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Nuclear cardiology is generally considered a clinical phenomenon of the past four decades. However, the field has its roots in earlier times. This chapter focuses on these historical roots as they have evolved into the present era. The initial application of radioisotopes to cardiac studies occurred in the mid-1920s. Ventricular function was evaluated in the 1960s and 1970s by first pass and equilibrium techniques. Myocardial stress perfusion imaging was first performed using potassium-43 and exercise in 1973. Stress imaging rapidly evolved thereafter with new tracers (thallium-201 and technetium-labeled agents) and from planar to SPECT approaches. Perfusion imaging rapidly proved its value diagnostically and in assessing prognosis. Infarct imaging reached its peak use in the 1970s but is now no longer employed. Advances in hybrid imaging, combining CT with radionuclide imaging has recently allowed attenuation correction as well as providing the combination of anatomic and physiologic data. PET myocardial perfusion studies have recently become a standard approach for evaluating perfusion, absolute coronary blood flow and coronary reserve. PET FDG studies of cardiac sarcoidosis have recently been established as a new approach for defining myocardial inflammation. New SPECT systems provide high sensitivity, high resolution studies, allowing for radiation dose reduction and high quality imaging studies.

Nuclear cardiology has made significant advances since the first reports of planar scintigraphy for the evaluation of left ventricular perfusion and function. While the current “state of the art” of gated myocardial perfusion single-photon emission computed tomographic (SPECT) imaging offers invaluable diagnostic and prognostic information for the evaluation of patients with suspected or known coronary artery disease (CAD), advances in the cellular and molecular biology of the cardiovascular system have helped to usher in a new modality in nuclear cardiology, namely, molecular imaging. In this review, we will discuss the current state of the art in nuclear cardiology, which includes SPECT and positron emission tomographic evaluation of myocardial perfusion, evaluation of left ventricular function by gated myocardial perfusion SPECT and gated blood pool SPECT, and the evaluation of myocardial viability with PET and SPECT methods. In addition, we will discuss the future of nuclear cardiology and the role that molecular imaging will play in the early detection of CAD at the level of the vulnerable plaque, the evaluation of cardiac remodeling, and monitoring of important new therapies including gene therapy and stem cell therapy.

The nuclear cardiology of the future will be based on new clinical and biologic targets. It will be driven by modern concepts of molecular and cell biology and molecular genetics. A major effort involves detection of atherosclerosis and vascular vulnerability. Approaches include targeting proliferating smooth muscle cells, angiogenesis, vascular injury, inflammation through a variety of mechanisms, defining cell death and protease activation, and imaging gene expression. Another new clinical target involves imaging stem cells and various progenitor cells. To meet these new objectives, advanced imaging technology is required. This involves the development of micro-single photon emission computed tomography and micro-positron emission tomography systems as well as fusion technology involving radiologic computed tomography imaging together with nuclear imaging. Vascular lesion detection imaging may require intravascular detectors. The future of nuclear cardiology, based on molecular imaging, is extraordinarily exciting. The newly defined biologic targets will allow the answering of many of the key clinical questions that will dominate cardiovascular care in cardiovascular investigation over the next decade.

Background— The α v β 3 integrin plays a critical role in cell proliferation and migration. We hypothesized that vascular cell proliferation, a hallmark of injury-induced remodeling, can be tracked by targeting α v β 3 integrin expression in vivo. Methods and Results— RP748, a novel 111 In-labeled α v β 3 -specific radiotracer, was evaluated for its cell-binding characteristics and ability to track injury-induced vascular proliferation in vivo. Three groups of experiments were performed. In cultured endothelial cells (ECs), TA145, a cy3-labeled homologue of RP748, localized to α v β 3 at focal contacts. Activation of α v β 3 by Mn 2+ led to increased EC binding of TA145. Left common carotid artery wire injury in apolipoprotein E −/− mice led to vascular wall expansion over a period of 4 weeks. RP748 (7.4 MBq) was injected into groups of 9 mice at 1, 3, or 4 weeks after left carotid injury, and carotids were harvested for autoradiography. Relative autographic intensity, defined as counts/pixel of the injured left carotid area divided by counts/pixel of the uninjured right carotid area, was higher at 1 and 3 weeks (1.8±0.1 and 1.9±0.2, respectively) and decreased significantly by 4 weeks after injury (1.4±0.1, P v and β 3 integrin expression was maximal at 1 week and decreased by 4 weeks after injury. The proliferation index, as determined by Ki67 staining, followed a temporal pattern similar to that of RP748 uptake. Dynamic gamma imaging demonstrated rapid renal clearance of RP748. Conclusions— RP748 has preferential binding to activated α v β 3 integrin and can track the injury-induced vascular proliferative process in vivo.

