Prevention of endothelial damage during preparation of saphenous veins for bypass grafting.

Abundant experimental evidence indicates that damage to vascular endothelium decreases intimal fibrinolytic activity, causes mural platelet and fibrin deposition, encourages proliferation of the exposed subintimal fibrocytes and smooth muscle cells, and increases endothelial permeability. These processes lead to thrombosis, subendothelial hyperplasia, or accelerated atherosclerosis. We have demonstrated in monkeys that distention of veins at high pressures (700 mm Hg), as commonly done clinically in preparation for coronary bypass, causes severe damage to the endothelium (as seen by scanning electron microscopy), and increased lipid uptake by the vein wall. The endothelium of veins distended at lower pressures (300-400 mm Hg) was not significantly different from that of undistended veins. Because of the potential late consequences of early endothelial damage to vein grafts, distention of veins before grafting to overcome spasm and to identify leaks must be done at controlled pressures. A convenient balloon device has been developed which limits the maximum pressure that can be applied when the vein is dilated.