Expression of platelet-bound stromal cell-derived factor-1 in patients with non-valvular atrial fibrillation and ischemic heart disease

Authors

  • K. STELLOS,

    1. Medizinische Klinik III, Kardiologie und Kreislauferkrankungen, Eberhard Karls-Universität Tübingen, Tübingen
    2. Department of Cardiology, Centre of Internal Medicine III, Johann-Wolfgang-Goethe-Universität Frankfurt am Main, Frankfurt, Germany
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  • A. RAHMANN,

    1. Medizinische Klinik III, Kardiologie und Kreislauferkrankungen, Eberhard Karls-Universität Tübingen, Tübingen
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  • A. KILIAS,

    1. Medizinische Klinik III, Kardiologie und Kreislauferkrankungen, Eberhard Karls-Universität Tübingen, Tübingen
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  • M. RUF,

    1. Medizinische Klinik III, Kardiologie und Kreislauferkrankungen, Eberhard Karls-Universität Tübingen, Tübingen
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  • K. SOPOVA,

    1. Medizinische Klinik III, Kardiologie und Kreislauferkrankungen, Eberhard Karls-Universität Tübingen, Tübingen
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  • K. STAMATELOPOULOS,

    1. Department of Clinical Therapeutics, Alexandra Hospital, University of Athens, Greece
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  • R. JORBENADZE,

    1. Medizinische Klinik III, Kardiologie und Kreislauferkrankungen, Eberhard Karls-Universität Tübingen, Tübingen
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  • S. WERETKA,

    1. Medizinische Klinik III, Kardiologie und Kreislauferkrankungen, Eberhard Karls-Universität Tübingen, Tübingen
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  • T. GEISLER,

    1. Medizinische Klinik III, Kardiologie und Kreislauferkrankungen, Eberhard Karls-Universität Tübingen, Tübingen
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  • M. GAWAZ,

    1. Medizinische Klinik III, Kardiologie und Kreislauferkrankungen, Eberhard Karls-Universität Tübingen, Tübingen
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  • H.-J. WEIG,

    1. Medizinische Klinik III, Kardiologie und Kreislauferkrankungen, Eberhard Karls-Universität Tübingen, Tübingen
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    • These authors contributed equally to this study.

  • B. BIGALKE

    1. Medizinische Klinik III, Kardiologie und Kreislauferkrankungen, Eberhard Karls-Universität Tübingen, Tübingen
    2. King’s College London, Division of Imaging Sciences and Biomedical Engineering, The Rayne Institute, St. Thomas′ Hospital, London, UK
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    • These authors contributed equally to this study.


Konstantinos Stellos, Medizinische Klinik III, Kardiologie und Kreislauferkrankungen, Eberhard-Karls Universität Tübingen, Otfried-Müller Str. 10, 72076 Tübingen, Germany.
Tel.: +49 17696543101; fax: +49 7071295749.
E-mail: konstantinos.stellos@gmail.com

Abstract

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.

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