Haemostatic activity in patients with atrial fibrillation treated with low-molecular-weight heparin before and after electrical cardioversion.
BACKGROUND
Electrical cardioversion of atrial fibrillation (AF) is associated with a thromboembolic risk, and this risk can be reduced by the use of antithrombotic therapy. International guidelines recommend an effective oral anticoagulant therapy (OAT) for at least 3 weeks before, and 4 weeks after cardioversion. We studied whether electrical cardioversion in it self causes changes in the level of activity in the haemostatic system during treatment with either low-molecular-weight heparin (LMWH).


METHODS
Thirty-eight patients with AF were randomised consecutively to either LMWH administered subcutaneous in a fixed daily dose, or conventional OAT. Changes in the biochemical markers prothrombin fragment 1+2 (F1+2), D-Dimer, and soluble fibrin, all reflecting the activity in the haemostatic system, were assessed at baseline, before and after electrical cardioversion in patients treated with LMWH for 3 weeks prior to cardioversion. A follow up compared the time spent on anticoagulation prior to cardioversion, and eventual complications in the two group (LMWH vs. OAT).


CONCLUSIONS
No significant differences between the levels of the biochemical markers measured before, and after cardioversion were seen, indicating that during anticoagulant therapy with LMWH, electrical cardioversion in itself, does not cause an increased activity in the haemostatic system. Also the level of F1+2 had declined significantly after cardioversion, when compared to baseline level in patients, whom had a normal sinus rhythm (NSR) re-established. This indicates that even in patients on a stable anticoagulant treatment, restoration of a NSR can cause a further decrease in thrombin generation. The median time spent on antithrombotic treatment prior to cardioversion, was significantly different between the LMWH (27 days) and the OAT group (138 days). Our study indicates that cardioversion in patients on LMWH does not cause a hypercoagulable state and that LMWH significantly shortens the time spent on anticoagulant therapy prior to cardioversion.
Zeuthen
Elisabeth L
EL
Department of Cardiology and Internal Medicine, Aarhus Sygehus, Aarhus University Hospital, 8000 Aarhus, Denmark. elz@dadlnet.dk
Lassen
Jens Flensted
JF
Husted
Steen E
SE
D000368:Aged; D001281:Atrial Fibrillation / Q000097:blood* / Q000188:drug therapy* / Q000628:therapy; D015415:Biomarkers / Q000097:blood; D004554:Electric Countershock / Q000009:adverse effects*; D005260:Female; D005337:Fibrin / Q000032:analysis; D005338:Fibrin Fibrinogen Degradation Products / Q000032:analysis; D006487:Hemostasis; D006495:Heparin, Low-Molecular-Weight / Q000008:administration & dosage*; D006801:Humans; D008297:Male; D008875:Middle Aged; D010446:Peptide Fragments / Q000097:blood; D011516:Prothrombin; D019851:Thrombophilia
D015415:Biomarkers; D005338:Fibrin Fibrinogen Degradation Products; D006495:Heparin, Low-Molecular-Weight; D010446:Peptide Fragments; C036309:fibrin fragment D; C045879:prothrombin fragment 1.2; D011516:Prothrombin; D005337:Fibrin