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Ann Thorac Surg 2003;76:458
© 2003 The Society of Thoracic Surgeons

Invited commentary

^a Cardiothoracic Department, Hammersmith Hospital, Du Cane Road, London W12 0NN, United Kingdom

Well-conducted studies addressing the issue of vein graft patency are of major importance. Data provided will determine the future use of vein grafts and reinforce the argument for or against total arterial revascularization. The study by Chello and colleagues provides comprehensive evidence that distension of vein grafts after harvesting, promotes endothelial injury and neutrophil-endothelial interaction in vitro. Important issues raised by this study concern the effects of graft handling on endothelial activation, early and late graft patency, and of course clinical outcome.

I was slightly puzzled by the fact that ICAM-1 and VCAM-1 upregulation appeared to have taken place only one to two hours after vein distension. While basal expression of these adhesion molecules is low, surface expression reaches peak levels at four to six hours, subject to DNA transcription [1, 2]. Longer incubation times, between mechanical stimulation and immunostaining, might have increased the potential of the study.

With regard to early graft occlusion, endothelial damage is a major event. The platelet, rather than the neutrophil, is likely to be the main cellular component. Exposure of subendothelial matrix and secretion of von Willebrand factor by endothelial cells promote primary haemostatic phenomena with platelet aggregation and thrombus formation. Expression of P-selectin, ICAM-1 and VCAM-1 with subsequent leucocyte sequestration is of lesser importance. Chello and colleagues could, however, address this issue in the future using assays of platelet aggregation with their model.

Finally, long term vein graft patency depends on the rate of intimal hyperplasia, possibly exacerbated by atheroclerotic obstruction. Neutrophil adhesion and migration into subendothelial tissues is certainly of major importance. The leucocyte integrin CD11b/CD18 is capable of binding both to subendothelial fibrinogen and endothelial ICAM-1. Evidence from animal models of vascular injury suggest that ICAM-1-mediated leucocyte adhesion plays a role in the progression of intimal hyperplasia [3, 4].

Although, by design, the study by Chello and colleagues does not answer the question: ‘Does distension of a vein graft after harvesting make it more likely to occlude?,’ it provides very interesting insight into the degree of endothelial damage 300 mm Hg of pressure causes. I predict that most surgeons who have read this article will now think twice before pressing the syringe.

References

1. Pober J.S., Gimbrone M.A., Jr, Lapierre L.A., Mendrick D.L., Fiers W., Rothlein R., Springer T.A. Overlapping patterns of activation of human endothelial cells by interleukin 1, tumor necrosis factor, and immune intereferone. J Immunol 1986;137:1893-1896.[Abstract]
2. Asimakopoulos G., Thompson R.D., Nourshargh S., Lidington E., Mason J.C., Haskard D.O., Ratnatunga R.C., Taylor K.M., Landis R.G. An anti-inflammatory property of aprotinin detected at the level of leukocyte extravasation. J Thorac Cardiovasc Surg 2000;120:361-369.[Abstract/Free Full Text]
3. Yasukawa H., Imaizumi T., Matsuoka H., Nakashima A., Morimatsu M. Inhibition of intimal hyperplasia after balloon injury by antibodies to intercellular adhesion molecule-1 and lymphocyte function-associated antigen-1. Circulation 1997;95:1515-1522.[Abstract/Free Full Text]
4. Rogers C., Edelman E.R., Simon D.I. A mAb to the b2-leukocyte integrin Mac-1 (CD11b/CD18) reduces intimal thickening after angioplasty or stent implantation in rabbits. Proc Natl Acad Sci USA 1998;95:10134-10139.[Abstract/Free Full Text]

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