Abstract

Introduction. Cardiovascular disease has been the leading cause of death and disability worldwide for many years. The widespread use of percutaneous coronary intervention has significantly improved clinical outcomes in patients with cardiovascular diseases. However, inflammatory reactions that occur in response to mechanical stretch, endothelial exposure and subintimal hemorrhage play a key role, triggering a cascade of proliferative processes leading to neointimal hyperplasia and restenosis. Aim. Aim of this review was to study the known mechanisms of coronary restenosis and to search possible new risk factors for in-stent restenosis. Material and methods. A review of current medical publications in PubMed, MedLine, Google Scholar, ScienceDirect was carried out. Search coverage included articles published from 1993 to 2021. Results and discussion. Risk factors for restenosis have been shown, such as genetic, mechanical (under exploitation, fracture, excessive dilatation, polymer damage), high level of systemic inflammation. In addition, it has been shown that vitamin D deficiency can also be a risk factor for atherosclerosis and immune inflammation. Conclusion. The in-stent restenosis is an actual problem. Incidence of in-stent restenosis has been reported in up to 10% after percutaneous coronary intervention. Multiple mechanical, genetic and inflammatory factors might contribute to in-stent restenosis. In recent years, serum levels of NT-proBNP, pentraxin-3, vitamin D have been studied as restenosis risk factors. Further research of this subject may allowed to develop methods for preventing this complication.

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