Acute Anticoagulation for AF

Anticoagulation is a two-step process involving acute and chronic treatment. The risk of cardioversion in the absence of anticoagulation increases proportionally with the time an individual is in AF. Although it is generally considered to be safe to cardiovert an unanticoagulated patient who has been in AF for less than 48 h, left atrial thrombus, spontaneous echo contrast, and stroke have been reported to occur within this 48-h window. Weigner et al. (2) retrospectively identified 375 patients with AF lasting less than 48 h. They found the incidence of thromboembolic events after resumption of normal sinus rhythm to be 0.8%. Interestingly, these individuals who had thromboembolic events had normal left ventricular function and no history of AF or prior thromboembolism, and would not have been traditionally characterized as "high risk" for embolism. Although this incidence of clinical thromboembolism is low compared to the 5-7% risk of stroke in unanticoagulated patients who have AF for greater than 48 h who undergo cardioversion, it is nevertheless a significant problem given the overall prevalence of AF in the population. Additionally, there is no difference in atrial mechanical function in patients who cardiovert spontaneously, pharmacologically, or electrically (3). Therefore, it would not be unreasonable to anticoagulate an individual as soon as AF is initially documented if you plan to cardiovert the patient or the patient is at high risk of thromboembolism.

Given the risk of thromboembolism with cardioversion—whether spontaneous, pharmacologic, or electrical—in patients with AF of greater than 48-72 h duration, anticoagulation is needed prior to and after cardioversion. Two approaches are currently acceptable. One method is to place the patient on warfarin and maintain an International Normalized Ratio (INR) of 2 or greater for at least 3-4 wk prior to cardioversion. After cardioversion, the patients need to remain on warfarin for at least 3 wk prior to discontinuing anticoagulation, since there can be a significant lag between the restoration of sinus rhythm and resumption of normal atrial mechanical function. This can lead to thromboembolism after cardioversion if the patient is not adequately anticoagulated. The importance of maintaining strict anticoagulation has been demonstrated in a study performed at the Ochsner Medical Institutions (4). One hundred and fifty patients with AF underwent elective electrical cardioversion. All patients were anticoagulated for at least 3 wk with weekly blood tests to ensure an INR of 2 or greater. If the patient's INR dipped below 2, the "clock" was restarted and the patient would have to demonstrate three more consecutive weeks of therapeutic INRs. Ninety-five percent of the patients were successfully cardioverted, and there were no thromboembolic events. Therefore, by maintaining a very strict level of precardioversion anticoagulation (INR greater than or equal to two or three consecutive weekly measurements) restoration of sinus rhythm can be achieved with minimal morbidity. In clinical practice, this can translate into several weeks or months for an individual patient to achieve this goal. This scenario can potentially result in a decreased effectiveness of cardioversion and antiarrhythmic therapy. The longer a patient is in AF, the more remodeling (i.e., dilatation and fibrosis) can occur, decreasing the likelihood of restoring sinus rhythm.

An alternative abbreviated approach to cardioversion in a patient with AF of greater than 2 d duration is to perform a transesophageal echocardiogram (TEE). If the TEE does not demonstrate left atrial thrombus, the patient can undergo cardioversion followed by anticoagulation for several weeks. Ideally, the patient would receive simultaneous warfarin and intravenous (iv) unfractionated heparin until the INR is therapeutic in order to minimize the time the patient has subtherapeutic levels of anticoagulation. The use of low mol-wt heparins as a substitute for iv heparin in this population is currently being studied in the ACUTE 2 trial.

TEE-expedited cardioversion has been compared to the traditional approach in the ACUTE pilot and main trials. In the pilot study, which was reported by Manning et al. (5), 230 patients with AF of greater than 2 d duration were placed on iv heparin and underwent TEEs. A total of 196 patients without thrombi underwent cardioversion (95% successful) and no patients had thromboembolism. The results of the main ACUTE trial were recently presented (5a). Among 1,222 patients randomized, the risk of stroke and transient ischemic attack was 0.6%, with no statistically significant difference between the TEE-expedited and traditional groups.

There may be a significant lag between the restoration of sinus rhythm as manifested by the presence of P waves on an electrocardiogram and the return of normal atrial transport function after a cardioversion is performed. This atrial electromechanical dissociation may place the patient at risk of thromboembolism in the period after successful cardioversion is performed. Therefore, it is recommended to maintain the patient at therapeutic levels of anticoagulation for at least 3-4 wk after cardioversion. In patients in whom the risk of recurrence of AF is high, anticoagulation may need to be used for several months until adequate assessment of arrhythmia suppression is determined.

Often, a physician or patient cannot determine the onset or duration of the arrhythmia. If the decision is made to cardiovert the patient in this situation, then either of these two approaches is a viable option. The major advantage of the TEE approach is that it reduces the duration of the waiting period prior to cardioversion. In a highly symptomatic patient, this may be the preferred option. Currently, the decision to proceed with cardioversion is based on clinical judgement without morbidity or mortality data to support this approach over rate control and long-term anticoagulation. Dense, spontaneous echo contact is a risk factor for subsequent thromboembolism (6), and it is not well-established when to proceed with cardioversion after TEE when dense, spontaneous echo contrast is seen. There is also uncertainty regarding when a patient in whom TEE has documented atrial thrombus can safely be cardioverted.

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