Ruptured atheromatous plaques in saphenous vein coronary artery bypass grafts: a mechanism of acute, thrombotic, late graft occlusion.

Although early occlusion of saphenous vein coronary artery bypass grafts is usually thrombotic, late occlusion is most often a result of progressive intimal fibromuscular proliferation or atheroma formation in the implanted vain. We describe another mechanism of late graft occlusion: atheromatous plaque rupture with superimposed occlusive thrombosis. Four men, ages 48-67 years underwent repeat bypass surgery for recurrent angina. Six of eight vein grafts excised 5-8 years after original bypass showed complete luminal occlusion by recent thrombus superimposed on ruptured atheromatous plaques. Similar findings were present at autopsy in two of three vein grafts from a 66-year-old man who died 7 years after bypass. These lesions are indistinguishable from those that occur in native coronary arteries of many patients with acute myocardial infarction. Unlike previously described graft occlusions, the present lesion represents a mechanism of acute, thrombotic, late graft occlusion. If recognized early, it may be amenable to nonsurgical intervention by angioplasty or thrombolysis.