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Background: Quantification of single photon emission computed tomography (SPECT) images is important for reproducible and accurate image interpretation. In addition, SPECT quantification provides important prognostic information. The purpose of this study was to validate the Yale circumferential quantification (Yale-CQ) method in phantom studies., Methods: Myocardial perfusion defects of varying extent and severities were simulated in a cardiac phantom with fillable defect inserts. Forty-five different phantom configurations simulated 45 different myocardial perfusion defect sizes, ranging from 1.6% to 32% of the cardiac phantom volume. Automatic processing was compared with manual processing in the phantom SPECT studies., Results: The automatic Yale-CQ algorithm performed well in all phantom studies. Compared with manual processing, the mean absolute error for automatically determined center of short axis slices was 0.27 pixel in the x direction, 0.45 pixel in the y direction, and 0.15 pixel in radius. Quantification of phantom defects with the Yale-CQ method correlated well with actual defect sizes (R = 0.99), but there was a systematic underestimation (mean error = -7.9%). With derived correction factors the overall correlation between 45 phantom defects and actual defect sizes was excellent, and the estimation error was significantly improved (R = 0.98, mean error = -0.82% for manual method and -0.95% for automatic method)., Conclusion: The automatic processing algorithm performs well for the phantom studies. Myocardial perfusion abnormalities can be quantified accurately by use of the Yale-CQ method. Quantified SPECT defect size can be expressed as a percentage of the left ventricle.

Background: 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., Patients and Methods: 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., Results: 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 (p < 0.0001). Of 37 patients with very large defects (defect integral > 30), 78% were inducible, whereas only 30% of 33 patients with defect integrals < 5 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., Conclusion: 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.

Unlabelled: Technetium-99m-tetrofosmin is a 99mTc-labeled perfusion tracer demonstrating promise for myocardial perfusion imaging. To determine if 99mTc-tetrofosmin tracks myocardial flow over a pathophysiologic range, the initial myocardial uptake and clearance of 99mTc-tetrofosmin relative to microsphere flow were evaluated in a canine model of ischemia during pharmacological vasodilatation., Methods: Six open-chest dogs were subjected to complete left anterior descending coronary artery occlusion. Dogs were injected with 99mTc-tetrofosmin and radiolabeled microspheres during pharmacological stress. Coincident with radiotracer injection, dynamic planar imaging and arterial sampling were performed to assess 99mTc-tetrofosmin clearance from blood, myocardium, lung and liver. Fifteen minutes after injection, hearts were excised for well counting of myocardial 99mTc-tetrofosmin activity and flow., Results: Myocardial 99mTc-tetrofosmin activity correlated linearly with microsphere flow (r = 0.84). Relative 99mTc-tetrofosmin activity underestimated flow at higher flow ranges (> 2.0 ml/min/g) and overestimated flow in low flow ranges (< 0.2 ml/min/g). Technetium-99m-tetrofosmin cleared rapidly from the blood and was retained in the myocardium. Resting target-to-background activity ratios (heart:lung = 3.57 +/- 1.01; heart:liver = 0.58 +/- 0.04) were acceptable 10 min after injection., Conclusion: Our experimental data support both the validity of 99mTc-tetrofosmin as a myocardial perfusion tracer and the use of early poststress 99mTc-tetrofosmin imaging for the assessment of myocardial perfusion in man.

