cardiovascularКардиоваскулярная терапия и профилактикаCardiovascular Therapy and Prevention1728-88002619-0125«SILICEA-POLIGRAF» LLC10.15829/1728-8800-2013-3-4-9cardiovascular-186Research ArticleИШЕМИЧЕСКАЯ БОЛЕЗНЬ СЕРДЦАCORONARY HEART DISEASEФАКТОРЫ РИСКА РЕСТЕНОЗА ПОСЛЕ КОРОНАРНОГО СТЕНТИРОВАНИЯ У ПАЦИЕНТОВ С ОЖИРЕНИЕМRESTENOSIS RISK FACTORS AFTER CORONARY ARTERY STENTING IN OBESE PATIENTSВеселовскаяН. Г.VeselovskayaN. G.

к.м.н., с.нс. отдела мультифокального атеросклероза

врач

ЧумаковаГ. А.ChumakovaG. A.

в.н.с. отдела мультифокального атеросклероза

д.м.н., профессор кафедры госпитальной и поликлинической терапии

Тел.: 8–903–910–80–40

tel.: 8–903–910–80–40

a.chumakova@mail.ruЕлыкомовВ. А.ElykomovV. A.

д.м.н., профессор, главный врач Алтайского краевого кардиологического диспансера

ГриценкоО. В.GritsenkoO. V.

аспирант кафедры госпитальной и поликлинической терапии

ДашковаА. А.DashkovaA. A.

н.с. отдела мультифокального атеросклероза

ТрубинаЕ. В.TrubinaE. V.

к.м.н., врач функциональной диагностики

КиселеваЕ. В.KiselevaE. V.

к.м.н., зав. отделением восстановительного лечения

ФГБУ НИИ Комплексных проблем сердечно-сосудистых заболеваний СО РАМН, Кемерово; Алтайский краевой кардиологический диспансер, БарнаулResearch Institute of Complex Cardiovascular Problems, Siberian Branch, Russian Academy of Medical Sciences, Kemerovo; Altay Region Cardiology Dispanser, BarnaulФГБУ НИИ Комплексных проблем сердечно-сосудистых заболеваний СО РАМН, Кемерово; Алтайский государственный медицинский университет, БарнаулResearch Institute of Complex Cardiovascular Problems, Siberian Branch, Russian Academy of Medical Sciences, Kemerovo; Altay State Medical University, BarnaulАлтайский краевой кардиологический диспансер, Барнаул; Алтайский государственный медицинский университет, БарнаулAltay Region Cardiology Dispanser, Barnaul; Altay State Medical University, BarnaulАлтайский государственный медицинский университет, БарнаулAltay State Medical University, BarnaulАлтайский краевой кардиологический диспансер, БарнаулAltay Region Cardiology Dispanser, Barnaul20132006201312349Copyright © Веселовская Н.Г., Чумакова Г.А., Елыкомов В.А., Гриценко О.В., Дашкова А.А., Трубина Е.В., Киселева Е.В., 20132013Веселовская Н.Г., Чумакова Г.А., Елыкомов В.А., Гриценко О.В., Дашкова А.А., Трубина Е.В., Киселева Е.В.Veselovskaya N.G., Chumakova G.A., Elykomov V.A., Gritsenko O.V., Dashkova A.A., Trubina E.V., Kiseleva E.V.Данная работа распространяется под лицензией Creative Commons Attribution 4.0.This work is licensed under a Creative Commons Attribution 4.0 License.https://cardiovascular.elpub.ru/jour/article/view/186Цель

Цель. Изучить роль эпикардиального ожирения (Ож) и других метаболических факторов в риске развития рестеноза коронарных артерий (КА) после стентирования.

Материал и методы

Материал и методы. В исследование были включены 68 мужчин с ишемической болезнью сердца (ИБС): стенокардией напряжения II–III функциональных классов (ФК), в возрасте 38–70 лет (средний возраст 54,4±9,1). Все пациенты имели Ож I–III степени, индекс массы тела (ИМТ) 33,71±3,02 кг/м2 . Ангиопластика со стентированием одной или двух КА всем больным выполнялась в плановом порядке по показаниям. Проводилась оценка основных и дополнительных метаболических фак- торов риска (лептин, резистин), провоспалительных маркеров — интерлейкин 6 (ИЛ-6), фактор некроза опухоли α (ФНО-α). Эпикардиальное ОЖ оценивалось с помощью трансторакальной эхокардиографии (ЭхоКГ) — в В-режиме проводилось линейное измерение толщины эпикардиальной жировой ткани (тЭЖТ) за правым желудочком.

