01 April 2005 : Original article
Med Sci Monit 2005; 11(4): RA127-135 :: ID: 15909
Apart from coronary artery bypass grafting, percutaneous transluminal coronary angioplasty (PTCA) and intracoronary stent placement are well established treatment strategies for CAD. Substantial differences exist in the mechanisms of restenosis between conventional PTCA and stenting. Arterial remodeling is the main contributor to lumen re-narrowing after PTCA, whereas neointimal hyperplasia is almost the sole mechanism of restenosis after stenting. Several reports have demonstrated that genetic factors may be involved in the pathogenesis of restenosis after PTCA and in-stent restenosis. In this review the candidate genes involved in the pathogenesis of restenosis are analyzed as potential genetic markers of restenosis after PTCA and in-stent restenosis. The I/D angiotensin-I converting enzyme gene polymorphism, gene polymorphisms of the endothelial nitric oxide synthase (Glu298Asp, –786T>C), the glycoprotein IIIa PlA1/A2 gene polymorphism, gene polymorphism of the estrogen (PvuII), allele 2 of the interleukin-1ra gene, and the GT repeats in heme oxygenase-1 gene promoter may be used as genetic markers for in-stent-restenosis. On the other hand, only the stromelysin-1 5A/6A gene polymorphism and allele 2 of the interleukin -1ra gene may be used as a genetic marker for restenosis after PTCA.
Keywords: Coronary Thrombosis - therapy, Renin-Angiotensin System - genetics, Amino Acid Substitution, Angioplasty, Balloon, Coronary, Coronary Restenosis - genetics, Coronary Thrombosis - therapy, Genetic Markers, Nitric Oxide Synthase - genetics, Peptidyl-Dipeptidase A - genetics, Polymorphism, Genetic, Renin-Angiotensin System - genetics, Sequence Deletion, Stents
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