The hallmark of endothelial activation, an early and critical step in many alloimmune and inflammatory responses, is the transcriptional induction and expression of endothelial adhesion molecules (eg, vascular cell adhesion molecule-1 [VCAM-1]). We assessed the feasibility of VCAM-1-targeted in vivo detection of endothelial activation using I-125-labeled-F(ab')2 fragments of E1/6, a monoclonal antibody against human but not murine VCAM-1. The Kd and Bmax, determined by saturation binding in tumor necrosis factor (TNF)-activated human endothelial cells (ECs), were 3.2 +/- 0.6 nmol/L and 5600 +/- 300 binding sites per EC, respectively. Biodistribution and in vivo binding characteristics of I-125-E1/6 F(ab')2 were assessed in a novel chimeric human/mouse model, in which human skin (as a source of human microvasculature) is grafted onto SCID/beige mice. I-125-E1/6 F(ab')2 localized to TNF-activated human skin grafts as detected by autoradiography and gamma well-counting. Relative uptakes (uptake in human skin graft/uptake in the surrounding mouse skin) were, respectively, 2.6 +/- 0.8 (n = 14) and 1.6 +/- 0.3 (n = 12) for E1/6 and MOPC-21, an isotype-matched control antibody (P < .01). The preferential uptake in human skin graft was not due to differences in tissue vascularity assessed by Tc-99m-labeled murine red blood cells. In conclusion, the chimeric human/mouse model is a novel experimental tool for in vivo evaluation of human endothelial cell-specific radiopharmaceuticals. Although I-125-E1/6 F(ab')2 localized to human skin grafts, the limited number of VCAM-1 molecules/endothelial cell adversely affects its suitability as a target for in vivo imaging of endothelial activation.

Because death by any means is a loss of functional tissue, should morphologic differentiation of the type of cell death be important at all? If any given injury results in morphologic hybrids of myocyte death, it is logical to presume that interventions to abrogate any one process may produce preventative benefits that exceed expectations.10 Cell death, at least in terminally differentiated cells, may therefore allow multiple avenues of intervention, and therefore appropriate diagnostic assessment of the cell death processes may become quite relevant. In the battlefield, where many heart muscle cells have fallen, we must exploit every cue to identify dead cells from not-so-dead cells.

In the past decade, significant advances have been made in the ability to image the heart with radionuclide tracers under stress and resting conditions in patients with suspected or known coronary artery disease (CAD) for the detection of ischemia, determination of prognosis, assessment of myocardial viability, preoperative risk assessment for patients undergoing noncardiac surgery, and evaluation of the efficacy of revascularization in patients undergoing coronary artery bypass surgery or an interventional procedure.1 For many years, planar imaging and SPECT with 201Tl constituted the only scintigraphic techniques available for detecting CAD and assessing prognosis in patients undergoing stress perfusion imaging. The major limitation of 201Tl scintigraphy is the high false-positive rate observed in many laboratories, which is attributed predominantly to image attenuation artifacts and variants of normal that are interpreted as defects consequent to a significant coronary artery stenosis. Although quantification of 201Tl images improves specificity, the false-positive rate remains problematic, particularly in women and in obese patients. Breast attenuation artifacts in women are sometimes difficult to distinguish from perfusion abnormalities secondary to inducible ischemia or myocardial scar. In recent years, new 99mTc-labeled perfusion agents have been introduced into clinical practice to enhance the specificity of SPECT and to provide additional information regarding regional and global left ventricular systolic function via ECG gating of images. It was immediately apparent that the quality of images obtained with these new 99mTc-labeled radionuclides was superior to that of images obtained with 201Tl because of the more favorable physical characteristics of 99mTc imaging with a gamma camera. With 99mTc, doses of ≈10 to 20 times higher than those that are feasible with 201Tl can be administered, yielding images with higher count density. 99mTc demonstrates less scatter and attenuation than 201Tl, which is associated …

