Article

The effects of direct current cardioversion for persistent atrial fibrillation on indices of endothelial damage/dysfunction

Haemostasis, Thrombosis, and Vascular Biology Unit, University Department of Medicine, City Hospital, Birmingham, England, UK
Thrombosis Research DOI:10.1016/j.thromres.2005.10.004 pp.479-485

ABSTRACT BackgroundAtrial 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.MethodsWe 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.ResultsPlasma 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.ConclusionAlthough 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.

0 0
 · 
0 Bookmarks
 · 
2 Views
  • Source
    Article: Lysophosphatidic acid stimulates thrombomodulin lectin-like domain shedding in human endothelial cells.
    Hua-Lin Wu, Chi-Iou Lin, Yuan-Li Huang, Pin-Shern Chen, Cheng-Hsiang Kuo, Mei-Shing Chen, Georgiana Cho-Chen Wu, Guey-Yueh Shi, Hsi-Yuan Yang, Hsinyu Lee
    [show abstract] [hide abstract]
    ABSTRACT: Thrombomodulin (TM) is an anticoagulant glycoprotein highly expressed on endothelial cell surfaces. Increased levels of soluble TM in circulation have been widely accepted as an indicator of endothelial damage or dysfunction. Previous studies indicated that various proinflammatory factors stimulate TM shedding in various cell types such as smooth muscle cells and epithelial cells. Lysophosphatidic acid (LPA) is a bioactive lipid mediator present in biological fluids during endothelial damage or injury. In the present study, we first observed that LPA triggered TM shedding in human umbilical vein endothelial cells (HUVECs). By Cyflow analysis, we showed that the LPA-induced accessibility of antibodies to the endothelial growth factor (EGF)-like domain of TM is independent of matrix metalloproteinases (MMPs), while LPA-induced TM lectin-like domain shedding is MMP-dependent. Furthermore, a stable cell line expressing TM without its lectin-like domain exhibited a higher cell proliferation rate than a stable cell line expressing full-length TM. These results imply that LPA induces TM lectin-like domain shedding, which might contribute to the exposure of its EGF-like domain for EGF receptor (EGFR) binding, thereby stimulating subsequent cell proliferation. Based on our findings, we propose a novel mechanism for the exposure of TM EGF-like domain, which possibly mediates LPA-induced EGFR transactivation.
    Biochemical and Biophysical Research Communications 03/2008; 367(1):162-8. · 2.48 Impact Factor
  • Source
    Article: Persistent atrial fibrillation is not associated with thrombomodulin level increase in efficiently anticoagulated patients.
    Beata Wożakowska-Kapłon, Radoslaw Bartkowiak, Urszula Grabowska, Grażyna Janiszewska
    [show abstract] [hide abstract]
    ABSTRACT: Atrial fibrillation (AF) is the most common arrhythmia and leads to a five-fold increased risk of stroke compared to persons with sinus rhythm. A soluble form of thrombomodulin (sTM) is a recognized marker of endothelial dysfunction and may contribute to the hypercoagulable state in AF. The aim of the study was to evaluate plasma concentration of sTM in persistent AF patients before and after sinus rhythm recovery following direct current cardioversion (CV). In 45 effectively anticoagulated consecutive patients, with persistent non-valvular AF, and normal left ventricular function, CV was performed. Blood samples for sTM assessment were collected twice: 24 hours before and 24 hours after CV. In 43 patients sinus rhythm was obtained. The mean plasma sTM level was significantly lower in AF patients compared to the control group with sinus rhythm and without anticoagulation (38.5 ±9.9 ng/ml vs. 44.1 ±9.1 ng/ml, p = 0.04). Plasma sTM levels did not change 24 hours after successful CV (36.7 ±9.5 ng/ml vs. 38.5 ±9.9 ng/ml, p = 0.16). Plasma sTM concentration was lower in patients with persistent AF and normal left ventricle systolic function than in patients with sinus rhythm, presumably due to chronic oral anticoagulant therapy in the AF group. CV has no impact on sTM plasma level evaluated 24 hours after sinus rhythm restoration.
    Archives of medical science : AMS. 12/2010; 6(6):887-91.
Data provided are for informational purposes only. Although carefully collected, accuracy cannot be guaranteed. The impact factor represents a rough estimation of the journal's impact factor and does not reflect the actual current impact factor. Publisher conditions are provided by RoMEO. Differing provisions from the publisher's actual policy or licence agreement may be applicable.

Keywords

20 healthy controls
 
4 weeks
 
AF group
 
cardioversion.ConclusionAlthough plasma vWF levels
 
cardioversion.ResultsPlasma levels
 
cause alterations
 
Circulating Endothelial Cells
 
electrical cardioversion.MethodsWe
 
endothelial cell function
 
endothelial cells post-cardioversion
 
endothelial damage
 
endothelial function
 
endothelial injury
 
persistent AF
 
Plasma levels
 
prothrombotic state
 
resultant endothelial dysfunction
 
sinus rhythm
 
thromboembolic risk
 
vascular endothelial function