Re: spatial and temporal quantitation of plane thallium myocardial images.
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Biomedical subjects
Publications and source records attributed to P Steele.
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Platelets may contribute to the pathogenesis of atherosclerotic coronary artery disease (CAD), and platelet reactivity may be activated by exercise. Fourteen men with CAD participated in a double-blind, crossover study of aspirin (ASA), dipyridamole (DPY), ASA-DPY, and placebo. The ASA therapy increased platelet survival time (autologous labelling with 51Cr), but had no effect on either the duration of angina-limited treadmill exercise or the heart rate-systolic blood pressure product (x 10(-2)) at peak exercise. The combination DPY-ASA had a greater effect on platelet survival, but did not substantially increase the duration of exercise. Administration of DPY alone at a higher dosage increased the exercise duration and had a similar effect on platelet survival. At the time that control exercise was completed with the higher dosage of DPY, the rate-pressure product was decreased. The results suggest that DPY and ASA favorably alter the platelet survival in men with CAD, and that DPY, but not ASA, favorably alters exercise performance. Although ASA and ASA-DPY may alter platelet response to exercise, the effect is not shown in hemodynamic measurements during exercise. In higher dosages, DPY may be an effective coronary vasodilator for men with CAD.
Polioencephalomalacia (PEM) was induced in sheep, with an overall incidence of 63 per cent, using local bracken fern (Pteridium esculentum) rhizomes as a source of thiaminase type 1 and pyridine as a basic cosubstrate. The condition was thiamin responsive and PEM was confirmed by histopathological examination. In a separate experiment to examine the effect of pyridine, it was shown that, for the duration of the experiment, pyridine had no toxic effect and caused no histologically detectable brain lesions.
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Outbreaks of ovine weaner nutritional myopathy occurring in the southwest of Western Australia outside the recognised selenium-responsive areas have been investigated. One hundred and five sheep died in 3 outbreaks following 5 months grazing cereal stubble paddocks. Liver selenium and glutathione peroxidase activities, measured as an index of biological availability of dietary selenium, indicated that the selenium status of the animals was probably adequate. A comparison fo liver selenium and alpha-tocopherol concentrations and glutathione peroxidase activity was made with both selenium supplemented sheep and sheep affected with selenium-responsive nutritional myopathy. In all cases investigated in this study liver alpha-tocopherol levels in affected animals were low and this may be important in the aetiology of this myopathy.
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Positive end-expiratory pressure (PEEP) ventilation is frequently associated with reduction in cardiac output despite unchanged transmural left ventricular (LV) end-diastolic pressure. These findings have been interpreted to indicate decreased contractility, but could also be explained by altered LV diastolic pressure-volume characteristics. To study this possibility, radiopaque markers were inserted into a plane of the LV in nine dogs. Transmural pressure (LV-pericardial) was synchronized with LV area during ventilation with zero end-expiratory pressure and with 15 cmH2O PEEP. Mean polynomial curves derived from the diastolic pressure-area data demonstrated that PEEP shifted the curves upward so that a given diastolic area was associated with a higher transmural LV pressure (P less than 0.0001). PEEP decreased end-diastolic area and stroke area, both of which were normalized with dextran volume expansion. Restoration of stroke area by normalizing end-diastolic area with volume expansion suggests the initial changes with PEEP were due to a decrease in preload rather than in contractility.
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Left ventricular ejection fraction (LVEF) was measured at rest and during supine bicycle exercise in 31 men with arteriographically defined coronary disease and in 15 normal men. LVEF was calculated from a left ventricular time vs activity curve (collimated scintillation probe, 99m Technetium) as the fracitonal fall in count-rate divided by the background-corrected left ventricular end-diastolic count-rate. In normal men LVEF at rest averaged .59 +/- .06 (+/-SD) and during exercise was .72 +/- .08. LVEF did not increase with exercise in men with coronary disease (.55 +/- .03 to .57 +/- .03; N = 31; AVE +/-SEM; NS). In 17 men with coronary disease who had ST segment depression with exercise, LVEF either decreased or was unaltered in all (55 +/- .04 to .49 +/- .03; P less than 0.05); whereas in 14 without ST depression, LVEF increased in 10 (71 per cent) and was unaltered in 4 (29 per cent) (.54 +/- .04 to .66 +/- .04; P less than 0.01). Results suggest that LVEF during exercise normally increases, but in men with coronary disease LVEF either fails to increase or actually decreases. In addition there appears to be a relationship between ST segment changes during exercise and ejection fraction.
