The effects of direct current cardioversion for persistent atrial fibrillation on indices of endothelial damage/dysfunction.
BACKGROUND
Atrial fibrillation is associated with increased thromboembolic risk, and this risk may occur even following cardioversion. Atrial fibrillation has been hypothesised to cause alterations in endothelial cell function through the influences of altered flow dynamics, and resultant endothelial dysfunction may be contributory to the generation of a prothrombotic state. The aim of this study was therefore to assess endothelial function before and after electrical cardioversion.


METHODS
We studied 30 consecutive patients undergoing elective cardioversion for AF and compared them with 20 healthy controls. Plasma levels of endothelial damage/dysfunction [von Willebrand factor (vWF), E-selectin (E-sel), soluble thrombomodulin (sTM)] and Circulating Endothelial Cells (CECs, an index of endothelial damage) in whole blood were measured in all subjects and on the AF group at baseline (pre-cardioversion) and at 2 h and 4 weeks following cardioversion.


RESULTS
Plasma levels of vWf were significantly increased in persistent AF at baseline compared to healthy controls (p<0.001). With restoration of sinus rhythm, vWF levels were significantly decreased at 4 weeks (p=0.0001), whilst levels of CECs (p=0.01) and sTM (p=0.022), although not increased at baseline, were significantly increased following cardioversion.


CONCLUSIONS
Although plasma vWF levels decreased post-cardioversion, suggesting some improvement in vascular endothelial function, the increases in sTM and CECs at 4 weeks may indicate endothelial injury sustained peri-cardioversion. This (delayed) injury and shedding of endothelial cells post-cardioversion may contribute to late thromboembolic risk.
Freestone
Bethan
B
Haemostasis, Thrombosis, and Vascular Biology Unit, University Department of Medicine, City Hospital, Birmingham, England, UK.
Chong
Aun Yeong
AY
Blann
Andrew D
AD
Lip
Gregory Y H
GY
D000368:Aged; D001281:Atrial Fibrillation / Q000150:complications / Q000503:physiopathology* / Q000628:therapy; D004554:Electric Countershock / Q000009:adverse effects* / Q000295:instrumentation / Q000379:methods; D042783:Endothelial Cells / Q000473:pathology; D004730:Endothelium, Vascular / Q000503:physiopathology*; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D012044:Regression Analysis; D012307:Risk Factors; D013923:Thromboembolism / Q000150:complications / Q000503:physiopathology / Q000628:therapy; D016896:Treatment Outcome; D014841:von Willebrand Factor / Q000032:analysis
D014841:von Willebrand Factor