Is Cardioversion After Acute Atrial Fibrillation Safe Without Anticoagulation?
Abstract & Commentary
Edward P. Gerstenfeld, MD
Professor of Medicine, Chief, Cardiac Electrophysiology, University of California, San Francisco
Dr. Gerstenfeld does research for Biosense Webster, Medtronic, and Rhythmia Medical.
This article originally appeared in the November 2013 issue of Clinical Cardiology Alert. It was edited by Michael H. Crawford, MD, Professor of Medicine, Chief of Clinical Cardiology, University of California, San Francisco, and peer reviewed by Ethan Weiss, MD, Assistant Professor of Medicine, Division of Cardiology and CVRI, University of California, San Francisco. Dr. Crawford reports no financial relationships relevant to this field of study, and Dr. Weiss is a scientific advisory board member for Bionovo.
Source: Airaksinen KE, et al. Thromboembolic complications after cardioversion of acute atrial fibrillation: The FinCV (Finnish CardioVersion) Study. J Am Coll Cardiol 2013;62:1187-1192.
In clinical practice, patients with atrial fibrillation (AF) duration < 48 hours often undergo cardioversion without systemic anticoagulation. The Finnish CardioVersion (FinCV) study reviewed the comprehensive database from three Finnish hospitals to identify all patients undergoing cardioversion with AF onset < 48 hours prior without prior systemic anticoagulation. All AF episodes were confirmed by 12-lead ECG. The primary endpoint was thromboembolic event within 30 days after cardioversion. There were 5116 cardioversions performed in 2481 patients who all had AF onset < 48 hours and no prior anticoagulation. There were 38 definite embolic events (0.7%, 95%CI, 0.5-1.0%) in the 30 days after cardioversion, 31 strokes, four transient ischemic attacks, two pulmonary embolisms, and one systemic embolism. In addition, 11 patients died within 30 days, including two from fatal strokes. Independent predictors of embolic events included age (odds ratio [OR], 1.05; 95% CI, 1.02-1.08); female sex (OR, 2.1; 95% CI, 1.1-4.0), heart failure (OR, 2.9; 95% CI 1.1-7.3), and diabetes (OR, 2.3; 95% CI, 1.1-4.9). The highest risk of thromboembolism (9.8%) was identified in patients with heart failure and diabetes, whereas those without heart failure and < 60 years of age had the lowest risk (0.2%). None of the patients with failed cardioversions had embolic events. The authors concluded that the risk of thromboembolic complications post-cardioversion of AF of < 48 hours’ duration is high in certain categories of patients when anticoagulation is not used.
It has often been taught that patients with AF < 48 hours’ duration can undergo cardioversion without transesophageal (TEE) echocardiogram or prior anticoagulation, while in patients with prior AF lasting > 48 hours, either 3 weeks of therapeutic anticoagulation or a TEE is needed. One of the challenges of this approach is uncertainty regarding the prior duration of AF. Unless a patient is hospitalized or has an implanted pacemaker, symptoms from AF can be unreliable. Nevertheless, there are some patients who can tell the minute their AF initiates, and then call to undergo cardioversion. It is well described that immediately after cardioversion, there is "stunning" of the left atrium, and that left atrial appendage velocities actually decrease as spontaneous thrombus can form immediately. This occurs whether cardioversion is electrical, chemical, or spontaneous. However, the duration of stunning is related to the prior duration of AF, so those with brief prior AF duration may recover left atrial function quickly. It is for this reason that some have performed cardioversion of low-risk patients on aspirin if they present within 48 hours. This study points out that although the overall stroke risk in this patient group with AF < 48 hours is low (1%), it is higher in those with stroke risk factors (~10%). Fortunately, the same risk factors that predict stroke in AF patients, namely age, diabetes, and congestive heart failure, were predictive of recurrent stroke in this study. Therefore, it seems prudent that in patients with any CHADS2 stroke risk factors, anticoagulation should be initiated and continued for 30 days after cardioversion, even if the AF duration is < 48 hours. This is much easier to do with the newer oral anticoagulants. The need for continued anticoagulation can be reassessed after 30 days, depending on the patients’ rhythm. If the duration of AF prior to presentation is at all unclear, then either 3 weeks of oral anticoagulation or a TEE should be performed prior to cardioversion. Importantly, if a TEE is being performed, one should achieve therapeutic anticoagulation before cardioversion in these patients. This can be achieved by giving the first oral dose of a novel anticoagulant 2 hours prior to cardioversion. For those with truly lone AF and clear recent onset AF, the risk of stroke with cardioversion is low (< 0.2%). I still tend to start a novel anticoagulant prior to and for at least 48 hours after cardioversion in these patients, given the possible deleterious effect of left atrial stunning and low risk of bleeding with short-term anticoagulant use.