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The effects of direct current cardioversion for persistent atrial fibrillation on indices of endothelial
Bethan Freestone1, Aun Yeong Chong, Andrew D Blann
1Haemostasis, Thrombosis, and Vascular Biology Unit, University Department of Medicine, City Hospital, Birmingham, England, UK.
Insights
Electrical cardioversion for atrial fibrillation (AF) improved some markers of endothelial function but increased markers of endothelial injury. This suggests a potential for delayed endothelial damage contributing to late thromboembolic risk after AF treatment.
Area of Science:
- Cardiology
- Vascular Biology
- Thrombosis
Background:
- Atrial fibrillation (AF) is linked to heightened thromboembolic risk, persisting even after cardioversion.
- Altered blood flow in AF may cause endothelial dysfunction, promoting a prothrombotic state.
Purpose of the Study:
- To evaluate endothelial function before and after electrical cardioversion in patients with AF.
- To assess specific markers of endothelial damage and dysfunction.
Main Methods:
- 30 patients undergoing elective cardioversion for AF and 20 healthy controls were studied.
- Plasma levels of von Willebrand factor (vWF), E-selectin (E-sel), soluble thrombomodulin (sTM), and circulating endothelial cells (CECs) were measured.
- Measurements were taken at baseline (pre-cardioversion) and at 2 hours and 4 weeks post-cardioversion.
Main Results:
- Persistent AF showed significantly higher baseline vWF levels compared to controls.
- Post-cardioversion, vWF levels decreased significantly at 4 weeks.
- Levels of CECs and sTM, not elevated at baseline, significantly increased after cardioversion.
Conclusions:
- While decreased vWF suggests improved vascular endothelial function post-cardioversion, increased sTM and CECs indicate potential endothelial injury.
- This delayed endothelial injury and cell shedding may contribute to the late thromboembolic risk observed after cardioversion.
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.
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