These authors contributed equally to this study.
Expression of platelet-bound stromal cell-derived factor-1 in patients with non-valvular atrial fibrillation and ischemic heart disease
Article first published online: 4 JAN 2012
© 2011 International Society on Thrombosis and Haemostasis
Journal of Thrombosis and Haemostasis
Volume 10, Issue 1, pages 49–55, January 2012
How to Cite
STELLOS, K., RAHMANN, A., KILIAS, A., RUF, M., SOPOVA, K., STAMATELOPOULOS, K., JORBENADZE, R., WERETKA, S., GEISLER, T., GAWAZ, M., WEIG, H.-J. and BIGALKE, B. (2012), Expression of platelet-bound stromal cell-derived factor-1 in patients with non-valvular atrial fibrillation and ischemic heart disease. Journal of Thrombosis and Haemostasis, 10: 49–55. doi: 10.1111/j.1538-7836.2011.04547.x
- Issue published online: 4 JAN 2012
- Article first published online: 4 JAN 2012
- Accepted manuscript online: 1 NOV 2011 11:58AM EST
- Received 2 July 2011, accepted 14 October 2011
- atrial fibrillation;
- ischemic heart disease;
- stromal cell-derived factor-1
Summary. Aims: Blood cell infiltration and inflammation are involved in atrial remodelling during atrial fibrillation (AF) although the exact mechanisms of inflammatory cell recruitment remain poorly understood. Platelet-bound stromal cell-derived factor-1 (SDF-1) is increased in cases of ischemic myocardium and regulates recruitment of CXCR4+ cells on the vascular wall. Whether platelet-bound SDF-1 expression is differentially influenced by non-valvular paroxysmal or permanent atrial fibrillation (AF) in patients with stable angina pectoris (SAP) or acute coronary syndrome (ACS) has not been reported so far. Methods and results: A total of 1291 consecutive patients with coronary artery disease (CAD) undergoing coronary angiography were recruited. Among the patients with SAP, platelet-bound-SDF-1 is increased in patients with paroxysmal AF compared with SR or to persistent/permanent AF (P < 0.05 for both). Platelet-bound SDF-1 correlated with plasma SDF-1 (r = 0.488, P = 0.013) in patients with AF and ACS, which was more pronounced among patients with persistent AF (r = 0.842, P = 0.009). Plasma SDF-1 was increased in persistent/permanent AF compared with SR. Patients with ACS presented with enhanced platelet-bound-SDF-1 compared with SAP. Interestingly, among patients with ACS, patients with paroxysmal or persistent/permanent AF presented with an impaired platelet-bound SDF-1 expression compared with patients with SR. Conclusions: Differential expression of platelet-bound and plasma SDF-1 was observed in patients with AF compared with SR which may be involved in progenitor cell mobilization and inflammatory cell recruitment in patients with AF and ischemic heart disease. Further in vivo studies are required to elucidate the role of SDF-1 in atrial remodeling and the atrial fibrillation course.