Circulating endothelial cells in atrial fibrillation with and without acute cardiovascular disease

被引:38
作者
Freestone, B [1 ]
Lip, GYH [1 ]
Chong, AY [1 ]
Nadar, S [1 ]
Lee, KW [1 ]
Blann, AD [1 ]
机构
[1] Univ Birmingham, Haemostasis Thrombosis & Vasc Biol Unit, City Hosp, Dept Med, Birmingham B18 7QH, W Midlands, England
关键词
circulating endothelial cells; endothelial damage; soluble E-selectin; soluble thrombomodulin; von Willebrand factor; atrial fibrillation;
D O I
10.1160/TH05-02-0093
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Normal adults have very few circulating endothelial cells (CECs) in their blood, but increased levels have been shown in association with conditions associated with endothelial damage such as myocardial infarction and stroke. As atrial fibrillation (AF) is associated with a hypercoagulable state and abnormalities of plasma indices of endothelial damage/dysfunction, we hypothesised that CECs would also be raised in this condition, and would correlate with these plasma markers. We measured CECs (by immunofluoresence) as an indicator of frank endothelial damage, alongside 3 plasma indices of endothelial perturbation: von Willebrand factor (vWf), soluble E-selectin and soluble thrombomodulin (sTM) (all ELISA) in 28 patients with chronic 'stable' AF, 63 patients with AF plus an acute cardiovascular or cerebrovascular event as positive controls, and 20 healthy subjects in sinus rhythm as negative controls. Chronic 'stable' AF patients had significantly higher levels of plasma vWf (p < 0.001),but comparable numbers of CECs (p = 0.1638) in comparison to healthy controls. In patients with AF associated with an acute cardiovascular or cerebrovascular event, levels of CECs (p < 0.0001) and sTM (p=0.004), but not vWf or sEsel, were significantly increased in comparison to chronic 'stable' AF patients. Patients with uncomplicated AF have abnormal systemic endothelial damage/dysfunction, as evident by increased plasma vWf levels, but normal numbers of CECs, compared to subjects in sinus rhythm. However, following clinical complications, such as stroke or significant haemodynamic compromise, further endothelial disturbance (as indicated by high levels of sTM and CECs) suggests additional endothelial damage.
引用
收藏
页码:702 / 706
页数:5
相关论文
共 31 条
[1]   S-Endo 1, a pan-endothelial monoclonal antibody recognizing a novel human endothelial antigen [J].
Bardin, N ;
George, F ;
Mutin, M ;
Brisson, C ;
Horschowski, M ;
Frances, V ;
Lesaule, G ;
Sampol, J .
TISSUE ANTIGENS, 1996, 48 (05) :531-539
[2]   Circulating endothelial cells - Biomarker of vascular disease [J].
Blann, AD ;
Woywodt, A ;
Bertolini, F ;
Bull, TM ;
Buyon, JP ;
Clancy, RM ;
Haubitz, M ;
Hebbel, RP ;
Lip, GYH ;
Mancuso, P ;
Sampol, J ;
Solovey, A ;
Dignat-George, F .
THROMBOSIS AND HAEMOSTASIS, 2005, 93 (02) :228-235
[3]   Circulating endothelial cells in pulmonary hypertension [J].
Bull, TM ;
Golpon, H ;
Hebbel, RR ;
Solovey, A ;
Cool, CD ;
Tuder, RM ;
Geraci, MW ;
Voelkel, NF .
THROMBOSIS AND HAEMOSTASIS, 2003, 90 (04) :698-703
[4]   Endothelial dysfunction and damage in congestive heart failure - Relation of flow-mediated dilation to circulating endothelial cells, plasma indexes of endothelial damage, and brain natriuretic peptide [J].
Chong, AY ;
Blann, AD ;
Patel, J ;
Freestone, B ;
Hughes, E ;
Lip, GYH .
CIRCULATION, 2004, 110 (13) :1794-1798
[5]   Atrial fibrillation in the setting of acute myocardial infarction: The GUSTO-I experience [J].
Crenshaw, BS ;
Ward, SR ;
Granger, CB ;
Stebbins, AL ;
Topol, EJ ;
Califf, RM .
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 1997, 30 (02) :406-413
[6]   Hemostatic state and atrial fibrillation (The Framingham Offspring Study) [J].
Feng, DL ;
D'Agostino, RB ;
Silbershatz, H ;
Lipinska, I ;
Massaro, J ;
Levy, D ;
Benjamin, EJ ;
Wolf, PA ;
Tofler, GH .
AMERICAN JOURNAL OF CARDIOLOGY, 2001, 87 (02) :168-171
[7]   Hypoxia/reoxygenation of human endothelium activates PMNs to detach endothelial cells via a PAF mechanism [J].
Franciose, RJ ;
Moore, EE ;
Moore, FA ;
Read, RA ;
Carl, VS ;
Banerjee, A .
JOURNAL OF SURGICAL RESEARCH, 1996, 61 (02) :459-462
[8]  
GEORGE F, 1992, THROMB HAEMOSTASIS, V67, P147
[9]   ENDOTHELIAL CELL-DAMAGE AND THROMBUS FORMATION AFTER PARTIAL ARTERIAL CONSTRICTION - RELEVANCE TO THE ROLE OF CORONARY-ARTERY SPASM IN THE PATHOGENESIS OF MYOCARDIAL-INFARCTION [J].
GERTZ, SD ;
URETSKY, G ;
WAJNBERG, RS ;
NAVOT, N ;
GOTSMAN, MS .
CIRCULATION, 1981, 63 (03) :476-486
[10]   COAGULATION-FACTORS AND THE INCREASED RISK OF STROKE IN NONVALVULAR ATRIAL-FIBRILLATION [J].
GUSTAFSSON, C ;
BLOMBACK, M ;
BRITTON, M ;
HAMSTEN, A ;
SVENSSON, J .
STROKE, 1990, 21 (01) :47-51