循环中脂蛋白相关磷脂酶A2与stanford B型主动脉夹层支架置入术后不良事件的相关性

Abstract
Figure/Table
References
Related Citation (15)

Download: PDF (742 KB) HTML (1 KB)
Export: BibTeX | EndNote (RIS)

Abstract Objective To investigate the correlations between Lp-PLA2 in circulation and the incidence of adverse events after Stanford type B aortic dissection with stent implantation. Methods The clinical data on 369 cases of Stanford type B aortic dissection with TEVAR treated between September 2017 and May 2021 was retrospectively analyzed. These patients were divided into the rehabilitation group (332 cases) and the adverse event group (37cases). The basic information, results of blood routine examination, indexes of renal function and liver function, and levels of CRP and Lp-PLA2 were collected and compared. The association between Lp-PLA2 and adverse events was analyzed. All the patients were followed up for 6 months. Independent sample t-test, non-parametric rank sum test, chi-square test or multivariate logistic regression analysis were used. SPSS22.0 software was used to analyze the independent influencing factors of the outcome. Results The levels of Lp-PLA2,WBC,CRP and UA in adverse event group were higher than those of the rehabilitation group (all P＜0.05).Multivariate logistic regression analysis showed that levels of Lp-PLA2, WBC and CRP were factors related to adverse events. Conclusions The expression of Lp-PLA2 is correlated with adverse events. Therefore, Lp-PLA2 may serve as a predictor of adverse events after thoracic endovascular aortic repair of Stanford type B aortic dissection.

Key words： lipoprotein-associated phospholipase A2 aortic dissection Stanford type B aortic dissection TEVAR inflammatory response

Received: 25 April 2021

ZTFLH:

R543.1

	Service

	E-mail this article
	Add to my bookshelf
	Add to citation manager
	E-mail Alert
	RSS
	Articles by authors
	LIANG Xiaohui
	CHENG Li
	HUANG Jifeng
	JIN Jun

Cite this article:

LIANG Xiaohui,CHENG Li,HUANG Jifeng等. Correlations between lipoprotein-associated phospholipase A2 in circulation and the incidence of adverse events after Stanford type B aortic dissection with aortic stent implantation[J]. Med. J. Chin. Peop. Armed Poli. Forc., 2021, 32(12): 1033-1037.

URL:

http://journal08.magtechjournal.com/Jwk_wjyx/EN/ OR http://journal08.magtechjournal.com/Jwk_wjyx/EN/Y2021/V32/I12/1033

[1]	Alfson D B, Ham S W. Type B aortic dissections: current guidelines for treatment[J]. Cardiol Clin,2017,35(3):387-410.
[2]	Jang H, Kim M D, Kim G M,et al. Risk factors for stent graft-induced new entry after thoracic endovascular aortic repair for Stanford type B aortic dissection[J]. J Vasc Surg, 2017,65(3):676-685.
[3]	Howard D P, Banerjee A, Fairhead J F,et al. Population-based study of incidence and outcome of acute aortic dissection and premorbid risk factor control:10-year results from the Oxford vascular study[J]. Circulation,2013,127(20):2031-2037.
[4]	Olsson C, Thelin S, Ståhle E,et al. Thoracic aorticaneurysm and dissection: increasing prevalence and improved outcomesreported in a nationwide population-based study of more than 14,000 cases from 1987 to 2002[J]. Circulation,2006,114(24):2611-2618.
[5]	Del Porto F,di Gioia C, Tritapepe L,et al. The multitasking role of macrophages in Stanford type A acute aortic dissection[J]. Cardiology,2014,127(2):123-129.
[6]	Younus A, Humayun C, Ahmad R, et al. Lipoprotein-associated phospholipase A2 and its relationship with markers of subclinical cardiovascular disease: a systematic review[J]. J Clin Lipidol,2017,11(2):328-337.
[7]	Donato L J,Meeusen J W,Callanan H, et al.Advantages of the lipoprotein- associated phospholipase A2 activity assay[J].Clin Biochem,2016,49(1):172-175.
[8]	Ballantyne C M, Hoogeveen R C, Bang H,et al. Lipoprotein-associated phospholipase A2, high-sensitivity C-reactive protein, and risk for incident coronary heart disease inmiddle-aged men and women in the atherosclerosis risk in communities (ARIC) study[J].Circulation,2004,109(7): 837-842
[9]	Packard C J, O'Reilly D S, Caslake M J,etal.Lipoprotein-associated phospholipase A2 as an independent predictor of coronary heart disease. West of Scotland coronary prevention study group[J]. N Engl J Med,2000,343(16):1148-1155.
[10]	Khuseyinova N,Koenig W. Predicting the risk of cardiovascular disease: where does lipoprotein-associated phospholipase A(2) fit in? [J]. Mol Diagn Ther, 2007,11(4): 203-217.
[11]	王瑞,张春扬,王引利. 2014年欧洲心脏病学会主动脉疾病诊断及治疗指南(部分)[J]. 心血管病学进展, 2014, 35(5):617-621.
[12]	Harris K M, Strauss C E, Eagle K A, et al. Correlates of delayed recognition and treatment of acute type a aortic dissection: the international registry of acute aortic dissection (IRAD) [J]. Circulation,2011,124(18):1911-1918.
[13]	Nienaber C A, Divchev D, Palisch H, et al. Early and late management of type B aortic dissection[J]. Heart,2014,100(19):1491-1497.
[14]	Koullias G J, Ravichandran P, Korkolis D P,et al.Increased tissue microarray matrix metalloproteinase expression favors proteolysis in thoracic aortic aneurysms and dissections[J]. Ann Thorac Surg,2004,78(6):2106-2110.
[15]	Hahn A W, Jonas U, Bühler F R,et al. Activation of human peripheral monocytes by angiotensin II[J]. FEBS Lett,1994,347(2-3):178-180.
[16]	Porto F, Proietta M, Tritapepe L,et al. Inflammation and immune response in acute aortic dissection[J]. Ann Med,2010,42(8):622-629.
[17]	Epps K C,Wilensky R L. Lp-PLA2- a novel risk factor for high-risk coronary and carotid artery disease[J]. Intern Med,2011,269(1): 94-106.
[18]	郑剑飞. 349 例主动脉夹层患者的流行病学初步分析及 MBD2 在主动脉夹层中表达意义[D]. 长沙: 中南大学, 2013.
[19]	Liu Y S, Hu X B, Li H Z,et al. Association of lipoprotein-associated phospholipase A2 with characteristics of vulnerable coronaryatherosclerotic plaques [J] . Yonsei Med, 2011,52(6): 914-922.
[20]	Lavi S, McConnell J P, Rihal C S, et al. Local production of lipoprotein-associated phospholipase A2 and lysophosphatidylcholine in the coronary circulation: association with early coronary atherosclerosis and endothelial dysfunction in humans[J].Circulation,2007,115(21): 2715-2721.
[21]	Mannheim D, Herrmann J, Versari D, et al.Enhanced expression of Lp-PLA2 and lysophosphatidylcholine in symptomatic carotid atherosclerotic plaques[J]. Stroke, 2008,39(5):1448-1455.
[22]	Saigusa R,Asano Y,Yamashita T,et al.Fli1 deficiencycontributes to the downregulation of endothelial protein C receptor in systemic scle- rosis: a possible role in prothrombotic condition[J].Br J Dermatol,2016,174(2):338-347.