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Ann Thorac Surg 2001;72:S2252
© 2001 The Society of Thoracic Surgeons
a Division of Cardiothoracic Surgery, Beth Israel-Deaconess Medical Center, Harvard Medical School, 110 Francis Street, #LMOB Suite 2A, Boston, MA 02215, USA
e-mail: fsellke{at}caregroup.harvard.edu
I would like to congratulate Drs Thatte and Khuri on a very nice presentation. Their paper and presentation nicely describe the influence of endothelial cell viability and function on graft patency. Although there is little evidence that suggests that endothelial injury has much to do with short-term patency of grafts provided the anastomoses is technically sound and of sufficient caliber, there is significant evidence that, within several weeks postoperatively, the health of the vascular tissue (particularly the endothelium) can have a dramatic effect on the patency of bypass grafts. This is due, of course, to the production of nitric oxide, prostacyclin, and other endothelially derived vasodilators, and also to the inhibitory effect by these substances on platelet and neutrophil aggregation. These substances may have a dramatic effect on long-term patency.
I have several comments regarding the paper. First, a minor point. It was stated that adenosine was released from the endothelial cells. The vast majority of adenosine is released from the vascular smooth muscle and, probably more importantly, also from the myocardium. Second, it was mentioned that intimal hyperplasia is generally not observed with normal endothelium in intact saphenous veins. It is difficult to make this assertion, as endothelial function after vein harvesting probably is never normal, although it is suggested that this may be the case if one uses the GALA solution. A correlation between endothelial function and intimal hyperplasia has, to my knowledge, not been well demonstrated, and the development of intimal hyperplasia may likely be observed with or without the presence of functional endothelium in vein grafts. As mentioned in the presentation, one of the reasons that arterial grafts have a much higher patency than venous grafts is that the arterial endothelium is far more adherent to the basement membrane and the underlying vascular smooth muscle than the venous endothelium. In addition, the production of nitric oxide, prostacyclin, and other vasoactive metabolites occurs more in the arterial grafts than in the vein grafts. These antiadhesion substances decrease the development of platelet adhesion and thrombus formation. In the paper it was hypothesized that sympathetic and parasympathetic control of the IMA and other arterial grafts might play an important role in maintaining the patency of these conduits. Such a role, again, has not been clearly shown.
The authors demonstrated a new method for imaging arterial and venous bypass grafts. It may have considerable promise, especially in the development of new preservation solutions. Careful handling of the venous bypass conduits has a great impact on long-term patency that has truly been underestimated. It is easy to get the vein out and to distend it with about 400 pounds of pressure per square inch, but this can have very damaging effects on the endothelium and, consequently, on the long term patency. This should not be underestimated. As was mentioned in the presentation, there is good evidence that the addition of blood, albumin, or other preservative components can improve graft patency through preservation of the vascular endothelium. The addition of blood is potentially a very simple method to improve long term patency, especially in the venous grafts. Other novel preservative solutions have included newly developed polymers that can have a dramatic effect on endothelial preservation. This too is an underestimated and underused technique that has great promise for clinical use.
As the authors demonstrated, overdistention can have very harmful effects on veins and arterial grafts as well. However, some distention is necessary to ensure that there are no leaks and that the patient does not have to be brought back to the operating room because of bleeding the night after surgery. Distention causes activation of protein kinases and mitogen-activated protein (MAP) kinases, which initiate proliferative mechanisms and which, in addition, may be involved in the chemotactic pathways. Therefore, care should be taken not to overdistend the venous grafts.
Finally, attention should be given to protecting the endothelium, not only in the conduits but also in the native coronary arteries. The use of blood or magnesium supplementation in the crystalloid cardioplegia can inhibit calcium influx, and can also have a marked effect on preserving endothelial function in the native circulation. Therefore, these simple measures may decrease the incidence of early graft thrombosis due to reduced runoff. They may lessen the likelihood of postoperative spasm in the native circulation, and they may also decrease the incidence of intimal hyperplasia and late arteriosclerosis, not only in the arterial and vein grafts but also in the native circulation. It has been demonstrated in certain models that endothelial function can be recovered after several weeks. However, these studies were performed largely in the arterial circulation; whether the venous endothelium will recover is doubtful and has not been tested.
All these considerations underscore the importance of preserving the endothelium at the time of surgery. The effects of the above measures on long-term graft patency still need to be determined, but these are all avenues that we should pursue to improve the outcome after coronary bypass surgery.
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