Результаты

Результаты. В течение первого года после стентирования у 28% пациентов был выявлен рестеноз в зоне вмешательства. Максимальный вклад в развитие рестеноза по результатам дискри- минантного анализа показали: ИЛ-6, адипонектин, тЭЖТ, лептин. Значения тЭЖТ у пациентов с рестенозом составили 8 (5;10) мм, и были почти в 2 раза выше, чем у мужчин без рестеноза 4,3 (3;6) мм (р3 мм рестеноз КА определялся у 38%, при показателях тЭЖТ>5 мм рестеноз определяли у 52% пациентов, при тЭЖТ >7 мм — у 66%. Результаты многофакторного анализа выявили, что сочетание эпикардиального Ож с исходным повышением ИЛ-6 и лептина оказывало значимое влияние на развитие рестеноза (ОШ 18,9; 95%ДИ 8–145; р<0,001).

Заключение

Заключение. Повышенные показатели тЭЖТ по данным ЭхоКГ связаны с риском развития рестеноза. Сочетание эпикардиального Ож с исходным повышением провоспалительных маркеров и показателей нейрогуморальной активности висцерального жира оказывает значимое влияние на развитие осложнений после реваскуляризации миокарда.

Aim

Aim. To assess the role of epicardial obesity (O) and other metabolic factors in the development of coronary artery (CA) restenosis after CA stenting.

Material and methods

Material and methods. The study included 68 men with coronary heart disease (CHD), Functional Class II–III effort angina, aged 38–70 years (mean age 54,4±9,1 years). All participants had Stage I–III O, with the mean body mass index (BMI) of 33,71±3,02 kg/m2. All patients underwent planned angioplasty and stenting of one or two CA. The levels of major and additional metabolic risk factors (leptin, resistin) and proinflammatory markers (interleukin (IL) 6, tumour necrosis factor (TNF) α) were measured. Epicardial obesity was assessed using transthoracic echocardiography (EchoCG) in B-mode, with the linear measurement of epicardial adipose tissue (EAT) behind the right ventriculum.

Results

Results. During the first year after CA stenting, 28% of the patients developed in-stent restenosis. The most important determinants of the restenosis risk were IL-6, adiponectin, EAT thickness, and leptin. In patients with restenosis, the mean EAT thickness value (8 (5–10) mm) was almost twice as large as in restenosis-free patients (4,3 (3–6) mm; p<0,001). In participants with EAT thickness >3 mm, 38% had CA restenosis; for patients with EAT thickness of >5 mm and >7 mm, the respective figures were 52% and 66%. The multivariate analysis results suggested that the combination of epicardial O and baseline elevation of IL-6 and leptin significantly increases the risk of restenosis (odds ratio 18,9; 95% confidence interval 8–145; p<0,001).

Conclusion

Conclusion. Increased EAT thickness at EchoCG was linked to the risk of restenosis. The combination of epicardial O and baseline elevation of pro-inflammatory markers and markers of neurohumoral activation of visceral fat tissue has a significant impact on the risk of myocardial revascularisation complications.

