Abstract
In the last 10 years the World has increased significantly the frequency of joint replacement in patients with coronary artery disease. Coronary angioplasty with stenting significantly improve the capacity and effectiveness of the treatment of coronary artery disease. However, an important factor limiting the effectiveness of endovascular treatment of restenosis remains the stented area.The article presents an overview of the most studied gene polymorphisms of hemostasis, inflammation system, the renin-angiotensin system, endothelial nitric oxide synthase, which can play a key role in the development of in-stent restenosis. Research in this area are significant and may help in understanding the mechanisms and risk stratification of restenosis after angioplasty.
Highlights
ОБЗОРЫ И ЛЕКЦИИВ последнее десятилетие в мире значительно выросла частота применения эндопротезирования при лечении лиц, страдающих ишемической болезнью сердца (ИБС)
The angiotensinogen gene 235T variant is associated with an increased risk of restenosis after percutaneous transluminal coronary angioplasty // Clin
An important factor limiting the effectiveness of endovascular treatment of restenosis remains the stented area.The article presents an overview of the most studied gene polymorphisms of hemostasis, inflammation system, the renin-angiotensin system, endothelial nitric oxide synthase, which can play a key role in the development of in-stent restenosis
Summary
В последнее десятилетие в мире значительно выросла частота применения эндопротезирования при лечении лиц, страдающих ишемической болезнью сердца (ИБС). Тем не менее важным фактором, ограничивающим эффективность эндоваскулярного лечения, остается развитие рестеноза стентированного участка. В настоящее время среди генетических механизмов развития рестеноза в стенте наиболее освещена роль полиморфизмов генов системы воспаления [11, 13, 20, 27, 37, 40, 45], системы гемостаза [3, 38, 39], ренин-ангиотензиновой системы [16, 23, 30,31,32, 42, 44], а также полиморфизмов генов эндотелиальной синтазы оксида азота [4, 14, 15, 17, 22, 35, 36]
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