cardiovascularКардиоваскулярная терапия и профилактикаCardiovascular Therapy and Prevention1728-88002619-0125«SILICEA-POLIGRAF» LLCcardiovascular-1207Research ArticleМНЕНИЕ ПО ПРОБЛЕМЕФакторы риска рестеноза после коронарного стентирования у больных с метаболическим синдромомRestenosis risk factors after coronary stenting in metabolic syndrome patientsДаниловН. М.DanilovN. M.ndanilov@yandex.ruГоргадзеТ. Т.GorgadzeT. T.ndanilov@yandex.ruСавченкоА. П.SavchenkoA. P.ndanilov@yandex.ruЧазоваИ. Е.ChazovaI. E.ndanilov@yandex.ruНИИ клинической кардиологии им. А.Л. Мясникова ФГУ РКНПК Росздрава, МоскваРоссияA.L. Myasnikov Institute of Clinical Cardiology, Russian Cardiology Scientific and Clinical Complex, State Federal Agency for Health and Social Development, MoscowRussian Federation200720042007627174Copyright © Данилов Н.М., Горгадзе Т.Т., Савченко А.П., Чазова И.Е., 20072007Данилов Н.М., Горгадзе Т.Т., Савченко А.П., Чазова И.Е.Danilov N.M., Gorgadze T.T., Savchenko A.P., Chazova I.E.This work is licensed under a Creative Commons Attribution 4.0 License.https://cardiovascular.elpub.ru/jour/article/view/1207

Настоящий обзор посвящен проблеме формирования рестенозов коронарных артерий после имплантации стентов у больных с метаболическим синдромом (МС). Известно, что целый ряд клинических факторов повышает риск развития рестенозов. На первом месте в этом ряду стоит сахарный диабет. В последнее время появились убедительные данные, указывающее на то, что МС является заболеванием, ускоряющим развитие коронарных рестенозов. Такие проявления МС, как пониженное высвобождение NO после перорального теста толерантности к глюкозе, повышенный уровень лептина, гиперинсулинемия и инсулинорезистентность являются важными предикторами развития рестеноза внутри стента у больных ишемической болезнью сердца (ИБС) с нормальными уровнями глюкозы натощак и гликированного гемоглобина. Совокупность проанализированных данных позволяет выделить группу больных ИБС с МС, которым следует рекомендовать использование стентов нового поколения с антипролиферативным покрытием.

This review is devoted to coronary restenosis after stent implantation in metabolic syndrome (MS) patients. It is known that some clinical factors increase restenosis risk, first of all, diabetes mellitus. Recently, MS has also been regarded as a pathology enhancing coronary restenosis risk. Certain MS features (reduced NO release after oral glucose tolerance test; increased leptin level; hyperinsulinemia, insulin resistance) are important predictors of intra-stent restenosis in coronary heart disease (CHD) patients with normal fasting levels of glucose and glycated hemoglobin. In CHD and MS patients, new, antiproliferative drug-coated stent use could be recommended.

коронарное стентированиеметаболический синдромпокрытые стентыфакторы рискарестенозcoronary stentingmetabolic syndromecoated stentsrisk factorsrestenosisReferencesMyers PR, Webel R, Thondapu V, et al. Restenosis is associated with decreased coronary artery nitric oxide synthase. Int J Cardiol 1996; 55: 183-91.Myers PR, Webel R, Thondapu V, et al. Restenosis is associated with decreased coronary artery nitric oxide synthase. Int J Cardiol 1996; 55: 183-91.Wu TC, Chen YH, Chen JW, et al. Impaired forearm reactive hyperemia is related to late restenosis after coronary stenting. Am J Cardiol 2000; 85: 1071-6.Wu TC, Chen YH, Chen JW, et al. Impaired forearm reactive hyperemia is related to late restenosis after coronary stenting. Am J Cardiol 2000; 85: 1071-6.Ikeda U, Yamamoto K, Maeda Y, et al. Endothelin-1 inhibits nitric oxide synthesis in vascular smooth muscle cells. Hypertension 1997; 29: 65-9.Ikeda U, Yamamoto K, Maeda Y, et al. Endothelin-1 inhibits nitric oxide synthesis in vascular smooth muscle cells. Hypertension 1997; 29: 65-9.Piatti PM, Fragasso G, Monti LD, et al. Acute intravenous L-arginine infusion decreases endothelin-1 levels and improves endothelial function in patients with angina pectoris and normal coronary arteriograms: correlation