the left main and left anterior descending coronary artery. Repeat testing after successful aortocoronary bypass grafting revealed improved exercise capacity and a normal 201Tl myocardial scintigram. The data indicate that patients with mitral valve prolapse alone do not have regional myocardial ischemia and that the presence of a defect on 201Tl myocardial scintigraphy following maximal stress testing would suggest the existence of concomitant coronary artery disease.

Distributions of several agents useful in imaging myocardial infarcts.

Myocardial cell death due to infarction is accompanied by an influx of calcium ion. The calcium ion seems to localize in crystalline structures that form within mitochondria and resemble hydroxyapatite. Based on this phenomenon 99mTc-stannous pyrophosphate has been successfully used to image myocardial infarcts within 24 hr of infarction and 1 hr following tracer administration both in dogs and patient volunteers. In this report, canine distribution studies of 99m-Tc-pyrophosphate are compared with similar studies with 99mTc-stannous polyphosphate, 99mTc-stannous 1, hydroxy-ethylidene-1, 1-disodium phosphonate diphosphonate), and 18F as sodium fluoride. Pyrophosphate polyphosphate, and diphosphonate are each potentially useful in myocardial infarct imaging but bone uptake of 18F occurs sufficiently early to prevent the use of this radionuclide in infarct scintigraphy.

Fatty acid accumulation and abnormal lipid deposition in peripheral and border zones of experimental myocardial infarcts.

Twenty-eight dogs with acute anterior myocardial infarcts due to proximal occlusion of the left anterior descending coronary artery (LAD) were studied at various periods following the occlusion to determine: (a) the time course and location of abnormal lipid accumulation after infarction, (b) the degree of muscle-cell injury associated with increased lipid deposition, and (c) whether uptake of fatty acid from the circulating fat pool contributes to lipid accumulation in certain myocardial regions. The findings show that myocardial lipid accumulation begins as early as 6 hr after proximal LAD occulsion. The increased lipid deposition occurs as nonmembrane-bound lipid droplets in muscle cells with and without ultrastructural evidence of irreversible injury. Analysis of tissue uptake of intravenoulsy injected [14C] oleic acid conjugated with albumin revealed relatively selective concentration of label in the peripheral and border regions of the infarct, but occasionally even the central subendocardial portion of the infarct concentrated the fatty acid. Thin-layer chromotography showed that most of the label was associated with the triglyceride fraction when the radiolabeled fatty acid was injected 6 or 24 hr after LAD occlusion. These myocardial cellular and topographical alterations will have to be considered when labeled fatty acids are used for imaging acute myocardial infarcts and/or if attempts are made to identify myocardial fat-laden cells scintigraphically.

Effects of noise on the determination of ejection fraction from left ventricular time-activity curves.

The effects of Poisson noise on three estimates of ejection fraction made from left-ventricular time-activity curves have been investigated. All three methods are based on a sinusoidal model of left-ventricular volume changes. The first, developed by Schelbert et al., overestimates the ejection fraction for low-activity levels and low ejection fractions. The second estimate, which is merely a first-order correction for the contribution of Poisson noise to the first estimate, appears to be more accurate when both estimators are applied to simulated time-activity curves, and the resulting ejection fractions are compared. A third, "maximum likelihood" estimator, when applied to the same data, is apparently more accurate than the first two.

Measurement of acute myocardial infarcts in dogs with 99mTc-stannous pyrophosphate scintigrams.

Myocardial scintigrams using 99mTc-stannous pyrophosphate (99mTc-PYP) can be used to measure myocardial infarcts produced in dogs by proximal ligation of the left anterior descending coronary artery. Seven dogs had 99mTc-PYP myocardial scintigraphy performed 24--32 hr after ligation of the proximal left anterior artery. In each dog the scintigrams showed increased 99mTc-PYP uptake in the distribution of the artery. The scintigraphically visible areas of infarction, measured using interactive computer-aided techniques, were compared subsequently with independent histologic measurements of myocardial infarct size. Several methods for using the area measurements to estimate infarct size were tested. The most successful method (r = 0.92, p less than 0.01) assumed a linear relationship between the largest scintigraphic infarct area and the histologically determined infarct weight. The results suggest that 99mTc-PYP myocardial scintigrams provide a useful noninvasive method for measuring infarct size in dogs with proximal ligation of the left anterior descending coronary artery.

Acute myocardial infarction imaged with 99mTc-stannous pyrophosphate and 201Tl: a clinical evaluation.

Twenty-six patients suspected of having acute myocardial infarction (AMI) underwent myocardial scintigraphy sequentially with 201Tl and 99mTc-stannous pyrophosphate (99mTc-PPi). Of the 26 patients, 24 had AMI documented by enzyme and electrocardiographic changes. Nineteen had transmural and five had subendocardial myocardial infarctions. The remaining two patients had "unstable angina pectoris." The mean time from onset to imaging was 4 days. Of the 24 patients with AMI, 22 had positive 99mTc-PPi scintigrams. In 20 the area of acute myocardial damage appeared to be the same by 99mTc-PPi scintigram as by ECG; in two, the location could not be precisely determined. The two patients with negative 99mTc-PPi scintigrams at the time of combined myocardial imaging had had positive 99mTc-PPi images previously. In all 24 patients, the 201Tl images were abnormal in at least the location suggested by the electrocardiogram. In seven patients, the area of decreased 201Tl activity was grossly equal to the positive area on the 99mTc-PPi images; in 15, the 201Tl defect was definitely larger; and in two, the 201Tl defect appeared slightly smaller. Although the 99mTc-PPi and 201Tl myocardial images provide different information, both are valuable in determining the overall integrity of the myocardium in patients with ischemic heart disease.

Renal displacement visualized on myocardial scintigram: case report.

Myocardial scinitgrams, using 99mTc-stannous pyrophosphate, showed an acute posterior infarction and an abnormally placed left kidney in a 24-year-old hypertensive man; Further study revealed that the kidney was displaced by a mass later proven to be a pheochromocytoma. The latter was the cause of his hypertension and probably instigated the acute myocardial infarction.