эпикардиальное ожирениеадипокиныинтерлейкин-6коронарное стентированиесердечно-сосудистые осложненияepicardial obesityadipokinescoronary artery stentingcardiovascular complicationsReferencesDogdu O, Yarlioglues M, Kaya MG, et al. Long term clinical outcomes of brachytherapy, bare-metal stenting, and drug-eluting stenting for de novo and in-stent restenosis lesions: Five year follow-up. Cardiol J 2011; 18 (6): 654–6.Dogdu O, Yarlioglues M, Kaya MG, et al. Long term clinical outcomes of brachytherapy, bare-metal stenting, and drug-eluting stenting for de novo and in-stent restenosis lesions: Five year follow-up. Cardiol J 2011; 18 (6): 654–6.Gustafsson F, Kragelund CB, Torp-Pedersen C, et al. Effect of obesity and being overweight on long-term mortality in congestive heart failure: influence of left ventricular systolic function. Eur Heart J 2005; 26 (1): 58–64.Gustafsson F, Kragelund CB, Torp-Pedersen C, et al. Effect of obesity and being overweight on long-term mortality in congestive heart failure: influence of left ventricular systolic function. Eur Heart J 2005; 26 (1): 58–64.Lavie CJ, Osman AF, Milani RV, et al. Body composition and prognosis in chronic systolic heart failure: the obesity paradox. Am J Cardiol 2003; 91 (7): 891–4.Lavie CJ, Osman AF, Milani RV, et al. Body composition and prognosis in chronic systolic heart failure: the obesity paradox. Am J Cardiol 2003; 91 (7): 891–4.Montani JP, Carroll JF, Dwyer TM. Ectopic fat storage in heart, blood vessels and kidneys in the pathogenesis of cardiovascular diseases. Int J Obes Relat Metab Disord 2004; 28 (4): 58–65.Montani JP, Carroll JF, Dwyer TM. Ectopic fat storage in heart, blood vessels and kidneys in the pathogenesis of cardiovascular diseases. Int J Obes Relat Metab Disord 2004; 28 (4): 58–65.Iacobellis G, Barbaro G. The double role of epicardial adipose tissue as pro- and anti-inflammatory organ. Horm Metab Res 2008; 40 (7): 442–5.Iacobellis G, Barbaro G. The double role of epicardial adipose tissue as pro- and anti-inflammatory organ. Horm Metab Res 2008; 40 (7): 442–5.Jeong JW, Jeong MH, Yun KH, et al. Echocardiographic epicardial fat thickness and coronary artery disease. Circ J 2007; 71 (4): 536–9.Jeong JW, Jeong MH, Yun KH, et al. Echocardiographic epicardial fat thickness and coronary artery disease. Circ J 2007; 71 (4): 536–9.Eroglu S, Sade LE, Yildirir A, et al. Epicardial adipose tissue thickness by echocardiography is a marker for the presence and severity of coronary artery disease. Nutr Metab Cardiovasc Dis 2009; 19 (3): 211–7.Eroglu S, Sade LE, Yildirir A, et al. Epicardial adipose tissue thickness by echocardiography is a marker for the presence and severity of coronary artery disease. Nutr Metab Cardiovasc Dis 2009; 19 (3): 211–7.Curcio A, Torella D, Indolf C. Mechanisms of smooth muscle cell proliferation and enothelial regeneration after vascular injury and stenting. Circulation J 2011; 75: 1287–97.Curcio A, Torella D, Indolf C. Mechanisms of smooth muscle cell proliferation and enothelial regeneration after vascular injury and stenting. Circulation J 2011; 75: 1287–97.Cheng KH, Chu CS, Lee KT, et al. Adipocytokines and proinflamatory mediators from abdominal and epicardial adipose tissue in patients with coronary artery disease. Int J Obes (Lond) 2008; 32 (2): 268–74.Cheng KH, Chu CS, Lee KT, et al. Adipocytokines and proinflamatory mediators from abdominal and epicardial adipose tissue in patients with coronary artery disease. Int J Obes (Lond) 2008; 32 (2): 268–74.Eiras S, Teijeira-Fernández E, Shamagian LG, et al. Extension of coronary artery disease is associated with increased IL-6 expression and decreased adiponectin gene expression in epicardial adipose tissue. Cytokine 2008; 43 (2): 174–80.Eiras S, Teijeira-Fernández E, Shamagian LG, et al. Extension of coronary artery disease is associated with increased IL-6 expression and decreased adiponectin gene expression in epicardial adipose tissue. Cytokine 2008; 43 (2): 174–80.Iacobellis G, Willens HJ. Echocardiographic Epicardial Fat: A Review of Research and Clinical Applications. JASE 2009; 22: 1311–9.Iacobellis G, Willens HJ. Echocardiographic Epicardial Fat: A Review of Research and Clinical Applications. JASE 2009; 22: 1311–9.Danesh J, Kaptoge S, Mann AG, et al. Long-term interleukin-6 levels and subsequent risk of coronary heart disease: two new prospective studies and a systematic review. PLoS Med 2008; 5 (4): 78–85.Danesh