scholarly journals Genetic predictors of early coronary in-stent restenosis

2020 ◽  
pp. 54-55
Author(s):  
К.Б. Богатырева ◽  
М.М. Азова ◽  
З.Х. Шугушев ◽  
Аисса А. Аит ◽  
А.В. Агаджанян ◽  
...  
Keyword(s):  
Endothelial Nitric Oxide Synthase ◽  
Genetic Factors ◽  
Percutaneous Coronary Interventions ◽  
Stent Restenosis ◽  
Genetic Predictors ◽  
Percutaneous Coronary ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide ◽  
Folate Cycle ◽  
In Stent Restenosis

В настоящее время рестеноз является основной проблемой, возникающей после чрескожных коронарных вмешательств. К причинам повторного сужения артерии после стентирования относятся клинические, ангиографические и генетические факторы. В представленной работе изучены некоторые полиморфные локусы генов ренин-ангиотензин-альдостероновой системы, фолатного цикла и эндотелиальной синтазы оксида азота. Выявлены генетические варианты, ассоциированные с рестенозом, развивающимся в различные сроки после стентирования (до 6 месяцев или позже). Currently, restenosis is a major challenge arising after percutaneous coronary interventions. Causes of re-narrowing of the artery after stenting include clinical, angiographic, and genetic factors. Some polymorphic loci of the renin-angiotensin-aldosterone system, folate cycle, and endothelial nitric oxide synthase genes have been studied. Genetic variants associated with the restenosis developing at different time periods after stent implantation (within the first 6 months or later) have been identified.

Hyperinsulinemia and impaired leptin-adiponectin ratio associate with endothelial nitric oxide synthase polymorphisms in subjects with in-stent restenosis

2008 ◽  
Vol 294 (5) ◽  
pp. E978-E986 ◽  
Author(s):  
Elena Galluccio ◽  
PierMarco Piatti ◽  
Lorena Citterio ◽  
Pietro C. G. Lucotti ◽  
Emanuela Setola ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Cardiovascular Disease ◽  
Endothelial Dysfunction ◽  
Nitric Oxide Synthase ◽  
Endothelial Nitric Oxide Synthase ◽  
Stent Restenosis ◽  
Nos3 Gene ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide ◽  
In Stent Restenosis

Little is known about the association of endothelial nitric oxide synthase (NOS3) gene polymorphisms and the presence of insulin resistance and the early evolution of atherosclerosis in nondiabetic subjects with cardiovascular disease (CAD) and stent implantation. The present study was performed in an attempt to better understand whether metabolic, endothelial, and angiographic findings characteristic of subjects with cardiovascular disease and in-stent restenosis are related to NOS3 variants. This is a case-control study performed from 2002 to 2006. All subjects admitted to the study were recruited in the Nord-Centre of Italy, most from Milan and its surrounding towns. Measures of glucose tolerance, insulin sensitivity, markers of endothelial dysfunction, forearm vasodilation, and adipokine levels were determined and associated to the frequency of two single-nucleotide polymorphisms of NOS3, i.e., Glu298Asp (rs1799983, G/T) and rs753482 (intron 18 A/C). A total of 747 subjects, not known to have diabetes, were evaluated: 333 subjects had asymptomatic CAD, 106 subjects had unstable angina and were evaluated for in-stent restenosis 6 mo after stent placement, and 308 were control subjects. The presence of TT and CC minor alleles was significantly greater in case groups compared with control subjects. At phenotypic level, subjects with the polymorphisms were characterized by hyperinsulinemia and reduced reactive hyperemia, whereas increased leptin and decreased adiponectin levels were present in subjects with restenosis in the presence of reduced minimal lumen diameter and length of stenosis almost doubled. Hyperinsulinemia, endothelial dysfunction, and a more atherogenic profile seem to be peculiar features of subjects with asymptomatic CAD and restenosis carrying NOS3 gene variants.

Designing Biomedical Stents for Vascular Therapy

2013 ◽  
pp. 216-239
Author(s):  
Arghya Paul
Keyword(s):  
Stent Thrombosis ◽  
Vascular Tissue ◽  
Medical Industry ◽  
Percutaneous Coronary Interventions ◽  
Late Stent Thrombosis ◽  
Comprehensive Overview ◽  
Stent Restenosis ◽  
Tissue Therapy ◽  
Percutaneous Coronary ◽  
In Stent Restenosis

The breakthrough technologies of stent have revolutionized the medical industry, particularly in the field of percutaneous coronary interventions and other vascular therapies. However, recent concerns of late stent thrombosis and in-stent restenosis have rekindled an interest in developing new and improved therapeutic stent devices. A multidisciplinary approach of regeneration therapy, biomedicine, and nanotechnology is the next frontier for this. The chapter presented here gives a comprehensive overview of the evolving stent technologies for efficient vascular tissue therapy and articulates the potential of these technologies to design the next generation of therapeutic stent. In addition, the chapter also encompasses upcoming technologies to develop bioactive stents for efficient healing and remodeling of damaged local vascular biology.

scholarly journals 'Miracle stents' - a future without restenosis

2020 ◽  
Vol 10 (2) ◽  
Author(s):  
Huda Hamid ◽  
John Coltart
Keyword(s):  
Coronary Intervention ◽  
Coronary Stenting ◽  
Percutaneous Coronary Interventions ◽  
Vascular Response ◽  
Stent Restenosis ◽  
Percutaneous Coronary ◽  
Drug Eluting ◽  
Artery Disease ◽  
In Stent Restenosis

Over the last three decades, percutaneous coronary intervention (PCI) technology has revolutionized the field of cardiology. PCI began in the form of balloon angioplasty, and was followed by coronary stenting. In-Stent restenosis is the main limitation of coronary stenting, and has been delayed to some extent by the development of drug eluting stents. Coronary angioplasty with stenting is currently the most popular non-medical treatment of coronary artery disease therefore solving the problem of in-stent restenosis could change the future role of other types of coronary intervention. This review examines the types of percutaneous coronary interventions, the mechanisms leading up to in-stent restenosis, and how previous and current treatments of in-stent restenosis influence the vascular response to injury.

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