Obligatory urinary and fecal nitrogen losses and urinary urea nitrogen and creatinine excretion levels were determined in 11 young women (four of whom used oral contraceptives), eight older men, and five young men. Values for obligatory nitrogen losses in the young women who did not use oral contraceptives were similar to those observed previously in young women and lower than those reported for young men. Our values for older men were lower than previously reported values for obligatory losses observed in young and elderly men, but similar to previously reported values for young women and to values for our women who did not use oral contraceptives. The four oral contraceptive users had significantly higher levels of total urinary and fecal obligatory nitrogen losses than the nonusers in our study. When values from our study and values from other recent studies are considered, variations in obligatory nitrogen losses appear to be larger among individuals within an age-sex group than the observed differences between groups. When the intakes of protein recommended as safe by the Food aculated from obligatory nitrogen losses per se, the recommended levels appear to be only marginally adequate.
Thromboembolism (TE) occurs in about 20% of patients with rheumatic mitral valve disease, and platelet survival time in these patients has correlated with TE. In patients with mitral valve prolapse, TE appears to occur very infrequently. Platelet survival (autologous labeling with chromium-51) was performed in 26 patients with mitral prolapse. Five patients had a history of stroke, as well as normal cerebrovascular arteriography and shortened platelet survival (average half-time +/- SEM 2.3 +/- 0.18 days; normal half-time 3.7 +/- 0.03 days; n = 26; p less than 0.01). Platelet survival was shortened in seven of 21 patients without TE (33%) (3.3 +/- 0.06 days; p less than 0.01 vs patients with TE). In 138 patients with rheumatic heart disease, platelet survival was shortened in 40 of 41 (98%) with a history of TE (2.3 +/- 0.08 days) and in 76 of 97 (78%) without TE (2.9 +/- 0.07 days; p less than 0.001 vs patients with TE). In patients with mitral prolapse, sulfinpyrazone increased platelet survival (2.4 +/- 0.16 to 2.7 +/- 0.19 days; n = 7; p less than 0.05). Our results suggest that platelet survival time is shortened in patients with mitral prolapse and rheumatic heart disease who have had TE. Of those without TE there is an increased frequency of shortened platelet survival in patients with rheumatic heart disease (78%) compared with those with mitral prolapse (33%), consistent with the infrequency of TE in mitral prolapse.
Platelet survival time (SURV) has correlated with thromboembolism in patients with prosthetic cardiac valves. Sulfinpyrazone increases SURV. SURV (autologous labeling with 51Chromium) was measured in 126 patients who had aortic or mitral valve replacement. These patients were followed prospectively. Ninety-four with shortened SURV received sulfinpyrazone; 32 with normal SURV were not treated with platelet suppressants. Eighty-seven patients were anticoagulated with warfarin--67 with shortened SURV and 20 with normal SURV. Eleven patients have had thromboembolism, and all had shortened SURV (2.4 +/- 0.08 days; average half-time +/- SEM; normal 3.7 +/- 0.03 days; n = 26) none had an increase of SURV with sulfinpyrazone (2.3 +/- 0.09 days). Of 83 patients with shortened SURV who did not have embolism, sulfinpyrazone increased SURV in 59 (71%) 2.6 +/- 0.05 to 2.9 +/- 0.06 days). Of 35 patients with shortened SURV who failed to increase SURV with sulfinpyrazone, 11 (31%) had embolism; none of 59 (0%) with an increase of SURV with sulfinpyrazone had thromboembolism. These results suggest that patients with thromboembolism after prosthetic cardiac valve replacement have shortened SURV and that patients treated with slufinpyrazone who have thromboembolism do not have an increased SURV.