Current assessment of regional left ventricular function with electrocardiogram (ECG)-gated single photon emission computed tomography (SPECT) imaging is generally performed by visual inspection. The objective of this study was to develop and validate a new computer algorithm for quantifying regional left ventricular wall thickening on ECG-gated SPECT images. Regional wall thickening was measured from count density changes during the cardiac cycle observed in 24-sector circumferential count distribution profiles generated from each of 8 frames of an ECG-gated SPECT study. Wall thickening was expressed as the percent count increase during systole relative to end diastole. The program was tested in a phantom simulation and in patient studies consisting of a pilot study (n=40) and a validation study (n=33). In the phantom study varying degrees of wall thickening were simulated. The pilot study included 20 normal subjects with low likelihood (

In this issue of iJACC (JACC: Cardiovascular Imaging) , Botvinick et al. ([1][1]) perform a complex study involving the performance of equilibrium radionuclide myocardiography with phase analysis during ventricular tachycardia. The authors identify specific characteristics that define tolerability

Objectives. We sought to investigate the mechanism of a mental stress–induced fall in left ventricular ejection fraction (LVEF) in patients with coronary artery disease. Background. Mental stress induces a fall in LVEF in a significant proportion of patients with coronary artery disease. This is accompanied by an increase in heart rate, blood pressure and rate–pressure product. Whether the mental stress–induced fall in LVEF is due to myocardial ischemia, altered loading conditions or a combination of both is not clear. Methods. Left ventricular (LV) function was studied noninvasively by serial equilibrium radionuclide angiocardiography and simultaneous measurement of peak power, a relatively afterload-independent index of LV contractility, in 21 patients with coronary artery disease (17 men, 4 women) and 9 normal subjects (6 men, 3 women) at baseline, during mental stress and during exercise. Peripheral vascular resistance (PVR), cardiac output (CO), arterial and end-systolic ventricular elastance (Ea, Ees) and ventriculoarterial coupling (V/AC) were also calculated. Patients underwent two types of mental stress—mental arithmetic and anger recall—as well as symptom-limited semisupine bicycle exercise. Results. Nine patients (43%) had an absolute fall in LVEF of ≥5% (Group I) in response to at least one of the mental stressors, whereas the remaining patients did not (Group II). Group I and Group II patients were similar in terms of baseline characteristics. Both groups showed a significant but comparable increase in systolic blood pressure (15 ± 7 vs. 9 ± 10 mm Hg, p = 0.12) and a slight increase in heart rate (7 ± 4 vs. 8 ± 7 beats/min, p = 0.6) and a comparable increase in rate–presure product (2.2 ± 0.9 vs. 1.9 ± 1.2 beats/min × mm Hg, p = 0.6) with mental stress. However, PVR increased in Group I and decreased in Group II (252 ± 205 vs. −42 ± 230 dynes·s·cm−5, p = 0.006), and CO decreased in Group I and increased in Group II (−0.2 ± 0.4 vs. 0.6 ± 0.7 liters/min, p = 0.02) with mental stress. There was no difference in the change in peak power (p = 0.4) with mental stress. With exercise, an increase in systolic blood pressure, heart rate, rate–pressure product and CO and a fall in PVR were similar in both groups. Of the two mental stressors, anger recall resulted in a greater fall in LVEF and a greater increase in diastolic blood pressure. Exercise resulted in a fall in LVEF in 7 patients (33%). However, exercise-induced changes in LVEF and hemodynamic variables were not predictive of mental stress–induced changes in LVEF and hemodynamic variables. Conclusions. Abnormal PVR and Earesponses to mental stress and exercise are observed in patients with a mental stress–induced fall in LVEF. Peripheral vasoconstrictive responses to mental stress contribute significantly toward a mental stress–induced fall in LVEF.

Current protocols for use of tissue-type plasminogen activator in acute myocardial infarction include heparin estimated by the activated partial thromboplastin time (aPTT). Recent reports indicate a risk of recurrent ischemic events with long aPTT values. Longer aPTT values in the Thrombolysis in Myocardial Infarction-II (TIMI II) Trial, obtained within the first 48 hours, were associated with patency at 18 to 48 hours and better left ventricular function at discharge (average 9.6 days), but also with emergency catheterizations within the first 48 hours and, weakly, with recurrent ischemia during the first 18 hours. A moderate decrease in fibrinogen, compared with a “small” decrease, was also associated with patency, but a “large” decrease was associated with hemorrhagic events. Patency was associated with higher fibrinogen values and higher plasminogen values at baseline. The aPTT results support frequent monitoring during the first 24 to 48 hours to ensure optimal clinical outcome. The coagulation factor results suggest that there may be an optimum window for fibrinogenolysis in this setting. (Am Heart J 1998;135:29-37.)