with asymmetric dimetylarginine levels. Circulation 2003; 107: 429-36.Piatti PM, Fragasso G, Monti LD, et al. Acute intravenous L-arginine infusion decreases endothelin-1 levels and improves endothelial function in patients with angina pectoris and normal coronary arteriograms: correlation with asymmetric dimetylarginine levels. Circulation 2003; 107: 429-36.Piatti PM, Colombo A, Carlo DM, et al. Association of Insulin Resistance, Hyperleptinemia, and Impaired Nitric Oxide Release With In-Stent Restenosis in Patients Undergoing Coronary Stenting. Circulation 2003; 108: 2074-81.Piatti PM, Colombo A, Carlo DM, et al. Association of Insulin Resistance, Hyperleptinemia, and Impaired Nitric Oxide Release With In-Stent Restenosis in Patients Undergoing Coronary Stenting. Circulation 2003; 108: 2074-81.Cooke JP, Oka RK. Does leptin cause vascular disease? Circulation 2002; 106: 1904-5.Cooke JP, Oka RK. Does leptin cause vascular disease? Circulation 2002; 106: 1904-5.Recchia FA, Vogel TR, Hintze TH. NO metabolites accumulate in erythrocyte in proportion to carbon dioxide and bicarbonate concentration. Am J Physiol Heart Circ Physiol 2000; 279: H852-6.Recchia FA, Vogel TR, Hintze TH. NO metabolites accumulate in erythrocyte in proportion to carbon dioxide and bicarbonate concentration. Am J Physiol Heart Circ Physiol 2000; 279: H852-6.Piatti P, Fragasso G, Monti LD, et al. Endothelial and metabolic characteristics of patients with angina and angiographically normal coronary arteries: comparison with subjects with insulin resistance syndrome and normal controls. JACC 1999; 34: 1452-60.Piatti P, Fragasso G, Monti LD, et al. Endothelial and metabolic characteristics of patients with angina and angiographically normal coronary arteries: comparison with subjects with insulin resistance syndrome and normal controls. JACC 1999; 34: 1452-60.Yamagishi SI, Edelstein D, Du XL, et al. Leptin induces mito4 chondrial superoxide production and monocyte chemoattractant protein-1 expression in aortic endothelial cells by increasing fatty acid oxidation via protein kinase. A J Biol Chem 2001; 276: 25096-100.Yamagishi SI, Edelstein D, Du XL, et al. Leptin induces mito4 chondrial superoxide production and monocyte chemoattractant protein-1 expression in aortic endothelial cells by increasing fatty acid oxidation via protein kinase. A J Biol Chem 2001; 276: 25096-100.Wallace AM, Mc Mahon AD, Packard CJ, et al. Plasma leptin and the risk of cardiovascular disease in the West of Scotland Coronary Prevention Study (WOSCOPS). Circulation 2001; 104: 3052-6.Wallace AM, Mc Mahon AD, Packard CJ, et al. Plasma leptin and the risk of cardiovascular disease in the West of Scotland Coronary Prevention Study (WOSCOPS). Circulation 2001; 104: 3052-6.Doehner W, Rauchhaus M, Godsland IF, et al. Insulin resistance in moderate chronic heart failure is related to hyperleptinemia, but not to norepinephrine or TNF-alpha. Int J Cardiol 2002; 83: 73-81.Doehner W, Rauchhaus M, Godsland IF, et al. Insulin resistance in moderate chronic heart failure is related to hyperleptinemia, but not to norepinephrine or TNF-alpha. Int J Cardiol 2002; 83: 73-81.Soderberg S, Stegmayr B, Ahlbeck4Glaber C, et al. High leptin levels are associated with stroke. Cerebrovasc Dis 2003; 15: 63-9.Soderberg S, Stegmayr B, Ahlbeck4Glaber C, et al. High leptin levels are associated with stroke. Cerebrovasc Dis 2003; 15: 63-9.Versaci F, Gaspardone A, Tomai F, et al. Immunosuppressive therapy for the prevention of restenosis after coronary artery stent implantation (IMPRESS Study). JACC 2002; 40: 1935-42.Versaci F, Gaspardone A, Tomai F, et al. Immunosuppressive therapy for the prevention of restenosis after coronary artery stent implantation (IMPRESS Study). JACC 2002; 40: 1935-42.Schillinger M, Exner M, Mlekusch W, et al. Acute-phase response after stent implantation in the carotid artery: association with 6-month in-stent restenosis. Radiology 2003; 227: 516-21.Schillinger M, Exner M, Mlekusch W, et al. Acute-phase