Association of monocyte count on admission with angiographic no-reflow after primary percutaneous coronary intervention in patients with ST-segment elevation myocardial infarction

被引:20
作者
Wang, Zuoyan [1 ]
Ren, Lihui [1 ]
Liu, Na [2 ]
Lei, Licheng [1 ]
Ye, Huiming [1 ]
Peng, Jianjun [1 ]
机构
[1] Capital Med Univ, Beijing Shijitan Hosp, Dept Caridol, 10 Tieyi Rd, Beijing 100038, Peoples R China
[2] Capital Med Univ, Beijing Shijitan Hosp, Dept Clin Lab, Beijing, Peoples R China
关键词
monocyte count; no-reflow phenomenon; primary percutaneous coronary intervention; acute myocardial infarction; MICROVASCULAR OBSTRUCTION; TISSUE FACTOR; PLATELET; ANGIOPLASTY; INJURY; MICROPARTICLES; INFLAMMATION; ACTIVATION; CHEMOKINES; ISCHEMIA;
D O I
10.5603/KP.a2016.0065
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Background: The no-reflow phenomenon during primary percutaneous coronary intervention (pPCI) in patients with ST-elevation myocardial infarction (STEMI) can lead to poor outcomes. It has been shown that the monocytes may be involved in the pathogenesis of coronary artery disease and associated with high risk of myocardial infarction. Aim: To assess the relation between admission monocyte count and angiographic no-reflow after pPCI. Methods: A total of 236 patients with acute STEMI, who underwent pPCI, were enrolled. The patients were divided into two groups (no-reflow and normal reflow) based on post-pPCI Thrombolysis in Myocardial Infarction (TIMI) flow grade. No reflow was defined as TIMI flow grades <= 2, and normal reflow was defined as TIMI 3 flow grade. The monocyte count and other laboratory parameters were measured on admission before pPCI. Results: There were 43 (18.2%) patients in the no-reflow group and 193 (81.8%) patients in the normal-reflow group. Patients with no-reflow had significantly higher admission monocyte count (0.76 +/- 0.48 x 10(9)/L vs. 0.55 +/- 0.29 x 10(9)/L, p = 0.004). Also, white blood cell and neutrophil counts were significantly higher while haemoglobin was significantly lower in the no-reflow group. In multivariate analysis, monocyte count remained an independent predictor of angiographic no-reflow phenomenon (odds ratio [OR] 2.665, 95% confidence interwal [CI] 1.102-6.445, p = 0.030) together with low haemoglobin concentration (OR 0.978, 95% CI 0.961-0.995, p = 0.013). Conclusions: Monocyte count on admission and low haemoglobin concentration were independent clinical predictors of no-reflow following pPCI in patients with STEMI. Our findings suggest that admission monocyte count may be available for early risk stratification of no-reflow after pPCI and might allow the improvement of strategies to prevent this phenomenon.
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收藏
页码:1159 / 1165
页数:7
相关论文
共 27 条
[1]   ADHESION MOLECULES AND INFLAMMATORY INJURY [J].
ALBELDA, SM ;
SMITH, CW ;
WARD, PA .
FASEB JOURNAL, 1994, 8 (08) :504-512
[2]   Differential contributions of monocyte- and platelet-derived microparticles towards thrombin generation and fibrin formation and stability [J].
Aleman, M. M. ;
Gardiner, C. ;
Harrison, P. ;
Wolberg, A. S. .
JOURNAL OF THROMBOSIS AND HAEMOSTASIS, 2011, 9 (11) :2251-2261
[3]   PROGRESSIVE IMPAIRMENT OF REGIONAL MYOCARDIAL PERFUSION AFTER INITIAL RESTORATION OF POSTISCHEMIC BLOOD-FLOW [J].
AMBROSIO, G ;
WEISMAN, HF ;
MANNISI, JA ;
BECKER, LC .
CIRCULATION, 1989, 80 (06) :1846-1861
[4]  
Arbel Y, 2015, ISR MED ASSOC J, V17, P500
[5]   Interaction between chemokines and oxidative stress:: Possible pathogenic role in acute coronary syndromes [J].
Aukrust, P ;
Berge, RK ;
Ueland, T ;
Aaser, E ;
Damås, JK ;
Wikeby, L ;
Brunsvig, A ;
Müller, F ;
Forfang, K ;
Froland, SS ;
Gullestad, L .
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 2001, 37 (02) :485-491
[6]   Coronary no-reflow is caused by shedding of active tissue factor from dissected atherosclerotic plaque [J].
Bonderman, D ;
Teml, A ;
Jakowitsch, J ;
Adlbrecht, C ;
Gyöngyösi, M ;
Sperker, W ;
Lass, H ;
Mosgoeller, W ;
Glogar, DH ;
Probst, P ;
Maurer, G ;
Nemerson, Y ;
Lang, IM .
BLOOD, 2002, 99 (08) :2794-2800
[7]   Effects of distal embolization on the timing of platelet and inflammatory cell activation in interventional coronary no-reflow [J].
Charron, Thierry ;
Jaffe, Ronen ;
Segev, Amit ;
Bang, K. W. Annie ;
Qiang, Beiping ;
Sparkes, John D. ;
Butany, Jagdish ;
Dick, Alexander J. ;
Freedman, John ;
Strauss, Bradley H. .
THROMBOSIS RESEARCH, 2010, 126 (01) :50-55
[8]   Targeting the chemokines in myocardial inflammation [J].
Frangogiannis, NG ;
Entman, ML .
CIRCULATION, 2004, 110 (11) :1341-1342
[9]   The inflammatory response in myocardial infarction [J].
Frangogiannis, NG ;
Smith, CW ;
Entman, ML .
CARDIOVASCULAR RESEARCH, 2002, 53 (01) :31-47
[10]   Myeloperoxidase may contribute to the no-reflow phenomenon in patients with acute myocardial infarction [J].
Funayama, Hiroshi ;
Ishikawa, San-e ;
Sugawara, Yoshitaka ;
Kubo, Norifumi ;
Momomura, Shin-ichi ;
Kawakami, Masanobu .
INTERNATIONAL JOURNAL OF CARDIOLOGY, 2010, 139 (02) :187-192