Circulating progenitor cells in patients with atrial fibrillation and their relation with serum markers of inflammation and angiogenesis.
The pathophysiological inter-relationships and underlying 'drivers' of a prothrombotic state in atrial fibrillation (AF) are complex but may include endothelial abnormalities. Circulating progenitor cells (CPCs) have been recently described as a cell population that may promote repair of endothelial damage. We hypothesised abnormalities in this cell population, alongside abnormal markers of endothelial damage/dysfunction (von Willebrand factor, soluble E-selectin), apoptosis (soluble Fas, soluble Fas ligand), angiogenesis (vascular endothelial growth factor) and inflammation (interleukin-6) in 135 consecutive AF patients (14 with lone AF), who were compared to 33 'disease controls' and 13 healthy controls. We also explored whether restoration of sinus rhythm would alter these indices. No significant differences in research indices were observed between AF and disease controls, apart from soluble Fas levels (p<0.001). Median CPC levels in lone AF were higher compared to 'non-lone AF' (that is, AF patients with co-morbidities) [p<0.001], apparently because of difference in age and presence of co-morbidities. There was an increase in CPC counts (p=0.007), but in not other markers following DC cardioversion. CPCs increased significantly in the 17 patients who were successfully cardioverted into sinus rhythm (p=0.003). In a stepwise multiple regression analysis, age (p=0.014), hyperlipidaemia (p=0.001) and use of statins (but not AF) was predictive of CPC counts (p=0.014). In conclusion, AF is unlikely to be independently associated with abnormalities in CPCs. Successful cardioversion is associated with a modest but significant increase in CPCs.
Haemostasis Thrombosis and Vascular Biology Unit, University of Birmingham Centre for Cardiovascular Sciences, City Hospital, Birmingham B18 7QH, UK.
Timothy
T
Watson
Eduard
E
Shantsila
Andrew
A
Blann
Gregory Y H
GY
Lip
D000368:Aged; D042501:Angiogenic Proteins / Q000097:blood*; D017209:Apoptosis; D001281:Atrial Fibrillation / Q000097:blood / Q000276:immunology / Q000473:pathology* / Q000628:therapy; D015415:Biomarkers / Q000097:blood; D016022:Case-Control Studies; D002452:Cell Count; D003430:Cross-Sectional Studies; D019040:E-Selectin / Q000097:blood; D004554:Electric Countershock; D053222:Fas Ligand Protein / Q000097:blood; D005260:Female; D006801:Humans; D018836:Inflammation Mediators / Q000097:blood*; D015850:Interleukin-6 / Q000097:blood; D008297:Male; D008875:Middle Aged; D012044:Regression Analysis; D018570:Risk Assessment; D012307:Risk Factors; D013234:Stem Cells / Q000378:metabolism / Q000473:pathology*; D013997:Time Factors; D016896:Treatment Outcome; D042461:Vascular Endothelial Growth Factor A / Q000097:blood; D019014:fas Receptor / Q000097:blood; D014841:von Willebrand Factor / Q000378:metabolism
D042501:Angiogenic Proteins; D015415:Biomarkers; D019040:E-Selectin; C491901:FAS protein, human; C505661:FASLG protein, human; D053222:Fas Ligand Protein; C508600:IL6 protein, human; D018836:Inflammation Mediators; D015850:Interleukin-6; C546936:SELE protein, human; C467484:VEGFA protein, human; D042461:Vascular Endothelial Growth Factor A; D019014:fas Receptor; D014841:von Willebrand Factor