Open AccessEffects of Aspirin, Dipyridamole, and Cod Liver Oil on Accelerated Myointimal Proliferation in Canine Veno-Arterial Allografts
Author(s) -
William M. DeCampli,
Jon C. Kosek,
R. Scott Mitchell,
Cynthia E. Handen,
D. Craig Miller
Publication year - 1988
Publication title -
annals of surgery
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.153
H-Index - 309
eISSN - 1528-1140
pISSN - 0003-4932
DOI - 10.1097/00000658-198812000-00013
Subject(s) - medicine , dipyridamole , aspirin , intimal hyperplasia , prostacyclin , lesion , fissipedia , cardiology , carnivora , gastroenterology , surgery , urology , smooth muscle
The effects of the administration of aspirin (ASA), dipyridamole (DPM), and cod liver oil (CLO) on graft patency rate and degree of intimal hyperplasia were investigated in a canine, hypercholesterolemic veno-arterial allograft model in an attempt to modify this immunologically mediated vascular injury. The drug regimens were ASA 1 mg/kg/day, DPM 10 mg/kg/day, combined ASA and DPM (ASA + DPM), and CLO (1.8 g/day eicosapentanoic acid [EPA] and 1.2 g/day docosahexanoic acid [DHA]), and control. The early angiographic patency rate (1-3 weeks) was 81% +/- 10% (+/- 70% confidence limits); the 90-day overall patency rate was 60% +/- 4% (87/144), with no statistically significant differences among the groups (range 46 +/- 10-71 +/- 9%). Qualitatively, there was no difference in luminal thrombus, intimal hemorrhage, or lesion eccentricity. Considering the relatively short time of graft implantation, an extensive amount of microscopic disease was observed; quantitatively, the mean intimal thickness was 515 +/- 17 microgram overall but was not statistically different between the groups. The fraction of potential lumenal area occupied by intimal thickening was 0.37 +/- 0.01 but again did not differ significantly between the groups. These doses of ASA, DPM, ASA + DPM, and CLO did not alter graft occlusion or retard the marked degree of subintimal myointimal cell hyperplasia that was generated in this hypercholesterolemic canine veno-arterial allograft preparation. Possible explanations for these negative findings include inadequate dosage or form of omega-3 fatty acids and the antiplatelet drugs administered, excessive variability in graft response due to uncharacterized immunologic histocompatibility, and the possible influence of non-platelet-mediated mechanisms. Nevertheless, this preparation is attractive as a reproducible model of accelerated (immunologically mediated) experimental arteriosclerosis.