J, Kaptoge S, Mann AG, et al. Long-term interleukin-6 levels and subsequent risk of coronary heart disease: two new prospective studies and a systematic review. PLoS Med 2008; 5 (4): 78–85.Patterson CC, Smith AE, Yarnell JW, et al. The associations of interleukin-6 (IL-6) and downstream inflammatory markers with risk of cardiovascular disease: the Caerphilly Study. Atherosclerosis 2010; 209 (2): 551–7.Patterson CC, Smith AE, Yarnell JW, et al. The associations of interleukin-6 (IL-6) and downstream inflammatory markers with risk of cardiovascular disease: the Caerphilly Study. Atherosclerosis 2010; 209 (2): 551–7.Singh N, Singh H, Khanijoun HK. Echocardiographic Assessment of Epicardial Adipose Tissue — A Marker of Visceral Adiposity. Mcgill J Med 2007; 10 (1): 26–30.Singh N, Singh H, Khanijoun HK. Echocardiographic Assessment of Epicardial Adipose Tissue — A Marker of Visceral Adiposity. Mcgill J Med 2007; 10 (1): 26–30.Szkodzinski J, Blazelonis A, Wilczek K, et al. The role of interleukin-6 and transforming growth factor-beta1 in predicting restenosis within stented infarct-related artery. Int J Immunopathol Pharmacol 2009; 22 (2): 493–500.Szkodzinski J, Blazelonis A, Wilczek K, et al. The role of interleukin-6 and transforming growth factor-beta1 in predicting restenosis within stented infarct-related artery. Int J Immunopathol Pharmacol 2009; 22 (2): 493–500.Funayama H, Ishikawa SE, Kubo N, et al. Close association of regional interleukin-6 levels in the infarct-related culprit coronary artery with restenosis in acute myocardial infarction. Circ J 2006; 70 (4): 426–9.Funayama H, Ishikawa SE, Kubo N, et al. Close association of regional interleukin-6 levels in the infarct-related culprit coronary artery with restenosis in acute myocardial infarction. Circ J 2006; 70 (4): 426–9.Correia ML, Haynes WG. Leptin, obesity and cardiovascular disease. Curr Opin Nephrol Hypertens 2004; 13: 215–23.Correia ML, Haynes WG. Leptin, obesity and cardiovascular disease. Curr Opin Nephrol Hypertens 2004; 13: 215–23.Chiba T, Shinozaki S, Nakazawa T. Leptin deficiency suppresses progression of atherosclerosis in apoE-deficient mice. Atherosclerosis 2008; 196: 68–75.Chiba T, Shinozaki S, Nakazawa T. Leptin deficiency suppresses progression of atherosclerosis in apoE-deficient mice. Atherosclerosis 2008; 196: 68–75.Han SH, Quon MJ, Koh KK. Reciprocal relationships between abnormal metabolic parameters and endothelial dysfunction. Curr Op Lipidol 2007; 18: 58–65.Han SH, Quon MJ, Koh KK. Reciprocal relationships between abnormal metabolic parameters and endothelial dysfunction. Curr Op Lipidol 2007; 18: 58–65.Schulze MB, Shai I, Rimm EB. Adiponectin and future coronary heart disease events among men with type 2 diabetes. Diabetes 2005; 54: 534–9.Schulze MB, Shai I, Rimm EB. Adiponectin and future coronary heart disease events among men with type 2 diabetes. Diabetes 2005; 54: 534–9.Kubota N, Terauchi Y, Yamauchi T. Disruption of adiponectin causes insulin resistance and neointimal formation. J Biol Chem 2002; 277: 25863–6.Kubota N, Terauchi Y, Yamauchi T. Disruption of adiponectin causes insulin resistance and neointimal formation. J Biol Chem 2002; 277: 25863–6.Piatti P, Di Mario C, Monti LD. 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 P, Di Mario C, Monti LD. Association of insulin resistance, hyperleptinemia, and impaired nitric oxide release with in-stent restenosis in patients undergoing coronary stenting. Circulation 2003; 108: 2074–81.Bienertová-Vasků JA, Hlinomaz O, Vasků A. Are common leptin promoter polymorphisms associated with restenosis after coronary stenting? Heart Vessels 2007; 22 (5): 310–5.Bienertová-Vasků JA, Hlinomaz O, Vasků A. Are common leptin promoter polymorphisms associated with restenosis after coronary stenting? Heart Vessels 2007; 22 (5): 310–5.Mazurek T, Zhang L, Zalewski A, et al. Human epicardial adipose tissue is a source of inflammatory mediators. Circulation 2003; 108: 2460–6.Mazurek T, Zhang L, Zalewski A, et al. Human epicardial adipose tissue is a source of inflammatory mediators. Circulation 2003; 108: 2460–6.Ahn SG, Lim HS, Joe DY. Relationship of epicardial adipose tissue by echocardiography to coronary artery disease. Heart 2008; 94: 7–13.Ahn SG, Lim HS, Joe DY. Relationship of epicardial adipose tissue by echocardiography to coronary artery disease. Heart 2008; 94: 7–13.

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