The coronary artery bypass conduit: I. Intraoperative endothelial injury and its implication on graft patency
Section snippets
Stage 1: thrombogenesis
Venous graft failure within 1 month after CABG surgery is thought to occur as a result of thrombogenesis 1, 2, 3, 4, 5, 6, 7, 8, 9, 11. Early pathologic changes observed in autogenous saphenous vein grafts implanted as arterial autografts include acute thrombosis, denudation of endothelium, platelet and fibrin accumulation, cellular intimal subendothelial infiltrates, myointimal proliferation, smooth muscle necrosis, and inflammation 1, 2, 3, 4, 5, 6, 7, 8, 9.
Endothelial cells are known to be
Measuremnt of endothelial function
The intraoperative preservation of harvested saphenous veins before performance of coronary artery bypass grafting is a factor in the protection of the endothelial cells. Short-term preservation of free vascular grafts is a daily routine in coronary operations, in which 1 to 2 hours may elapse between harvesting and reperfusion. This interval may affect both the structure and function of the graft, depending upon the composition of the storage solution, the storage temperature, or the duration
Structural assessment
The structural and functional viability of vessel endothelium is measured with a fluorescence-based, super-vitality, live–dead assay [24]. This assay measures the structural integrity of cells by allowing the membrane-permeable calcein AM ester dye to enter the cell and be transformed by the cellular esterases to produce green fluorescence in living cells, thus providing a measure of enzyme activity and cell viability. In contrast, the membrane impermeable ethidium homodimer enters compromised
Summary
Endothelial dysfunction is the primary determinant in the interrelated pathogenesis of thrombosis, intimal hyperplasia, and arteriosclerosis in aorto-coronary saphenous vein graft failure. The plethora of risk factors that can cause endothelial abnormalities and graft failure include (but are not restricted to) surgical trauma, ischemia, storage conditions, distension, and arterialization of venous grafts. Inherent deficiencies of the vein as a bypass conduit, structural and functional damage
Acknowledgements
We thank Vaidya (Dr.) Ajit S. Kolatkar for sharing his knowledge of blood circulation and useful discussions. HST acknowledges Aditi Thatte for her encouragement and support. The editorial assistance of Mrs. Nancy Healey is greatly appreciated.
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