Summary
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.
Keywords
Atrial fibrillation - angiogenesis - progenitor cells - apoptosis - inflammation
