Transesophageal Echocardiography in Patients with Atrial Flutter
ABSTRACT & COMMENTARY
Synopsis: Atrial thrombus or spontaneous echo contrast are common in patients who present with atrial flutter of more than two days duration.
Source: Irani WN, et al. Circulation 1997;95:962-966.
Little is known about the prevalence of atrial thrombi and spontaneous echo contrast in patients presenting for conversion of atrial flutter. Irani et al identified 47 patients during a one-year period who presented with atrial flutter and were not taking warfarin anticoagulation. Patients with a prior history of documented atrial fibrillation or mitral valve disease were excluded. The final study group included 47 male patients with an average duration of 4 ± 9 weeks of atrial flutter. Fifty-three percent of the patients had abnormal left ventricular function, and most had either hypertension, diabetes, congestive heart failure, or coronary artery disease. Five of the 47 patients (11%) had had a prior cerebrovascular event. Patients underwent transthoracic and transesophageal echocardiography (TEE) prior to any attempt at cardioversion.At this initial study, atrial thrombus was seen in one patient, atrial thrombi and spontaneous echo contrast in four patients, and 11 patients only had spontaneous echo contrast. Peak left atrial appendage velocity was lower in patients with either atrial thrombi or spontaneous echo contrast. All 31 patients without thrombus or spontaneous echo contrast on TEE underwent cardioversion without anticoagulation, and no clinically recognized embolic events were observed during four weeks of follow-up. Four patients with spontaneous echo contrast initially underwent electrical cardioversion without anticoagulation. None of these four had an embolic event during follow-up.
In the other seven patients, cardioversion was deferred. Of these patients, one suffered a cerebrovascular accident four days after TEE, one failed cardioversion, two were successfully cardioverted after three weeks of anticoagulation, and three patients were lost to follow-up. All five patients in whom atrial thrombi were identified had cardioversion deferred and anticoagulation initiated. Four of these five patients converted either spontaneously (1) or electrically (3) after three weeks of anticoagulation with no embolic sequelae. One patient was lost to follow-up. Forty patients underwent pulsed Doppler examination immediately after successful electrical cardioversion. Eleven of these patients showed no atrial mechanical activity immediately after cardioversion.
The authors conclude that atrial thrombus or spontaneous echo contrast are common in patients who present with atrial flutter of more than two days’ duration. They recommend that a TEE-guided approach may be used to select those patients who require anticoagulation before cardioversion.
COMMENT BY JOHN P. DiMARCO, MD, PhD
The management guidelines for patients with atrial flutter with regard to cardioversion are in evolution. Prior to 1995, the recommendation was that patients with atrial flutter did not require anticoagulation before cardioversion. It was thought that atrial electrical and mechanical activity were more organized during atrial flutter than during atrial fibrillation and that this would eliminate the need for anticoagulation. However, this opinion was based on incomplete data. Most large retrospective series of cardioversion of atrial arrhythmias included a large number of patients with atrial fibrillation together with a smaller number of patients with atrial flutter. Quite often the breakdown was not evident from the report. In addition, patients with atrial flutter tend to be much less stable. Ventricular rates in atrial flutter are more difficult to control pharmacologically. Therefore, patients with atrial flutter often present earlier and are within the 48-hour window. Even when they present later, it is frequently not possible to defer cardioversion for three weeks because of an inability to control ventricular rate.This paper by Irani et al points out that, when ventricular rates can be safely controlled, consideration of embolic risks after cardioversion is appropriate even in patients with atrial flutter. The American Society of Chest Physicians had changed their prior recommendation with the 1995 guidelines (Chest 1995;108:352S-359S). At that time, they recommended anticoagulation before electric conversion of atrial flutter based on weak (class C) evidence. The paper by Irani et al provides further evidence to support this approach.
Therefore, at the present time, it is important to evaluate completely the patient who presents with atrial flutter. If the atrial flutter is of less than two days duration, it is still reasonable to proceed immediately with attempts at either pharmacologic or electrical conversion. In the patients with atrial flutter of more than two days duration, a more complicated approach is necessary. First, the hemodynamic status of the patient in atrial flutter and the ability to safely achieve rate control should be assessed. Patients who are highly symptomatic and whose rates cannot be adequately controlled should probably still undergo cardioversion as necessary. However, these patients should probably be anticoagulated after the procedure because of the atrial stunning after conversion detected by Irani et al. Patients who can be rate controlled should probably be treated according to the guidelines for patients with atrial fibrillation. At the present time, this is either three weeks of anticoagulation or a TEE-guided approach in which patients without atrial thrombi or spontaneous echo contrast are acutely anticoagulated with heparin, cardioverted, and then maintained on anticoagulation for at least four weeks.
Finally, we must admit that we do not at present know if the method of cardioversion used will have an effect on atrial stunning after sinus rhythm is restored. Atrial flutter can often be terminated by either pacing or drugs. It remains to be demonstrated that these alternate techniques will be better since some of the stunning observed may be the result of the prolonged period of tachycardia rather than the electrical shock itself.
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