**1.1. History of surgical revascularization**

The concept of surgical revascularization for coronary artery disease (CAD) originated in the early 20th century. A pioneer in this field is Beck, a surgeon who in 1935 developed an indirect technique of myocardial revascularization by grafting a flap of the pectoralis muscle over the exposed epicardium to create new blood supply. [1] Later, Beck also developed another revascularization technique by anastomosis between the aorta and the coronary sinus. [2] In 1946, the Vineberg procedure was introduced in which the internal mammary artery (IMA) was used to implant directly into the left ventricular and is hence considered the forerunner of coronary artery bypass grafting (CABG). This technique was the first intervention docu‐ mented to increase myocardial perfusion and was successfully performed in over 5,000 patients between 1950 till 1970. [3-5] The major breakthrough in surgery, however, was the invention of the heart-lung machine in 1953, which allowed surgeons to perform open-heart procedures on a non-beating heart and controlled operating field while protecting other vital organs. [6] Still it was not until 1960 when the first successful human coronary artery bypass surgery was performed by Goetz and Rohman, who used the IMA as the donor vessel for anastomosis to the right coronary artery. [7] The bypass graft technique as we know today was developed by Favaloro in 1967. [8] In his physiologic approach in the surgical management of coronary artery disease, Favaloro and his team initially used a saphenous vein autograft to bypass a stenosis of the right coronary artery. Shortly hereafter, Favaloro began to use the saphenous vein as a bypassing conduit. After the saphenous vein bypass procedure was extended to include the left arterial system by Johnson [9], the use of the IMA for bypass grafting was performed by Bailey and Hirose in 1968. [10] Arguably, the first successful IMA – coronary artery anastomosis was already performed 4 years earlier by the Russian surgeon Vasilii Kolesov. [11] Use of the radial artery (RA) as a bypass conduit was introduced by

© 2013 Beijk and Harskamp; licensee InTech. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. © 2013 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Carpentier in 1971 and fell into disrepute shortly after its introduction because of high failure rates but was revisited as many of these original grafts appeared widely patent at 6 years. [12, 13] Initially used as a free graft in a fashion similar to that of the saphenous vein graft, more recently the RA has been used as a T or Y graft from the left IMA (LIMA) or an extension graft from the distal right IMA (RIMA). On the basis of superior long-term outcomes of arterial conduits compared with vein grafts, other arteries have been used in CABG such as the gastroepiploic artery (GEA), the inferior epigastric artery (IEA), the splenic artery, the subscapular artery, the inferior mesenteric artery, the descending branch of the lateral femoral circumflex artery, and the ulnar artery. However none of these arteries have shown similar patency rates as the internal mammary artery.

The concept of the 'failing graft' is one of a patent graft whose patency is threatened by a hemodynamically significant lesion in the inflow or outflow tracts or within the body of the graft. Salvage of the failing and failed bypass graft remains an important clinical and technical challenge. The high incidence of graft failure has led to the evolution of graft surveillance programs to detect 'failing' grafts and research has focussed on means to control the devel‐

Treatment of Coronary Artery Bypass Graft Failure

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The saphenous vein consists of three layers: the intima, media, and adventitia. The intima is composed of a continuous layer of endothelial cells on the luminal surface of the vessel. Beneath lies the fenestrated basement membrane embedded with a fragmented internal elastic lamina. The media comprises of smooth muscle cells (SMC) arranged in an inner longitudinal and an outer circumferential pattern with loose connective tissue and elastic fibers interlaced. The middle muscle layer is most extensive at the insertion points of the valves and leaflets. The adventitia forms the outer layer and consists of longitudinally arranged SMC, collagen fibers and a network of elastin fibers, in addition to vascular and nerve supplies to the vessel.The great saphenous vein is the most frequently used conduit for myocardial revascu‐ larization but other venous conduits such the short saphenous vein or upper extremity veins

Studies of saphenous veins harvested for bypass procedures have shown that many have abnormal histological and physical attributes. [23,24] Moreover, the quality of the saphenous vein can have significant clinical consequences. Therefore, vein grafts in the arterial circulation

Several intrinsic and extrinsic factors may play a role in the mechanism of SVG failure. At the time of harvest, the quality of the saphenous veins may be poor, demonstrating a spectrum of pre-existing pathological conditions ranging from significantly thickened walls to post phlebitic changes and varicosities. Between 2% and 5% of saphenous veins are unusable and up to 12% can be considered diseased which reduce the patency rate by one half compared to non-diseased veins. [25] In addition, the inevitable vascular trauma that occurs during SVG harvesting itself can also lead to damage to the endothe‐ lium and SMC and thereby contribute to graft failure. Surgical manipulation and highpressure distension to reverse spasm during harvesting leads to loss of endothelial integrity and the antithrombogenic attributes of the endothelium, rendering the SVG prone to subsequent occlusive intimal hyperplasia and/or thrombus formation. [26] Dur‐ ing harvesting the vasa vasorum and nervous network of the SVG are devided, making the graft dependent on diffusion for weeks until adequate circulation is esthablished.

must be considered as a viable, constantly adapting and evolving conduit.

opment of intimal hyperplasia. [22]

**3. Histology of saphenous vein**

(cephalic and basilica) can be used as well.

**4. Saphenous vein graft failure**

*Surgical revascularization in the current era -* A number of studies and trials have consistently shown the benefit of CABG in select patient populations. Indisputable, surgical revasculari‐ zation which in most cases is performed utilizing the saphenous vein for bypassing non LADlesions and arterial bypass grafts for LAD lesions, has dramatically changed the management of patients with ischemic heart disease. Currently, over 300,000 patients undergo CABG in the United States each year. [14] Although the short-term outcomes of CABG are generally excellent, patients remain at risk for future cardiac events due to progression of native coronary disease and/or coronary bypass graft failure. [15-18] To illustrate, over half of saphenous vein grafts (SVG) are occluded at 10 years post CABG and an additional 25% show significant stenosis at angiographic follow-up. [19] Additionally, diseased grafts represent an increasing proportion of culprit lesions and acute graft occlusion may cause acute coronary syndromes (ACS). [20] In the next paragraphs we will describe in further detail the pathophysiologic mechanisms that lead to coronary artery bypass graft failure, and elude to management strategies.
