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• W2025220133 abstract "AMAJOR AND MUCH-NEEDED ADVANCE FOR CARDIAC surgeons and patients requiring coronary artery bypass graft (CABG) surgery would be the availability of an easily applied intervention that would improve long-term patency rates for saphenous vein grafts to those achieved with internal thoracic artery grafts. With newer endoscopic techniques, the saphenous vein can be harvested with minimal trauma and without compromising short-term patency rates. While saphenous vein grafts are the easiest conduits to use technically, especially for sequential grafting, the internal thoracic artery, with its excellent long-term patency (especially when used to the left anterior descending vessel), will remain the preferred primary conduit in the vast majority of cases. Saphenous vein graft failure has a trimodal distribution. Early failure occurs within the first 1 to 2 months, probably from primary thrombosis due to technical factors, poor runoff into small or severely diseased distal coronary arteries, or unrecognized intrinsic saphenous vein disease. Late failure occurs after 3 to 5 years and results from the known tendency for saphenous veins to develop accelerated atherosclerosis. These processes may be considerably modified by currently available antiplatelet and lipid-lowering drug therapy. Intermediate failure of saphenous vein grafts is due to the development of neointimal hyperplasia, which is most prominent in the first year after CABG surgery, but can occur up to 3 years after implantation. Several factors act in concert to influence the development of neointimal lesions. These include ischemia of the venous wall, hemodynamic stress and mechanical trauma during vein harvesting and preparation, and inherent abnormalities within the vein exposed to arterial pressure, particularly in patients with multiple risk factors for atherosclerosis. Intimal hyperplastic lesions are composed of mesenchymal cells embedded in the extracellular matrix and result from complex interactions between endothelial cells, smooth muscle cells, inflammatory cells, and extracellular matrix macromolecules. Smooth muscle cells, the major component of these neointimal lesions, are believed to arise from phenotypically altered medial smooth muscle cells or possibly from CD34 cells present in peripheral blood. The initial response of a harvested saphenous vein to an operatively induced endothelial injury is smooth muscle cell proliferation. Although this process has been extensively studied in rodents, pigs, and nonhuman primates, little is known about the occurrence, duration, or importance of this proliferative response in humans. An increase in cell number and phenotypical alterations in the cytoskeleton of smooth muscle cells seem to be essential for their migration from the media into the intima and produce intimal thickening. Delineating signaling pathways implicated in smooth muscle cell proliferation, migration, and extracellular matrix production is critically important for designing novel therapies for inhibiting or limiting neointimal thickening. Gene profiling of culprit lesions may offer some insight into these events. Although the complementary DNA arrays of saphenous vein explanted after a mean of 94 months have been analyzed, few human graft explants are available for analysis within the proliferative phase of lesion formation. The E2F family of transcription factors consists of 8 known members and 2 partner proteins, DP1 and DP2, essential for E2F activity. Members 1, 2, and 3 of the E2F family have high-transcription activity and are responsible for G1/S progression of cells through the cell cycle and thus regulate smooth muscle cell proliferation. Other members of the E2F family have poor transcription activity and inhibit cellular proliferation. Targeting strategic transcriptional control of gene expression such as the G1/S transcription phase of the cell cycle with edifoligide, an oligonucleotide decoy, is a logical concept based on preliminary in vitro and in vivo studies. In this issue of JAMA, the PREVENT (Project of Ex-vivo Vein Graft Engineering via Transfection) IV investigators report the results of a large phase 3 multicenter randomized clinical trial evaluating edifoligide, which has been shown in experimental and preliminary clinical studies to inhibit neointimal hyperplasia in vein bypass grafts. In this study of 3014 patients undergoing primary CABG surgery with at least 2 planned saphenous vein grafts, edifoligide had no effect on the primary end point of per patient graft failure (45.2% in the edifoligide group vs 46.3% in the placebo group) or on the incidence of major adverse cardiac events at 1 year. All but 3% of vein graft failures were due to occlusions. Many of these occlusions were clinically important because the incidence of myocardial infarction early after operation was more than twice as high in the vein graft failure group and the incidence of subsequent cardiac events of death, myocardial infarction, or need for subsequent revascularization was 26%" @default.
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• W2025220133 date "2005-11-16" @default.
• W2025220133 modified "2023-09-25" @default.
• W2025220133 title "Gene Therapy and Vein Graft Patency in Coronary Artery Bypass Graft Surgery" @default.
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• W2025220133 doi "https://doi.org/10.1001/jama.294.19.2495" @default.
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