Restenosis pathophysiological mechanisms and genetic markers after percutaneous coronary interventions
Abstract
Coronary restenosis remains the main problem for effectiveness of percutaneous transluminal coronary angioplasty (PCA) and coronary stenting (CS). The aim of this review is to analyze pathogenetic mechanisms of coronary restenosis after PCA and CS, as well as various polymorphisms of relevant candidate genes as potential genetic markers of post‑PCA and post‑CS restenosis.
Both pathophysiological mechanisms and genetic basis are different for stent restenosis and post‑PCA, stent‑free restenosis. There are genes, which could be used as genetic markers of stent restenosis risk. For PCA restenosis risk, there are genes, also used as genetic markers. Genetic testing before percutaneous coronary interventions could identify patients with high restenosis risk, that, combined with new pharmaceutical approaches, will decrease coronary restenosis rates after PCA and CS.
About the Authors
Yu. A. Shuvalova
Russian Cardiology Scientific and Clinical Complex, State Federal Agency for Health and Social Development, Moscow
Russian Federation
Russian Federation
A. N. Meshkov
Russian Cardiology Scientific and Clinical Complex, State Federal Agency for Health and Social Development, Moscow
Russian Federation
Russian Federation
A. I. Kaminny
Russian Cardiology Scientific and Clinical Complex, State Federal Agency for Health and Social Development, Moscow
Russian Federation
Russian Federation
G. F. Piksina
Russian Cardiology Scientific and Clinical Complex, State Federal Agency for Health and Social Development, Moscow
Russian Federation
Russian Federation
V. V. Kukharchuk
Russian Cardiology Scientific and Clinical Complex, State Federal Agency for Health and Social Development, Moscow
Russian Federation
Russian Federation
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Review
For citations:
Shuvalova Yu.A., Meshkov A.N., Kaminny A.I., Piksina G.F., Kukharchuk V.V. Restenosis pathophysiological mechanisms and genetic markers after percutaneous coronary interventions. Cardiovascular Therapy and Prevention. 2007;6(5):107-114. (In Russ.)
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