Gene therapy for vein graft disease

Division of Cardiovascular Surgery, Mayo Clinic, 200 First Street SW, Rochester, MN, 55905, USA.
Current Cardiology Reports (Impact Factor: 1.93). 02/2001; 3(1):22-8. DOI: 10.1007/s11886-001-0006-0
Source: PubMed


The durability of coronary artery bypass grafting is intrinsically dependent upon the patency of the graft. The long term patency of arterial grafts, in particular internal mammary grafts, has been clearly defined by multiple groups to be greater than 90% at 10-20 years following construction. This has been fully addressed in Chaps. 13 and 14. Moreover, a recent randomized trial between radial artery and saphenous vein grafts demonstrated the superiority of radial artery conduits at 1 year [1].However, certain clinical scenarios require the use of venous grafts. The intrinsic limitations of saphenous vein bypass grafts and the subsequent acceptance of these imperfections guide our clinical decisions in a fundamental fashion. To address these shortcomings in saphenous vein grafts, a growing body of research has endeavored to improve the function of saphenous veins in an attempt to ultimately increase patency rates and durability of the surgical revascularization.

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    ABSTRACT: Gene therapy refers to the transfer of specific genes to the host tissue to intervene in a disease process, with resultant alleviation of the symptoms of a particular disease. Cardiovascular gene transfer is not only a powerful technique for studying the function of specific genes in cardiovascular biology and pathobiology, but also a novel and promising strategy for treating cardiovascular diseases. Since the mid-1990s, nitric oxide synthase (NOS), the enzyme that catalyzes the formation of nitric oxide (NO) from L-arginine, has received considerable attention as a potential candidate for cardiovascular gene therapy, because NO exerts critical and diverse functions in the cardiovascular system, and abnormalities in NO biology are apparent in a number of cardiovascular disease processes including cerebral vasospasm, atherosclerosis, postangioplasty restenosis, transplant vasculopathy, hypertension, diabetes mellitus, impotence and delayed wound healing. There are three NOS isoforms, i.e., endothelial (eNOS), neuronal (nNOS) and inducible (iNOS). All three NOS isoforms have been used in cardiovascular gene transfer studies with encouraging results. This review will discuss the rationale of NOS gene therapy in different cardiovascular disease settings and summarize the results of experimental NOS gene therapy from various animal models of cardiovascular disease to date.
    The Japanese Journal of Pharmacology 09/2002; 89(4):327-36. DOI:10.1254/jjp.89.327