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Dr. Dunn is Franklin E. Murphy Professor of Medicine Emeritus, and Dr. Marcum is a Fellow, Division of Cardiovascular Diseases, University of Kansas Medical Center.
Correspondence to: Marvin I. Dunn, MD, Master FCCP, Division of Cardiovascular Diseases, University of Kansas Medical Center, Kansas City, KS 66160-7378
Atrial fibrillation (AF) is the most common persistent and
intermittent arrhythmia seen in clinical practice. A recent large
cross-sectional study by Go et al1
found a prevalence of
AF of 0.95% in study patients 
20 years old. The prevalence ranged
from 0.1% in individuals < 55 years old to 9% in patients > 80
years old. These investigators estimated that there are currently 2.3
million adults with AF in the United States and that, since the
prevalence is age related, this number could increase to somewhere
between 5 million and 6.3 million by 2050. The implications of this
problem are many and include the financial burden associated with
treatment, effects on quality of life, and an increased risk of other
medical conditions, such as heart failure and thromboembolism. The most
potentially devastating associated problem is embolic cerebrovascular
accident (CVA).
The Atrial Fibrillation Investigators2 found that the incidence of CVA in patients with AF averages 5%/yr in those who are not treated with anticoagulation. The rate varies among those with AF, depending on the presence or absence of other medical conditions. These investigators identified independent risk factors for CVA through multivariate analysis of pooled data. They found previous CVA or transient ischemic attack, increased age, history of hypertension, and diabetes mellitus to significantly increase the risk of CVA in patients with AF. Patients in their study were classified into risk categories based on the presence or absence of these risk factors. The investigators found that the event rate in those with AF ranged from 1% in patients < 65 years old with no risk factors, to 8.1% in patients > 75 years old with one or more risk factors. Most of these strokes are secondary to stasis-induced thrombi within the left atrial appendage that subsequently embolize. The risk of CVA is greatly reduced with use of anticoagulation therapy. The risk reduction in patients treated with warfarin has been shown to be approximately 68%.3
Therapy for AF falls in two broad categories: (1) ventricular rate control and anticoagulation, or (2) cardioversion to sinus rhythm and maintenance of sinus rhythm with pharmacologic agents. Almost all would agree that every patient should have an attempt to restore regular rhythm with either electrical or pharmacologic cardioversion. This can be done with antiarrhythmic medication administered prior to cardioversion or immediately following. All would agree that the sooner cardioversion can be undertaken, the greater the likelihood of success and also the greater the likelihood of a persistence of regular rhythm.
Two major complications of cardioversion are thrombogenesis and atrial stunning, both of which predispose to thromboembolism. Thrombi usually form in the left atrial appendage, which is the only portion of the left atrium that is trabeculated. When functioning normally, the appendage contracts both longitudinally and circumferentially to express blood from its cavity. During fibrillation, blood is not actively expressed from the left atrial appendage and thrombus forms in the interstices of the trabeculae. These thrombi may embolize, especially after return of normal atrial function. Approximately 75% of initial emboli lodge in cerebral vasculature causing a CVA; 70% of such emboli result in severe neurologic disability or death. Bjerkelund and Orning4 found a 6.8% incidence of embolic events in patients with atrial arrhythmias who were not anticoagulated prior to direct-current cardioversion and who had a return to normal sinus rhythm. Patients in the comparative group, who were receiving anticoagulation, were noted to have a 1.1% incidence of embolic events after return to normal sinus rhythm. If AF has been present for < 48 h, anticoagulation is not necessary. If AF has been present for > 48 h or for an unknown period, then the patient should receive anticoagulation therapy. It is unclear whether the thrombogenicity of cardioversion is due to electrical injury to the atrial myocardium, the stunning of the atria, or both.
Postcardioversion CVAs occur most frequently within 2 to 3 days of the procedure, but may occur as long as 2 to 3 weeks after the procedure.5 There are two reasons for this: (1) the mechanical contraction of the left atrium may be delayed,6 and (2) it may take 2 to 3 weeks for thrombus that has formed in the left atrial appendage to become adherent to the wall of the appendage. The most recent recommendations7 for anticoagulation in patients undergoing elective cardioversion in whom the arrhythmia has been present for > 48 h are: (1) therapeutic warfarin (target international normalized ratio, 2.5; range, 2.0 to 3.0) anticoagulation for 3 weeks before elective cardioversion, and (2) anticoagulation for 4 weeks after successful cardioversion.
Recent studies have shown that transesophageal echocardiographically guided cardioversion may offer a safe alternative to these recommendations. The Assessment of Cardioversion Using Transesophageal Echocardiography Investigators8 studied a conventional approach to cardioversion vs an approach of transesophageal echocardiography (TEE) after diagnosis of AF with treatment guided by the results of that echocardiogram. Patients in whom no intracardiac thrombi were detected by TEE were treated with short-term anticoagulation and external direct-current cardioversion within 24 h to 5 days. Anticoagulation was continued for 4 weeks after cardioversion in both groups. The results showed no significant difference in the rate of embolic events between the two groups. There were, however, significantly fewer hemorrhagic events in the TEE-guided group. There was also a greater rate of successful restoration of sinus rhythm and shorter time to cardioversion in the TEE-guided group.
Another technique for cardioversion is internal electrical cardioversion. This technique utilizes catheter-based electrodes that are placed within the cardiac chambers and provide low-energy atrial defibrillation. Since extracardiac tissue is bypassed, the delivered electrical potential is greater. For this reason, the success rate of cardioversion by this technique should be superior to external cardioversion. Lévy et al9 found that this method of cardioversion was more effective than external cardioversion with no increase in complications. It was also shown10 to be effective in patients in whom external cardioversion was unsuccessful. Therefore, despite the potential for the complications associated with any invasive procedure, this procedure will continue to be utilized in patients who are deemed less likely to respond to external cardioversion or who have undergone unsuccessful external cardioversion.
In this issue of CHEST (see page 13), Lehmann et al report a randomized study of external vs internal cardioversion. They measured the time to return of "basal" atrial contraction of right and left atria using echocardiographic techniques and assessed tissue injury using enzymatic measurements. They found that there was no difference in the time of return to normal atrial mechanical performance. They found that the left atrium often remained stunned beyond day 7, with a return to basal function by day 28. They also found that the return to basal function of the right atrium was almost immediate. Finally, they found no evidence of significant cardiac tissue injury with either internal or external cardioversion. Given a propensity for both right and left atrial thrombus formation in patients with AF, there is the potential for pulmonary embolism, in addition to CVA. Therefore, the current American College of Chest Physicians’ recommendations for anticoagulation prior to and following electrical cardioversion seem vindicated.
Although the findings of this well-conducted study seem quite concise, the number of patients studied was relatively small and further studies are needed to corroborate these findings. Further studies are also indicated to determine if these findings apply to patients with atrial flutter, and whether patients with atrial flutter who are atrially paced into sinus rhythm also have atrial stunning and a propensity for thrombus formation and embolization. As further studies are reported, it may be possible to further refine therapy and increase the safety of cardioversion.
References
This article has been cited by other articles:
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  N. A. Metheny Preventing respiratory complications of tube feedings: evidence-based practice. Am. J. Crit. Care., July 1, 2006; 15(4): 360 - 369. [Abstract] [Full Text] [PDF]
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 G. D. Veenhuyzen, C. S. Simpson, and H. Abdollah Atrial fibrillation Can. Med. Assoc. J., September 28, 2004; 171(7): 755 - 760. [Abstract] [Full Text] [PDF]
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