The field of clinical medicine is littered with the bodies of sacred cows. Recent examples include the demise of vagotomy and pyloroplasty as a standard treatment for peptic ulcers and the absolute contraindication of beta blockers in the treatment of heart failure. I would like to suggest that the next sacred cow to be dispensed with is the routine use of electrical cardioversion in the treatment of atrial fibrillation, despite its inclusion as a therapeutic option in the National Institute for Health and Clinical Excellence (NICE) atrial fibrillation guidelines.[1]
Direct electrical cardioversion has been a mainstay of therapy for the treatment of atrial fibrillation for many years. The theory underpinning its utilisation has some face validity, that by restoring sinus rhythm any problems associated with atrial fbrillation will be ameliorated. This, however, does not take into account the underlying cause of the arrhythmia, with the majority of atrial fbrillation caused by ischaemic heart disease. It is only relatively recently, however, that evidence for the ineffectiveness of cardioversion has begun to emerge. Paradoxically this evidence has derived from trials designed to prove the effectiveness of the procedure.
The Evidence
The utility of cardioversion was originally explored in the Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM) study,[2] which recruited over 4,000 patients aged 65 and over with atrial fbrillation and one additional risk factor for stroke. Patients were randomised to either rhythm control, using electrical cardioversion and medication as necessary, or to rate control using drugs, such as beta blockers or digoxin. To the surprise of the investigators the primary outcome, mortality, was worse in the rhythm control group, as were secondary outcomes such as hospitalisation and serious arrhythmias. Importantly, oral anticoagulation could be stopped at the clinician's discretion following cardioversion.
The AFFIRM investigators conducted a post hoc on-treatment analysis that did show some survival advantage if sinus rhythm was maintained.[3] The caveat to this was that use of anti-arrhythmic drugs was associated with increased mortality and, in fact, the main predictor of survival was use of warfarin. This left even the AFFIRM investigators to conclude that any advantage from maintaining sinus rhythm through use of anti-arrhythmic agents was offset by their toxicity.
Despite the fact that these findings have been repeated in further studies[4,5] and the problems associated with ensuring adequate oral anticoagulation prior to undertaking the intervention, cardioversion has remained a common intervention in patients with atrial fibrillation, particularly if there is associated co-morbidity such as heart failure.
A recent paper also seems to lay this issue to rest. Roy and colleagues[6] in trying to establish the efficacy of cardioversion for patients with atrial fibrillation and heart failure (defined as left ventricular ejection fraction of 35% or less, or symptoms of congestive heart failure) recruited 1,376 patients who were randomised to rhythm control, comprising cardioversion within six weeks of randomisation with additional cardioversions as necessary, or rate control with adjusted doses of beta blockers with digoxin. There was no significant difference in primary outcome of death from cardiovascular causes, nor any significant differences in secondary outcomes including death from any cause, stroke, or worsening heart failure. The authors concluded that "in patients with atrial fibrillation and congestive heart failure, a routine strategy of rhythm control does not reduce the rate of death from cardiovascular causes as compared with a rate-control strategy".
Where Does This Leave Us?
If cardioversion therefore has no place in the routine treatment of atrial fibrillation, nor in the treatment of high-risk patients, for example those with heart failure, where does this leave us? To my mind, cardioversion should no longer be offered routinely to patients with atrial fibrillation. The only clinical scenarios where it may be a useful intervention are for patients presenting acutely, within 24 hours of onset, or for patients who are very symptomatic despite medical therapy. Even in these instances, oral anticoagulation should be considered long term because of the high rate of recurrence
References
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