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. CONCLUSION: 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.
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. CONCLUSION: 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.