The Aorta-to-Coronary Radial Artery Bypass Graft: A Technique Avoiding Pathological Changes in Grafts

Intimal Hyperplasia: A Cause of Radial Artery Aortocoronary Bypass Graft Failure

To determine the clinical significance of intimal proliferation as a cause of aortocoronary bypass vein graft obstruction, 492 vein grafts from 281 patients were studied 0 to 75 months postoperatively. All grafts had been inserted between 1968 and 1975 by one surgeon using one technique. The graft patency rate was 92 percent (55 to 60) in the first month; 91 percent (49 of 54) at 1 to 3 months; 84 percent (37 to 44) at 4 to 6 months; 77 percent (33 of 43) at 7 to 12 months; 81 percent (113 of 140) at 13 to 24 months; 82 percent (59 of 72) at 25 to 36 months; and 84 percent (66 of 79) at 37 to 75 months. Vein graft samples were obtained from 41 patients: In 27 patients with 51 grafts (early group), they were obtained 0 to 30 days (mean 14 days) postoperatively; in 14 patients with 27 grafts (late group) they were obtained 7 to 75 months (mean 34 months) postoperatively. Intimal proliferation was graded 1 to 4 corresponding to an intima/media thickness ratio of 1,2,3 or 4, respectively. In the early group, all 51 vein grafts howed grade 1 to 2 intimal proliferation; 5 of these grafts were occluded, all as a result of recent thrombosis. In the late group, 17 of the 27 grafts were studied histologically. All patent vein grafts showed grade 2 to 3 intimal prolferation. Four vein grafts were occluded but only one as a result of grade 4 intimal proliferation. In 14 patients in the late group, angiograms performed shortly before vein graft samples were obtained revealed 14 patent and 4 occluded vein grafts. Ten of the 14 patent vein grafts showed grade 2 to 3 intimal proliferation but were of uniformly good caliber angiographically (graft/artery ratio more than 1.5).

Vein graft patency and intimal proliferation after aortocoronary bypass: Early and long-term angiopathologic correlations

Aortocoronary saphenous vein grafts from 40 patients (total 62 grafts) were studied at autopsy. The earliest change seen was the insudation of blood constituents into the vein intima. Occluding thrombi were seen in six grafts from short-term survivors, and one organized thrombus was seen in a graft from a long-term survivor (28 months). Various degrees of intimai thickening were seen in grafts from all patients surviving for more than a month; this had progressed to diffuse occlusion in three cases. Gross and microscopic findings correlated well with postmortem angiographic findings in the long-term survivors. Electron microscopic examination showed smooth muscle cells, collagen fibers and ground substance in the thickened intima. Fibroblasts were not a feature of this thickening. Increased permeability of the graft endothelium, due to injury or hemodynamic factors, may result in exposure of medial smooth muscle cells to certain plasma factors and thus promote smooth muscle cell hyperplasia as has been produced in certain experimental models.

Pathologic changes in aortocoronary saphenous vein grafts

Changes in saphenous veins used as aortocoronary bypass grafts.

The histological modifications in 8 cases of autologous aorto-coronary saphenous vein grafts were studied. In the early stages, these showed intimal thickening and medial hypertrophy, particularly affecting the middle circular layer. The intimal thickening progressed, and the media later became largely replaced by dense fibrous tissue. No aneurysmal dilatations were observed, but in 3 cases the grafts were thrombosed. The pathogenesis of these changes is discussed.

J. N. Cox

Papers

Aorto-coronary by-pass with autogenous saphenous vein grafts: histopathological aspects.