Endothelial dysfunction mediated by interleukin-18 in patients with ischemic heart disease undergoing coronary artery bypass grafting surgery

被引:11
作者
Jadranko, Sokolic [1 ]
Tokmadzic, Vlatka Sotosek [1 ,2 ]
Danijel, Knezevic [2 ]
Igor, Medved [3 ]
Nada, Vukelic Damjani [4 ]
Sanja, Balen [4 ]
Marijana, Rakic [5 ]
Ana, Lanca Bastiancic [5 ]
Gordana, Laskarin [5 ,6 ]
机构
[1] Clin Hosp Ctr Rijeka, Clin Anesthesiol & Intens Care Med, Kresimirova 42, Rijeka 51000, Croatia
[2] Univ Rijeka, Fac Med, Dept Anesthesiol Reanimatol & Intens Care, B Branchetta 20, Rijeka 51000, Croatia
[3] Univ Rijeka, Fac Med, Dept Surg, Tome Strizica 3, Rijeka 51000, Croatia
[4] Clin Hosp Ctr Rijeka, Dept Transfus Med, Kresimirova 42, Rijeka 51000, Croatia
[5] Hosp Med Rehabil Hearth & Lung Dis & Rheumatism T, Div Cardiol, M Tita 188, Opatija 51410, Croatia
[6] Univ Rijeka, Med Fac, Dept Physiol & Immunol, B Branchetta 20, Rijeka 51000, Croatia
关键词
ACUTE MYOCARDIAL-INFARCTION; CARDIOPULMONARY BYPASS; DECIDUAL LYMPHOCYTES; CYTOTOXIC ACTIVITY; GLYCOCALYX; CELLS; INFLAMMATION; EXPRESSION; ADHESION; RISK;
D O I
10.1016/j.mehy.2017.05.009
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
When medication management or percutaneous coronary intervention is not successful in patients with advanced ischemic heart disease, surgical revascularisation predominantly coronary artery bypass grafting (CABG) is considered the gold standard. However, CABG surgery can lead to ischemia/reperfusion injury, which is characterized by a strong inflammatory response. Interleukin (IL)-18, is a strong inflammatory mediator, that is released from cardiomyocytes and can be found in the systemic circulation of patients during and immediately after CABG surgery. The existing damage of endothelial glycocalyx in patients with ischemic heart disease is further impaired concurrently during the surgery due to the anaesthesia-surgical technique used and intravascular fluid loading. This results in the increased incidence of adverse events, including myocardial infarction. IL-18 leads to the activation of lymphocyte cytotoxicity via cytotoxic mediators (Fas ligand, Tumour necrosis factor (TNF)-related apoptosis-inducing ligand, perfotin, and granulysin). We hypothesize that IL-18 is released locally in the heart and the systemic circulation in patients undergoing CABG surgery and may be correlated with the level of activity of circulating lymphocytes. In turn, this may lead to lymphocyte-mediated cytotoxicity directed toward damaged and activated endothelial cells. Shear stress glycocalyx, as well as damaged and activated endothelial cells then become the main the source of pro-inflammatory cytokines, chemokines, and adhesion molecules. These attract activated lymphocytes to adhere to the endothelium or enter the subintimal layer, increasing existing or initiating the formation of new plaques, which leads to the development of myocardial infarction during or shortly after surgery. To evaluate our hypothesis, we will measure the local concentration of IL-18 in the sinus coronarius and systemic circulation. These values will then be correlated with immunological and biochemical parameters, predominantly with the concentration of degradation products of glycocalyx and cytotoxic mediators in activated lymphocytes. If our hypothesis is correct, measuring the IL-18 concentration that is responsible for glycocalyx deterioration, may become a useful tool for predicting myocardial infarction occurrence in patients undergoing CABG surgery. (C) 2017 Elsevier Ltd. All rights reserved.
引用
收藏
页码:20 / 24
页数:5
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