Abstract

Given the number of patients who have undergone coronary bypass surgery in which vein grafts were used, the increasing incidence of vein graft disease over time, and the reluctance of most patients to see a cardiovascular surgeon professionally again after the first go-around, there is continued need for development of approaches to treat such patients. There are many unique characteristics of patients treated for vein graft disease: they are older than when they had their initial procedure, and more importantly, their vein grafts are also older. Beyond 1 year and particularly >3 years after surgery, atherosclerosis of vein grafts becomes increasingly prevalent.1 2 3 4 5 It may coexist with intimal fibromuscular proliferation and, in patients with acute ischemic syndromes, thrombus of varying ages. Atherosclerotic plaques in vein grafts are often large compared with plaques in native coronary arteries and are usually soft and friable, rich in necrotic debris, cholesterol crystals, blood elements, and foam cells; this is often referred to as gruel. Thrombus has been documented by angioscopy in up to 70% of vein graft lesions undergoing treatment.6 This substrate is primarily responsible for the problems encountered during interventional procedures, which include distal embolization, inadequate dilatation, and increased restenosis rates. Distal embolization is of the greatest concern because the treatment options for embolization are so limited. Saber et al7 assessed the histopathology of 6 vein grafts from 5 patients treated with balloon angioplasty. Two grafts were obtained during autopsy; the remainder were from surgical extirpation. The picture worth a thousand words (Figure⇓) tells the compelling story of the underlying pathophysiology: a 59-year-old woman 6 years after CABG surgery presented with an acutely occluded vein graft and was treated with streptokinase and PTCA. The patient developed profound hypotension and subsequently died. At postmortem examination, there was …

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