Early patency of free internal mammary artery (IMA) grafts for coronary artery bypass (CAB) is lower than that of in situ IMA grafts, and proximal anastomotic problems have been implicated in the pathogenesis of graft occlusion. To determine whether thrombotic phenomena might account for proximal graft narrowing, we examined platelet and fibrinogen deposition in 23 free IMA grafts in a canine model of CAB. Twelve animals had no antiplatelet therapy and were controls. Eleven animals received dipyridamole, 55 mg p.o. daily, 2 days before and each day after operation; aspirin, 325 mg p.o. daily, was given after CAB. Six of the 12 untreated dogs and 5 of the 11 treated dogs were sacrificed at 1 day after surgery; the remainder of each group was sacrificed on the 14th postoperative day. Platelet and fibrinogen depositions were quantitated by indium-111 tropolone and Iodine-125 labeling, respectively. Grafts were sectioned into five parts: proximal anastomosis (PA), proximal graft (PG), midgraft (MG), distal graft (DG), and distal anastomosis (DA). Platelet deposition was highest at the PA of free IMA grafts, and fibrinogen deposition was high at both anastomoses. Antiplatelet therapy significantly reduced platelet deposition at the PA at 14 days, but not at 1 day; fibrinogen deposition was significantly reduced at the DA at 1 day, and at both the PA and DA at 14 days. The ratio of fibrinogen molecules per platelet was unaffected by antiplatelet therapy, but was observed to increase with time at the DG and DA. Unexplained discrepancies were noted in the fibrinogen-to-platelet ratio between control IMA and control femoral artery. In contrast to in situ IMA grafts, patency of free IMA grafts may be improved with antiplatelet therapy.
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