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

Abstract

Early graft occlusion is usually caused by technical factors6"9 or compromised anatomic runoff0 12 and is almost always thrombotic."1 In contrast, late graft occlusion is usually a result of structural changes within the graft itself and is not usually associated with occlusive thrombosis.10-4 Progressive fibrous or fibromuscular intimal proliferation'0 11, 14-16 and, less frequently, atheromatous plaque formation 10, 1l-18 are the most common pathologic changes found in grafts that become occluded late after coronary artery bypass surgery. Recurrent symptoms of myocardial ischemia sometimes necessitate revascularization. [9][10][11][12][13][14][15][16][17][18][19][20][21] Excision of occluded grafts at reoperation has enabled us to study the pathologic changes responsible for acute late graft occlusion. In this communication we describe a lesion that has not been previously emphasized in saphenous vein grafts, although it is well recognized in native coronary arteries: atheromatous plaque rupture with superimposed occlusive thrombosis. This lesion, which we observed in five patients, represents a mechanism of graft occlusion that appears to occur as an acute event late after coronary artery bypass grafting. This lesion may be amenable to nonsurgical correction by percutaneous, intra- RW, a 53-year-old, obese, hypertensive male, presented with recurrent angina pectoris 5 years after saphenous vein coronary artery bypass. Angiography showed occlusion of grafts to the left anterior descending and the circumflex coronary arteries. At reoperation, new vein grafts were placed. The occluded grafts were excised and submitted for pathologic examination.Histologic sections of the vein graft to the left circumflex coronary artery showed complete luminal occlusion by recent thrombus superimposed on a ruptured atheromatous plaque ( fig.

2011 ACCF/AHA Focused Update Incorporated Into the ACC/AHA 2007 Guidelines for the Management of Patients With Unstable Angina/Non–ST-Elevation Myocardial Infarction

“…[817][818][819][820] In addition, post-CABG patients may develop atherosclerosis in their native vessels, and this can lead to UA/NSTEMI. 820,821 However, obstructive lesions are more likely to occur in SVGs (53% within 5 years, 76% at 5 to 10 years, and 92% at greater than 10 years), 822 and there is a high rate of early graft failure in current practice (occlusion in up to one third at 1 year). Spasm in grafts or native vessels 823,824 and technical complications may also play a role in the development of UA/NSTEMI during the early postoperative period.…”

2012 ACCF/AHA Focused Update Incorporated Into the ACCF/AHA 2007 Guidelines for the Management of Patients With Unstable Angina/Non–ST-Elevation Myocardial Infarction

“…[930][931][932][933] In addition, post-CABG patients may develop atherosclerosis in their native vessels, and this by guest on http://circ.ahajournals.org/ e768 Circulation June 11, 2013…”

“…933,934 However, obstructive lesions are more likely to occur in SVGs (53% within 5 years, 76% at 5 to 10 years, and 92% at greater than 10 years), 935 and there is a high rate of early graft failure in current practice (occlusion in up to one third at 1 year). Spasm in grafts or native vessels 936,937 and technical complications may also play a role in the development of UA/NSTEMI during the early postoperative period.…”

Histopathologic Insight into Saphenous Vein Bypass Graft Disease

“…However, few histopathologic studies exist on human saphenous vein bypass graft disease, partly because of difficulties in obtaining old vein grafts and the preference of some surgeons for keeping the old bypass grafts during the redo surgery [5,6,7,8,9,10]. Because of this, animal models have served as the conventional means of conducting research on aortocoronary vein graft stenosis and atherosclerosis [11,12,13].…”