Although myocardial perfusion imaging (MPI) is widely used in patients with coronary artery disease, few data are available concerning the relationship between myocardial scar and ischemia and arrhythmic potential.One hundred forty-four patients with chronic coronary artery disease who underwent electrophysiological studies (EPS) and MPI within 3 months constituted the study population. By history, 26% of the patients had sustained ventricular tachycardia (VT), 21% had cardiac arrest with ventricular fibrillation, and 53% had nonsustained VT. Eighty-five percent had previous myocardial infarction. Standard EPS protocol with up to three extra stimuli was used. Patients with a response of sustained monomorphic VT were defined as inducible. Quantitative MPI was used to define stress perfusion defect size and reversibility. The relations of ischemia (reversible defect) and scar (fixed defect) to inducibility on EPS were assessed by univariate analysis. Multivariate analysis was used to compare MPI results with known clinical predictors of inducibility.Fifty-two percent of the patients had inducible monomorphic sustained VT. MPI showed scar alone in 33%, scar with additional ischemia in 53%, ischemia alone in 8%, and no abnormality in 6%. No relation was found between the scintigraphic presence or size of ischemia and the likelihood of inducibility or to the type of arrhythmia history. In contrast, scar size was related to the result of EPS; inducible patients had significantly larger resting defect integrals (27 +/- 23 vs 14 +/- 15) than noninducible patients (p0.0001). Of 37 patients with very large defects (defect integral30), 78% were inducible, whereas only 30% of 33 patients with defect integrals5 were inducible. On multivariate analysis resting defect integral was an independent predictor of inducibility. In comparison with left ventricular ejection fraction (available in 122 patients), perfusion defect size was a better independent predictor of sustained VT on EPS.The presence or size of potentially ischemic myocardium does not appear to be related to the inducibility during EPS. Size of scar as quantified by myocardial perfusion imaging correlates well and better than the global left ventricular function with inducibility of sustained VT on EPS.

This study sought to determine the significance of abnormal thallium-201 (Tl-201) lung uptake on stress imaging in the absence of perfusion abnormalities.Abnormal Tl-201 lung uptake, represented by an increased lung/heart ratio (LHR), on stress imaging is a marker of stress-induced left ventricular dysfunction and poor prognosis in patients with coronary artery disease.We evaluate 1,271 patients from the Thrombolysis in Myocardial Infarction (TIMI)-IIIB trial (86% of TIMI-IIIB cohort) with unstable angina or non-Q wave myocardial infarction, who underwent predischarge exercise (92%) or dipyridamole stress (8%) Tl-201 imaging. An increased LHR (or = 0.50) was related to perfusion abnormalities and adverse cardiac events at 1 year.Of 1,271 patients, there were 762 (60%) with and 509 (40%) without perfusion abnormalities. An increased LHR was seen in 227 patients (18%) (173 [23%] with, 54 [11%] without perfusion abnormalities). Patients with an increased LHR had a lower left ventricular ejection fraction, higher body weight, lower exercise capacity and a higher prevalence of angina on exercise than patients with a normal LHR. In the two groups with increased LHR, there was no difference in age, hypertension, previous myocardial infarction, total exercise time, frequency of angina and ST segment depression on exercise. However, the group with an increased LHR and normal myocardial perfusion had a preponderance of women (65% vs. 30%, p0.001). At 1-year follow-up, patients with an increased LHR had a higher cardiac event rate than those with a normal LHR (18% vs. 10%, respectively, p = 0.001) despite a higher revascularization rate (28% vs. 15%, p0.001). An increased LHR was associated with increased adverse cardiac events, irrespective of the presence or absence of perfusion abnormalities.An increased LHR continues to be associated with higher adverse cardiac events in the current era of aggressive interventional management of coronary artery disease. An increased LHR in the absence of myocardial perfusion abnormality is seen mostly in women and overweight patients. However, despite the apparent absence of perfusion abnormalities, an increased LHR in this group is also associated with a higher rate of adverse cardiac events.

