The pathogenesis and prevention of aortocoronary vein bypass graft occlusion and restenosis after arterial angioplasty: Role of vascular injury and platelet thrombus deposition

Vascular injury during aortocoronary vein bypass graft surgery and arterial angioplasty initiates platelet thrombus deposition and mandates antithrombotic therapy, starting before the procedures to maximize protection against occlusion. This has been shown in studies in animals and in patients undergoing aortocoronary vein bypass graft operation where dipyridamole therapy was started before the operation, heparin was given intraoperatively and combined dipyridamole and aspirin therapy was started 7 hours after operation and markedly reduced vein graft occlusion in patients with grafts at both high and low risk for occlusion without increasing bleeding. Other alternative regimens, particularly preoperative dipyridamole followed postoperatively with aspirin alone, offer a promising future. Therapy should be continued for at least I year and perhaps indefinitely. Control of coronary risk factors appears important for long-term therapy to try to retard the atherosclerotic and occlusive process that leads to approximately 50% vein graft attrition by 10 years after operation. The possible role of cod liver oil and internal mammary artery bypass is discussed. Arterial angioplasty appears to cause deep arterial injury that activates both platelets and the coagulation system. These potentiate each other to form macroscopic mural thrombus within 1 hour in more than 90% of arteries that manifested deep arterial injury in pigs. Acute platelet thrombus deposition was retarded but not eliminated by only certain platelet-inhibitor agents. Implications for ongoing trials, current empiric therapy and future therapy are discussed.