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Page 2 of 10                                                     Gacad et al. Vessel Plus 2019;3:28  I  http://dx.doi.org/10.20517/2574-1209.2019.011
               now can be achieved by percutaneous coronary intervention (PCI) with endovascular implantation of
               drug eluting stents (DES), which target coronary obstructions that hamper myocardial perfusion during
               exercise [7-12] . The indications, benefits and shortcomings of surgical and endovascular CAR are evolving
               and a constant source of debate [6,13] . However, two aspects of CAR are overwhelmingly agreed on: the left
               internal mammary artery (LIMA) is the longest-lasting and most event free conduit for CABG and the
               completeness of CAR is an important determinant of its long-term outcome [14-16] .

               Due in part to LIMA long-lasting patency, CABG surgery is considered to be the CAR procedure of choice
                                                                                         [17]
               in patients with mCAD that encompasses the left anterior descending artery (LAD) . However while
               revascularization of non-LAD coronaries is commonly achieved with implantation of saphenous vein grafts
               (SVG) alongside the LIMA, another treatment option is a staged procedure, referred to as hybrid coronary
               revascularization (HCR), where revascularization of non-LAD coronaries is achieved by percutaneous
               implantation of 2nd generation DES [18,19] . Although it was advocated for ≥ 2 decades, HCR only represents
                                                          [20]
               < 0.5% of the total of CABG procedures performed .

               The rationale for HCR and the barriers to its widespread adoption are first discussed. A pragmatic approach
               to HCR, that may facilitate its adoption by the cardiovascular community, is then advocated.

               SAPHENOUS VEIN GRAFT PATENCY
               Autologous saphenous vein was the conduit used by Favaloro in his landmark CABG operation 50 years
                  [21]
               ago . SVG still account for > 80% of conduits used in CABG surgery [22,23] . The rate of SVG occlusions
               has been estimated be 15% 1-year post implantation, 1%-2% per year from year 1 to 6 and 4% per year
                                                                     [24]
               from year 6 to 10 resulting in a patency rate of 60% at 10 years . More recent data suggests 42.8% of SVG
               failure (defined by ≥ 75% stenosis) at 12-18 months after CABG surgery in 1828 patients who underwent
                                                          [25]
               angiography for clinical reasons or per protocol . The rate of SVG failure was similar 12-18 months
               implantation in 926 patients enrolled in the Project of EX-Vivo Vein Graft Engineering via Transfection
                                 [26]
               (PREVENT) IV trial . The bulk of SVG patency rate data was collected in large volume University or
               Veterans Administration medical centers when 400,000 CABG operations were performed annually in the
                          [27]
                                                                                     [6]
               United States . Nowadays with PCI being the most common procedure for CAR , CABG surgery is less
               performed and the current patency rate of SVG is unknown.

               Rapid development of SVG atherosclerosis is the primary reason for the low SVG patency rate 5-10 years
                               [28]
               after implantation . Systemic arterial pressure and harvesting-related trauma cause endothelial damage
               and intimal hyperplasia. An inflammatory response follows with recruitment of immune cells, activation
                                                                                                       [29]
               of pro-thrombotic factors, vascular smooth muscle cells migration and extra cellular matrix degradation .
               Macrophages and foam cells promote the development of necrotic chores that expand and eventually
                                                                                        [24]
               rupture leading to intra vascular thrombosis and clinically full-blown atherosclerosis . Due to its diffuse
               and friable nature, SVG atherosclerosis progresses rapidly and is not mitigated by implantation of DES .
                                                                                                       [28]
               Further, mobilization of embolic debris and serotonin-induced vasospasm during PCI may result in a no-
               reflow phenomenon and in-stent restenosis [30,31] . Targeted therapy at all the steps of the atherosclerosis
               cascade has failed to alter the progression of atherosclerosis in SVG. Atherosclerosis is diffuse and often
               concentric involving 90% to 100% of the graft circumference [30,32] .


               Redo revascularization is currently the only therapeutic option for diseased SVG [31,33] , and is seldom
               achieved by repeat CABG surgery due to technical difficulties and a mortality that is 5-fold greater than
               that of the initial operation [34-36] . Redo revascularization through PCI with implantation of bare metal stents
               or DES is also problematic [37-39] . Percutaneous interventions on diseased SVG are associated with a high-
               rate of in-stent restenosis, target vessel revascularization, peri-procedural myocardial infarction and in-
               hospital mortality [40,41] . Current wisdom advocates to focus revascularization efforts on the native vessel
               lesions and not on the diseased SVG [40,41] .
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