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Platelets may contribute to the pathogenesis of atherosclerosis and to the complications of coronary atherosclerosis, acute myocardial infarction, unstable angina, and sudden cardiac death. In addition, platelets may contribute to saphenous vein aortocoronary graft occlusion. Of 104 men with coronary artery disease, platelet survival (SURV) (chromium51 labeling) was shortened in 68% (3.1+/-0.03 days [average+/-SEM]; normal, 3.7+/-0.03 days; P greater than .001). Three platelet-suppressant drugs, sulfinpyrazone, clofibrate, and dipyridamole increased SURV. Saphenous vein graft occlusion was associated with shortened SURV. Of 36 men with occlusion of at least one graft, SURV was shortened in 35 (2.5+/-0.08 days), whereas in 19 with all grafts open, SURV was shortened in six (3.5+/-0.10 days; P less than .01). These drugs increased SURV (2.3 +/- 0.08 to 2.7 +/- 0.11 days; P less than 0.1) and were associated with improved graft patency (four of 32 grafts after initial bypass vs 30 of 34 grafts open after second operation).
Platelet survival time was measured in eight men who had an acute transmural myocardial infarction and were subsequently found to have a normal coronary arteriogram. Platelet survival (chromium-51 labeling) was shortened in all men (2.4 +/- 0.11 days; average half-time +/- standard error of the mean) and different from that in eight age-matched normal men (3.7 +/- 0.08 days) (P less than 0.001). Three patients had recurrent venous thromboembolism and one had had iliofemoral arterial thromboembolism. Platelet survival was shortened (2.9 +/- 0.12 days) in 11 of 16 age-matched men with transmural infarction who had arteriographic evidence of coronary obstructive disease. These results suggest that platelet survival time is shortened in patients with infarction who subsequently are shown to have a normal coronary arteriogram and that arterial thrombosis may be responsible for the infarction.
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Platelet survival time (SURV) (autologous labelling with 51Chromium) was shortened (3 +/- 0.03 days; average t 1/2 +/- SEM; normal t 1/2 3.7 +/- 0.03 days) in 88 out of 128 (69%) men with coronary disease. In 35 out of 47 men with hyperprebetalipoproteinemia, SURV was shortened (3 +/- 0.09 days) (74%). Of 30 men with hyperbetalipoproteinemia, SURV was shortened (2.5 +/- 0.10 days) in 26 (87%). Of 51 men without hyperlipoproteinemia, SURV was normal (3.3 +/- 0.10 days) in 24 (47%). Dietary alteration of serum triglyceride was undertaken in 12 men with hyperprebetalipoproteinemia, and in eight a decrease of triglyceride of more than 75 mg% was achieved (324 +/- 21-219 +/- 18 mg%; P less than 0.001) with an increase of SURV (2.2 +/- 0.11-2.8 +/- 0.13 days; P less than 0.001). In four, serum triglyceride increased by more than 75 mg% (279 +/- 14-451 +/- 28 mg%) and SURV decreased (2.7 +/- 0.16-2.3 +/- 0.21 days). Cholestyramine (16 g g.d.) and diet decreased serum cholesterol (348 +/- 7.6-319 +/- 6.3 mg%; P less than 0.001) in 15 men with hyperbetalipoproteinemia and SURV increased (2.3 +/- 0.08-2.7 +/- 0.07 days; P less than 0.001). Results suggest that SURV is shortened in men with coronary disease, particularly in those with hyperlipoproteinemia, and that alteration of triglyceride and cholesterol are associated with alteration of SURV.
A new method of multiplanar emission tomography is described; it uses a wide-field Anger scintillation camera (37.5 cm crystal diameter) and a seven-pinhole collimator. The pinholes (5.5 mm) acquire data simultaneously from the emissing source and project the data onto seven independent regions of the camera crystal. Multiple planes are reconstructed from the initial seven-view data acquisition through the use of a computerized addition-multiplication algorithm and variation of the superposition relationships among the projected views. These planes are then altered iteratively by a least-error criterion following ray-sum comparison with the original views. Planar resolution (full-width-half-maximum) is 1.0 cm and depth resolution is 1.5 cm. In 42 patients with angiographically demonstrated coronary-artery disease, studies of myocardial Tl-201 perfusion, under exercise, have shown improved detection sensitivity in comparison with scintigraphy using parallel-hole collimation.