Variation in serum visfatin levels 24 hours after coronary stent implantation

doi:10.3969/j.issn.2095-4344.2014.16.026

Abstract

Abstract:

BACKGROUND: Coronary stent implantation can cause blood vessel damage and wall reconstruction, leading to vascular stent restenosis. Studies have found that visfatin is associated with inflammatory reaction, and exhibits an increased expression at the site of plaque rupture in acute myocardial infarction.

OBJECTIVE: To investigate the influence of percutaneous coronary intervention on the levels of visfatin in patients with coronary heart disease.

METHODS: Thirty patients with acute myocardial infarction within 12 hours after the onset of the chest pain, 30 patients with unstable pectoris and 30 patients with stable angina pectoris were included. All patients were successfully treated by percutaneous coronary intervention. Meanwhile, 30 patients only undergoing coronary angiography but not stenting treatment were selected, and another 30 patients without any treatment served as normal control group.

RESULTS AND CONCLUSION: According to enzyme-linked immunosorbent method, the visfatin levels of acute myocardial infarction, unstable angina, stable angina and coronary angiography groups continue to rise at pre-operation, 30 minutes, 6 hours, 12 hours, 24 hours after operation, all of which were higher than that in the normal control group (P < 0.05). The results confirmed that within 24 hours after coronary stent implantation the visfatin levels continue to rise.

中国组织工程研究杂志出版内容重点：生物材料；骨生物材料; 口腔生物材料; 纳米材料; 缓释材料; 材料相容性；组织工程

全文链接：

Key words: coronary artery disease, coronary stenosis, inflammation, stents

CLC Number:

R318

Hou Yun, Ding Shi-fang, Wang Hui-jie, Jiang Ju-quan, Fu Wen-bo, Wang Hua, Chen Zhi-nan . Variation in serum visfatin levels 24 hours after coronary stent implantation[J]. Chinese Journal of Tissue Engineering Research, 2014, 18(16): 2619-2624.