The effect of positive end-expiratory pressure (PEEP) on right ventricular performance and myocardial blood flow was determined in 16 dogs before and after right coronary artery (RCA) occlusion. Right ventricular ejection fraction (RVEF), end-diastolic volume (EDV) and end-ejection volume were measured by thermodilution. Right ventricular end-ejection pressure-volume relations (RVEEPVR) were determined at baseline and at 20 cm H2O PEEP, both before and after RCA occlusion. In four of the dogs, RVEEPVR were also determined at 10 cm H2O PEEP after RCA occlusion. With intact RCA flow, RVEF declined with PEEP (37 +/- 5 to 19 +/- 6%) with no significant change in EDV (50 +/- 11 to 42 +/- 11 ml) or end-ejection volume (31 +/- 7 to 36 +/- 9 ml). RVEEPVR and right ventricular myocardial blood flow were also unchanged with PEEP. After RCA occlusion, RVEF declined with PEEP (27 +/- 4 to 15 +/- 5%) in association with a significant increase in end-ejection volume (39 +/- 8 to 49 +/- 10 ml), but no change in EDV (53 to 55 ml). In addition, RVEEPVR and myocardial blood flow declined with RCA occlusion, and declined further with 20 cm H2O, but not with 10 cm H2O PEEP, after RCA occlusion. Therefore, in this experimental model, right ventricular performance was adversely affected during PEEP when right coronary blood flow was limited.

Nitroglycerin is known to affect the electrophysiological properties of the ischaemic ventricle, possibly by altering regional myocardial blood flow. This study correlated the effects of nitroglycerin, given after acute coronary occlusion, on regional ventricular refractoriness and regional myocardial blood flow. Nitroglycerin returned ventricular refractory periods to their pre-occlusion values in spite of no significant effect on regional myocardial blood flow. Although the beneficial electrophysiological effects of nitroglycerin were not explained by increased regional flow to the ischaemic myocardium, an improved myocardial oxygen supply-demand balance may have produced these favourable effects. This study emphasises the need for electrophysiological evaluation of the effects of interventions intended to limit infarct size.

The emergence in the past 20 years of nuclear medicine as a distinct diagnostic discipline has been a major clinical advance. The relatively rapid evolution from the small laboratory limited primarily to the study of thyroid disease to the large unit in which radioactive tracers (radionuclides) are utilized to evaluate structure and function of most organ systems has been accelerated by major advances in instrumentation, new radioactive tracers and application of computer techniques. Application of these radionuclide techniques to the study of coronary artery disease has been quite recent, and has in part been limited by the need for a coordinated effort between the cardiologist and the specialist in nuclear medicine. However, realization of the potential usefulness of these techniques has fostered an increasingly productive liaison between the two specialties. The potential advantages of these radionuclides in evaluating patients with cardiovascular disease is twofold: first, they may permit the noninvasive or atraumatic acquisition of data that might otherwise be obtained only at the time of cardiac catheterization; second, and perhaps more important, they may permit the acquisition of physiologic measurements or observations not attainable by more conventional modes of study. Functionally, these techniques can be divided into those that evaluate cardiac performance and those that evaluate coronary blood flow, regional myocardial perfusion and myocardial viability.

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.

The external imaging patterns and the kinetics of infiltration of indium-111 labeled polymorphonuclear leukocytes (PMNs) occurring in the course of the inflammatory response associated with myocardial infarction were studied in dogs subjected to closed-chest anterior wall infarction. The effects of infarct age and regional residual myocardial blood flow upon PMN infiltration were investigated and quantified, and the capacity of indium-111 PMNs to image the experimental infarction was evaluated qualitatively. The epicardial accumulation of indium-111 PMNs occurred primarily in infarct zones with residual blood flow of 0.6 times normal and was maximal (14.8 +/- 3.8 times normal) in the lowest blood flow zone (less than 0.1 times normal). PMN accumulation in the endocardial infarct zones occurred in the regions with blood flow less than 0.6 times normal and was maximal (26.8 +/- 4.9 times normal) in the lowest blood flow zone. However, contrary to the maximal epicardial infiltration period, which occurred within the first 24 hours after infarction, the maximal endocardial infiltration occurred at 72 hours after infarction. In both endocardium and epicardium, PMN uptake was minimal at 120 hours after infarction. In vivo cardiac images were abnormal and revealed discrete, anatomically distinct areas of increased myocardial radioactivity uptake in the anterior wall of all dogs studied within 24--96 hours after infarction. All images obtained 120 hours after infarction were negative. Thus, indium-111 PMNs provide a noninvasive means of in vivo imaging of the inflammatory response to myocardial infarction and allow quantification of this response at a tissue level.

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.