Why the study?
Does aspirin and dipyridamole reduce platelet accumulation on PTFE grafts in a rabbit model?
Does aspirin and dipyridamole reduce platelet accumulation on PTFE grafts in a rabbit model?
Aspirin and dipyridamole significantly reduce early, but not late, platelet deposition on PTFE grafts in a rabbit model, suggesting short-term antiplatelet therapy may be sufficient.
Answers are grounded in this paper and cite their sources.
Supports early antiplatelet benefit in graft models; leaves open translation to human patency.
The optimal duration of antiplatelet therapy was evaluated by sequential measurement of platelet accumulation on polytetrafluoroethylene (PTFE) grafts. Sixty four New Zealand white rabbits received aspirin (ASA, 10 mg/kg/day) and dipyridamole (DPM, 10 mg/kg/day) (n = 34), or placebo (n = 30), beginning 3 days prior to insertion of a 10 mm x 3 mm PTFE interposition aortic graft. Using autologous In-111 labelled platelets, a graft platelet accumulation index (GPAI) was calculated as the grafttreference aorta ratio of activity of In-111. ASA/DPM significantly reduced mean GPAI from grafts and reference aorta removed 48 h after graft insertion from 217 ± 74 (mean ± SEM) on placebo (n = 8) to 43 ± 3 (n = 9), (p<0.05). Mean GPAI at 4 weeks were 55 ± 28 (n = 5) and 28 ± 6 (n = 5), (not significant), at 8 weeks 64 ± 17 (n = 5) and 49 ± 9 (n = 5) (not significant) and at 12 weeks 11 ± 4 (n = 4) and 25 ± 10 (n = 5), (not significant) for the control and ASA/DPM groups, respectively. We conclude that ASA/DPM significantly reduce early platelet deposition on PTFE grafts. These data support the use of antiplatelet therapy after vascular bypass procedures in man and further suggest that only a few months of antiplatelet therapy may be beneficial in man.
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Nordestgaard et al. (1990) studied this question.
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