response after stent implantation in the carotid artery: association with 6-month in-stent restenosis. Radiology 2003; 227: 516-21.Matthews DR, Hosker JP, Rudenski AS, et al. Homeostasis model assessment: insulin resistance and beta-cell function from fasting plasma glucose and insulin concentrations in man. Diabetologia 1985; 28: 412-9.Matthews DR, Hosker JP, Rudenski AS, et al. Homeostasis model assessment: insulin resistance and beta-cell function from fasting plasma glucose and insulin concentrations in man. Diabetologia 1985; 28: 412-9.Bergman RN. Lilly lecture 1989. Toward physiological understanding of glucose tolerance: minimal-model approach. Diabetes 1989; 38: 1512-27.Bergman RN. Lilly lecture 1989. Toward physiological understanding of glucose tolerance: minimal-model approach. Diabetes 1989; 38: 1512-27.Takagi T, Yoshida K, Akasaka T, et al. Hyperinsulinemia during oral glucose tolerance test is associated with increased neointimal tissue proliferation after coronary stent implantation in non diabetic patients: a serial intravascular ultrasound study. JACC 2000; 36: 731-8.Takagi T, Yoshida K, Akasaka T, et al. Hyperinsulinemia during oral glucose tolerance test is associated with increased neointimal tissue proliferation after coronary stent implantation in non diabetic patients: a serial intravascular ultrasound study. JACC 2000; 36: 731-8.Iozzo P, Chareonthaitawee P, Dutka D, et al. Independent asso4 ciation of type 2 diabetes and coronary artery disease with myocardial insulin resistance. Diabetes 2002; 51: 3020-4.Iozzo P, Chareonthaitawee P, Dutka D, et al. Independent asso4 ciation of type 2 diabetes and coronary artery disease with myocardial insulin resistance. Diabetes 2002; 51: 3020-4.Kahn SE. The relative contributions of insulin resistance and beta-cell dysfunction to the pathophysiology of type 2 diabetes. Diabetologia 2003; 46: 3-19.Kahn SE. The relative contributions of insulin resistance and beta-cell dysfunction to the pathophysiology of type 2 diabetes. Diabetologia 2003; 46: 3-19.Bergman RN, Finegood DT, Kanh SE. The evolution of beta-cell dysfunction and insulin resistance in type 2 diabetes. Eur J Clin Invest 2002; 32(Suppl 3): 35-45.Bergman RN, Finegood DT, Kanh SE. The evolution of beta-cell dysfunction and insulin resistance in type 2 diabetes. Eur J Clin Invest 2002; 32(Suppl 3): 35-45.The Decode Study Group. Glucose tolerance and mortality: comparison of WHO and American Diabetes Association diagnostic criteria. Lancet 1999; 354: 617-21.The Decode Study Group. Glucose tolerance and mortality: comparison of WHO and American Diabetes Association diagnostic criteria. Lancet 1999; 354: 617-21.Norhammar A, Tenerz A, Nilsson G, et al. Glucose metabolism in patients with acute myocardial infarction and no previous diagnosis of diabetes mellitus: a prospective study. Lancet 2002; 359: 2140-4.Norhammar A, Tenerz A, Nilsson G, et al. Glucose metabolism in patients with acute myocardial infarction and no previous diagnosis of diabetes mellitus: a prospective study. Lancet 2002; 359: 2140-4.Morice MC, Serruys PW, Sousa JE, et al. A randomized comparison of a sirolimus-eluting stent with a standard stent for coronary revascularisation. N Engl J Med 2002; 346: 1773-80.Morice MC, Serruys PW, Sousa JE, et al. A randomized comparison of a sirolimus-eluting stent with a standard stent for coronary revascularisation. N Engl J Med 2002; 346: 1773-80.Kaiser C, Brunner-La Rocca H, Buser P, et al. Incremental costeffectiveness of drug-eluting stents compared with a third-generation bare-metal stent in a real-world setting: randomised Basel Stent Kosten Effektivitats Trail (BASKET). Lancet 2005; 366: 921-9.Kaiser C, Brunner-La Rocca H, Buser P, et al. Incremental costeffectiveness of drug-eluting stents compared with a third-generation bare-metal stent in a real-world setting: randomised Basel Stent Kosten Effektivitats Trail (BASKET). Lancet 2005; 366: 921-9.

The authors declare that there are no conflicts of interest present.