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Analysis of indium 111 platelet kinetics and imaging in patients with aortic grafts and abdominal aortic aneurysms



Analysis of indium 111 platelet kinetics and imaging in patients with aortic grafts and abdominal aortic aneurysms



Arteriosclerosis 10(6): 1037-1044



To quantitatively characterize processes of platelet thrombus formation in vivo, the kinetics and incorporation into thrombus of autologous In-111-labeled platelets were compared in six patients with aortic aneurysms and in seven patients wiht prosthetic aortic grafts. Although platelet survival was comparably shortened in both patient groups (mean, 5.8 days), the maximum radioactivity (percentage of whole body radioactivity) as determined by gamma camera imaging was higher in the aneurysms than in the grafts (3.3% .+-. 1.6% vs. 1.6% .+-. 1.1%, p = 0.05). Maximum In-11 uptake was also attained more quickly in the aneurysm patients (2.3 .+-. 0.8 days vs. 3.5 .+-. 1.3 days; p = 0.07). The experimental platelet kinetic and imaging data were subsequently evaluated by compartmental analysis to estimate both normal and disease-related components of platelet destruction. This analysis indicated that deposited platelet radioactivity had a longer residence time on grafts (2.9 .+-. 1.7 days vs. 1.4 .+-. 0.9 days, p = 0.07) but accumulated at a faster rate in aneurysms (5.0% .+-. 3.4% per day vs. 1.4% .+-. 0.9% per day, p = 0.02). As determined by imaging, only a proportion of increased platelet destruction was specifically due to the aneurysms (55% .+-. 38%) or grafts (17% .+-. 11%, p = 0.03). This result indicates additional components of platelet destruction unrelated to graft and aneurysm thrombus formation which, in some graft patients, may reflect a greater severity of vascular disease or other mechanisms causing a preferential shortening of platelet survival. Thus, the analytical approach described may be a useful one for discriminating components of in vivo platelet utilization including platelet removal due to normal hemostatic and senescent mechanisms, localized thrombus formation, and more generalized vascular disease.

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Accession: 007016236

Download citation: RISBibTeXText

PMID: 2244854

DOI: 10.1016/0741-5214(91)90172-q


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