Figures/Tables 1

References

[1] Kuvin JT, Kimmelstiel CD. Infection causes of atherosclerosis. Am Heart J. 1999;(137):216-226.
[2] Hatanaka K, Li XA, Masuda K, et al. Immunohistochemical localization of C-reactive protein binding sites in human aortic lesions by a modified streptavid in-biotin-staining method. Pathol Int. 1995(3):635-641.
[3] Torzewski J, Torzewski M, Bowyer DE, et al. C-reactive protein frequently colocates with the teruninal complement complex in the intima of early atherosclerotic lesions of human coronaryarteries. Arterioscler Thromb Vasc Biol. 1998(6):1386-1392.
[4] 邓新桃,何情,赵建祥,等.冠状动脉病变严重程度、冠心病介人治疗对QT离散度的影响[J].实用临床医药杂志,2007,(1):95-96.
[5] 张文利,黄定.PCI后冠状动脉再狭窄机制及防治研究进展[J].中国循证心血管医学杂志,2011,3(2):125-128.
[6] Komowski R, Hong MK, Tio FO, et al. In-stent retenosis: contribution of inflammatory responses and arterial injury to neointimal hyperplasia. J Am Coll Cardiol. 1998;31(1): 224-230.
[7] 徐伟斌,俞璐,罗敏.内脏素-又一新的脂肪因子[J].中国糖尿病杂志,2006,14:153-154.
[8] Fukuhara A, Matsuda M, Nishizawa M, et al. Vacating: a protein secreted by visceral fat thatmimics the effects of insulin. Science. 2005;307(5708):426-430.
[9] Samal B, Sun Y, Stearns G, et al. Cloning and characterization of the cDNA encoding a novel human pre-B-cell colony-enhancing factor. Mol Cell Biol. 1994; 14(2):1431-1437.
[10] Dahl TB, Yndestad A, Skjelland M, et al. Increased expression of visfatin in macrophages of human unstable carotid and coronary atherosclerosis: possible role in inflammation and plaque destabilization. Circulation. 2007; 115(8):972-980.
[11] Moschen AR, Kaser A, Enrich B, et al. Visfatin, an adipocytokine with proinflamma- tory and immunomodulating properties. J Immunol. 2007;178(3):1748-1758.
[12] 李虎,秦涛,贾国良,等.直接支架植入术对冠脉循环白细胞及血小板功能的影响[J].中国现代医学杂志, 2007,15(13): 1989-1991.
[13] 李璇,马根山,陈忠,等.川芎嗪洗脱支架对猪冠状动脉平滑肌细胞增殖和凋亡的影响[J].现代医学, 2008,36(4):236-239.
[14] 贡军丽,王瑛,杨德琼,等.冠状动脉介入治疗后相关细胞因子含量的变化及其意义[J].心血管康复医学杂志, 2008,17(5):428-430.
[15] 卢长青,邱春光,宋文翔,等. 冠脉内置入药物涂层支架与金属裸支架对血浆C反应蛋白水平影响的对比观察[J].河南医学研究, 2007,16(4):311-313.
[16] Filippatos TD, Derdemezis CS, Gazi IF, et al. Increased plasma visfatin levels in subjects with the metabolic syndrome. Eur J Clin Invest. 2008;38(1):71-72.
[17] Iwen KA, Senyaman O, Schwartz A, et al. Melanocortin crosstalk with adipose functions: ACTH directly induces insulin resistance, promotes a pro-inflammatory adipokine profile and stimulates UCP-1 in adipocytes. J Endocrinol. 2008;196(3):465-472.
[18] Adya R, Tan BK, Puan A, et al. Visfatin induces human endothelial VEGF and MMP-2 /9 production via MAPK and P13K/Akt signaling pathways:novel insights into visfatin induced angiogenesis. Cardiovase Res. 2008;78(2): 356-365.
[19] Hatanaka K, L iX A, M asudaK, et al. Immunohistochemical localization of C-reactive protein binding sites in humanaortic lesionsbya modified streptavid in-biotin-staining method. Pathol Int. 1995;45:635-641.
[20] Zwaka TP, Hombach V, Torzewski J. C-reactive protein mediated low density lipoprotein uptake bymacrophages implications for atherosclerosis. Circulation. 2001;103(9): 1194-1197.
[21] Tataru MC, Heinrich J, Junker R, et al. C-reactive protein and the sever ity of atherosc leros is in m yocard ial in farction patients with stable angina pectoris. Eur Heart J. 2000;21(12): 1000-1008.
[22] 张慧平,孙福成,季福绥,等.C-反应蛋白与冠心病关系的研究[J].心血管康复医学杂志,2007,16:223-225.
[23] 王文清,宁波,王新宴,等.C-反应蛋白与冠心病病变程度的相关性[J].心脏杂志,2006,(3):323-325.
[24] Kai H, Ikeda H, Yasukawa H, et al. Peripheral blood levels of matrix metalloproteinase 2 and 9 are elevated in patients with acute coronary syndrome. J Am Coll Cardiol. 1998;32(2): 368-372.
[25] Huang T, Cheng J, Zheng YF. In vitro degradation and biocompatibility of Fe-Pd and Fe-Pt composites fabricated by spark plasma sintering. Mater Sci Eng C Mater Biol Appl. 2014;35:43-53.
[26] Li L, Mirhosseini N, Michael A, et al. Enhancement of endothelialisation of coronary stents by laser surface engineering. Lasers Surg Med. 2013;45(9):608-616.
[27] Martin D, Boyle F. Finite element analysis of balloon-expandable coronary stent deployment: influence of angioplasty balloon configuration. Int J Numer Method Biomed Eng. 2013;29(11):1161-1175.
[28] Boyle CJ, Lennon AB, Prendergast PJ. Application of a mechanobiological simulation technique to stents used clinically. J Biomech. 2013;46(5):918-924.
[29] Walker AM, Johnston CR, Rival DE. The quantification of hemodynamic parameters downstream of a Gianturco Zenith stent wire using newtonian and non-newtonian analog fluids in a pulsatile flow environment. J Biomech Eng. 2012; 134(11): 111001.
[30] Tambaca J, Canic S, Kosor M, et al. Mechanical behavior of fully expanded commercially available endovascular coronary stents. Tex Heart Inst J. 2011;38(5):491-501.
[31] Crowder SW, Gupta MK, Hofmeister LH, et al. Modular polymer design to regulate phenotype and oxidative response of human coronary artery cells for potential stent coating applications. Acta Biomater. 2012;8(2):559-569.
[32] Gastaldi D, Sassi V, Petrini L, et al. Continuum damage model for bioresorbable magnesium alloy devices - application to coronary stents. J Mech Behav Biomed Mater. 2011;4(3): 352-365.
[33] Boyle CJ, Lennon AB, Early M, et al. Computational simulation methodologies for mechanobiological modelling: a cell-centred approach to neointima development in stents. Philos Trans A Math Phys Eng Sci. 2010;368(1921):2919-2935.
[34] Karagkiozaki VC, Logothetidis SD, Kassavetis SN, et al. Nanomedicine for the reduction of the thrombogenicity of stent coatings. Int J Nanomedicine. 2010;5:239-248.