Receiver operating characteristic (ROC) curve analysis provides detailed information about the performance of a diagnostic test. As part of a multicenter phase III trial, 160 patients with known or suspected coronary artery disease underwent planar stress-rest99mTc-labeled tetrofosmin and stress-redistribution201Tl imaging within 14 days of each other, to compare the diagnostic accuracy of these imaging modalities by ROC curve analysis. Coronary arteriography was used as the reference standard and greater than 70% stenosis was considered significant. ROC curve analysis showed improved detection of coronary artery disease with99mTc-labeled tetrofosmin compared with201Tl, with ROC curve areas of 0.765 versus 0.644, respectively (p=0.02).99mTc-labeled tetrofosmin also better identified single-vessel disease in those without previous myocardial infarction (ROC curve areas of 0.684 vs 0.510 for99mTc-labeled tetrofosmin and201Tl, respectively;p=0.04) and enhanced the detection of multivessel disease in those with previous myocardial infarction (ROC curve areas of 0.764 vs 0.638, respectively;p=0.02). Detailed assessment of diagnostic performance by ROC curve analysis shows that, for planar imaging,99mTc-labeled tetrofosmin enhances the detection of coronary artery disease compared with201Tl.

Previous studies have shown an association between distortion of the terminal portion of the QRS (QRS[+] pattern: emergence of the J point ≥50% of the R wave in leads with qR configuration, or disappearance of the S wave in leads with an Rs configuration) on admission and in-hospital mortality in acute myocardial infarction (AMI). However, the mechanism for this association is not known. We assessed the relation between QRS(+) pattern and coronary angiographic findings, infarct size, and long-term prognosis in the Thrombolysis In Myocardial Infarction 4 trial. Patients were allocated into 2 groups based on the presence (QRS[+], n = 85) or absence (QRS[−], n = 293) of QRS distortion. The QRS(+) patients were older (mean ± SD: 61.1 ± 10.6 vs 57.5 ± 10.6 years, p = 0.004), had more anterior AMI (49% vs 37%, p = 0.04), and less previous angina (42% vs 54%, p = 0.05). QRS(+) patients had larger infarct size as assessed by creatine kinase release over 24 hours (209 ± 147 vs 155 ± 129, p = 0.003), and predischarge sestamibi (MIBI) defect (17.9 ± 15.9% vs 11.2 ± 13.4%, p

Background Insulin resistance, hyperinsulinemia, and myocardial hypertrophy frequently coexist in patients. Whether hyperinsulinemia directly affects myocardial protein metabolism in humans has not been examined, however. To test the hypothesis that hyperinsulinemia is anabolic for human heart protein, we examined the effects of insulin infusion on myocardial protein synthesis, degradation, and net balance in patients with ischemic heart disease. Methods and Results Eleven men (aged 57±3 years) with coronary artery disease who had fasted for 12 to 16 hours received a constant infusion of insulin (50 mU · m −2 · min −1 ) while plasma concentrations of glucose and amino acids were kept constant. Rates of myocardial protein synthesis, degradation, and net balance were estimated from steady state extraction and isotopic dilution of L-[ ring -2,6- 3 H]phenylalanine across the heart basally and 90 minutes into infusion. Subjects had elevated fasting plasma insulin concentrations (173±21 pmol/L) and used little exogenous glucose during insulin infusion, suggesting resistance to the effects of insulin on whole-body carbohydrate metabolism. Basally, myocardial protein degradation, as estimated by phenylalanine release (133±28 nmol/min), exceeded protein synthesis, estimated by phenylalanine uptake (31±15 nmol/min), resulting in net negative phenylalanine balance (−102±17 nmol/min). Insulin infusion reduced myocardial protein degradation by 80% but did not affect protein synthesis, returning net phenylalanine balance to neutral. Conclusions Acute hyperinsulinemia markedly suppresses myocardial protein degradation in patients with cardiovascular disease who are resistant to its effects on whole-body glucose metabolism. This antiproteolytic action represents a potential mechanism by which hyperinsulinemia could contribute to the development of myocardial hypertrophy in patients with cardiovascular disease.

