Atrial fibrillation, transesophageal echo, electrical cardioversion, and anticoagulation

Although successful electrical cardioversion is accomplished in most cases without any evidence of embolic stroke, a few patients have experienced this catastrophe. The current thinking is that when electrical energy is applied to the chest wall, the atrium, although it returns to sinus rhythm, is stunned. It is not known how long this stunning lasts in the individual patient nor whether high energy produces stunning and low energy does not. Nor is it known whether chemical conversion of atrial fibrillation to sinus rhythm affects the atrium in the same way. However, the atrium seems to recover more quickly in patients with a short duration of atrial fibrillation and these patients may not require the usual four weeks of postcardioversion anticoagulation. Based on what we know, or more precisely what we don't know, it seems reasonable to ensure that every patient with atrial fibrillation is anticoagulated during and after DC cardioversion to sinus rhythm. Of course, this is easy to do with intravenous heparin, but that requires hospitalization. Perhaps subcutaneous heparin in high doses would suffice until the patient can be anticoagulated with coumadin. From the research perspective it might be interesting to perform serial echo/Doppler studies on these patients to identify when the individual patient's atrial function returns to normal. This might provide a clinical rationale for discontinuing anticoagulation. Comparing the time to return of normal atrial function (as measured by Doppler echo) between patients undergoing pharmacologic cardioversion versus electrical cardioversion and studying the relationship of the amount of electrical energy required for cardioversion versus the duration of stunning would be clinical research projects of interest to clinicians.