Thirty patients with stable angina pectoris and ischemia on stress perfusion imaging underwent continuous ambulatory left ventricular (LV) function monitoring. Mental stress was induced by mental arithmetic. Fifteen patients developed transient LV dysfunction during mental arithmetic. Patients were followed for 2 years for adverse cardiac events. Twelve patients had cardiac events over 1 year (myocardial infarction in 4, and unstable angina in 8). Nine of 15 patients (60%) with and only 3 of 15 (20%) without mental stress-induced LV dysfunction developed cardiac events (p = 0.025). A higher proportion of patients with cardiac events were taking beta blockers (p = 0.01) and had lower resting heart rates (p = 0.002) than those without cardiac events. There was no difference in the baseline characteristics between the groups of patients with and without cardiac events. At 2-year follow-up, 10 of 15 patients (67%) with mental stress-induced LV dysfunction had adverse events compared with only 4 of 15 (27%) with no mental stress-induced LV dysfunction (p = 0.025). Thus, in this cohort of patients with stable angina pectoris, mental stress-induced LV dysfunction was associated with higher cardiac events on follow-up. The exact mechanism of this association is not clear. Mental stress may be a trigger for adverse cardiac events in these patients. Transient LV dysfunction in response to mental stress may be a marker of abnormal cardiovascular reactivity to emotional and psychological stimuli in patients with coronary artery disease and may be useful for risk stratification.

Regional and global left ventricular dysfunction caused by coronary artery disease may be reversible in a significant proportion of cases. This fact has important clinical implications. The choice of the optimal nuclear imaging technique for the detection of myocardial viability is a matter of ongoing debate. Currently the choice of technique depends on the clinical question to be answered, the local availability of the technique, and local expertise. Cost considerations may also play an important role in choice of technique.

Background Our objective was to compare the sensitivity and specificity of tetrofosmin, a new 99m Tc-labeled myocardial perfusion imaging agent for the detection of myocardial perfusion abnormalities, with those of 201 Tl and coronary angiography. Our hypothesis was that same-day stress/rest tetrofosmin imaging could provide data comparable to those of 201 Tl imaging. Myocardial perfusion imaging plays an important role for the evaluation of coronary artery disease. Newer 99m Tc-labeled agents offer several advantages over 201 Tl, the conventional myocardial perfusion imaging agent. Tetrofosmin is a new 99m Tc-labeled agent with promising results in preliminary studies. Methods and Results Two hundred fifty-two patients with suspected coronary artery disease were enrolled in 10 centers in the United States and Europe. All patients underwent exercise and rest myocardial perfusion imaging with 99m Tc-tetrofosmin using two separate injections of the radiotracer 4 hours apart on the same day. Planar images were obtained in three standard views 15 to 60 minutes after radiotracer injection. Patients also underwent standard exercise and redistribution planar 201 Tl imaging within 2 weeks of tetrofosmin imaging. In addition, 58 healthy subjects with low likelihood of coronary artery disease underwent exercise and rest tetrofosmin imaging. Coronary angiograms were available in 181 patients with suspected coronary artery disease. All radionuclide images were processed in the central core laboratory and interpreted blindly by a panel of four experienced readers. 201 Tl images and tetrofosmin images were read separately. Discrepancies were resolved by consensus. The workload, peak heart rate, and double products were comparable during exercise for both imaging agents. Technically acceptable paired 201 Tl and tetrofosmin images were available in 224 of 252 patients. Tetrofosmin images were generally of good quality, with low extracardiac activity, and easy to interpret. Patients were categorized as showing normal, ischemia, infarction, or mixture with each imaging modality. Precise concordance for each of these categories was 59.4% (κ=0.44; 95% CI, 0.35 to 0.53). When patients were categorized as normal or abnormal, the concordance was 80.4% (κ=0.55; 95% CI, 0.43 to 0.67). When each of five anatomic territories (septal, anterior, inferior, lateral, and apical) was categorized as normal versus abnormal, the concordance varied from 81% to 90%. When similar comparison was made for the specific category of abnormality, the concordance was 64% to 84%. When coronary angiography was used as the criterion, the sensitivity and positive and negative predictive accuracy of tetrofosmin and 201 Tl were comparable. The normalcy rate of tetrofosmin images in the healthy subjects with low likelihood of coronary artery disease was 97%. Conclusions 99m Tc tetrofosmin is a new myocardial imaging agent with favorable imaging characteristics with results comparable to those of 201 Tl.