Prospective Evaluation of Transesophageal Pacing for the Interruption of Atria1 Flutter WYNNE~RAWFORD, M.D., VANCE J. PLUMB, M.D., ANDREW E. EPSTEIN, M.D., G. NEAL KAY, M.D. Birmingham, Alabama PURPOSE: Although transesophageal pacing has been used successfully for the interruption of car- diac arrhythmias, the efficacy of this technique for the interruption of spontaneous atrial flutter re- mains poorly defined. The utility of transesophage- al pacing to interrupt atrial flutter that was persis- tent despite standard antiarrhythmic drug therapy (mean duration: 70.3 days; range: one day to more than 365 days) was studied prospectively in 39 con- secutive patients. PATIENTS AND METHODS: After written informed consent was obtained from each patient, transe- sophageal pacing was performed with a program- mable stimulator, using the distal electrode as the cathode and the proximal electrode as the anode. All patients continued to receive a type 1 antiar- rhythmic drug or amiodarone throughout the peri- od of transesophageal pacing. The response to transesophageal pacing was classified as follows: (1) direct conversion; (2) indirect conversion; or (3) failure to interrupt atria1 flutter. RESULTS: The mean stimulus amplitude and pulse duration required for atria1 capture were 19.8 f 7.5 mA and 18.4 f 7.9 msec. Atria1 flutter was success- fully converted to sinus rhythm by transesophageal pacing in 82% of patients. In 38% of patients, atrial flutter was converted directly to sinus rhythm without another intervening arrhythmia (direct conversion). The mean pacing rate required for di- rect conversion was 341 f 27 beats/minute. In 44% of patients, the cycle length of atria1 flutter was accelerated to less than 180 msec or was converted to atria1 fibrillation with spontaneous conversion to sinus rhythm within 24 hours (mean 8.4 f 9.3 hours, indirect conversion). The mean pacing rate inducing accelerated atria1 flutter or transient atria1 fibrillation was 372 f 61 beats/minute (p = NS compared to direct conversion). Atrial flutter was not interrupted or atrial fibrillation was in- duced that did not spontaneously convert to sinus rhythm within 24 hours in an additional seven pa- tients (18% ). The underlying cardiac disease, age, previous drug therapy, atria1 size, atria1 flutter cy- cle length, history of prior atrial fibrillation, left ventricular function, and concomitant medical ill- nesses did not predict the efficacy of transesopha- geal pacing. CONCLUSION: The present study suggests that transesophageal pacing is highly effective for in- terrupting spontaneous atria1 flutter that does not terminate with standard antiarrhythmic drug therapy. A trial flutter is often persistent despite antiar- rhythmic drug therapy and frequently requires electrical cardioversion or rapid pacing for termina- tion. Intracardiac electrophysiologic studies have demonstrated a re-entrant basis for chronic atria1 flut- ter [l-3], and the role of rapid atria1 pacing to tran- siently entrain and interrupt this arrhythmia is well established [4-61. Although atria1 flutter can be termi- nated by rapid atria1 pacing using endocardial or epi- cardial electrodes in most patients [4-121, Waldo et al [6] have described a faster form of atria1 flutter (type II) that cannot be interrupted by rapid pacing [4,5]. However, antiarrhythmic drugs that prolong the cycle length of atria1 flutter may enhance the likelihood of successful interruption by atria1 pacing [12]. Prior reports of transesophageal pacing for the in- terruption of atria1 flutter have demonstrated this technique to be highly effective [7-111. However, these studies have included patients with arrhythmias that have been induced in the electrophysiologic laboratory [7,9] or that have developed following cardiac surgery [P61, conditions in which atria1 flutter is likely to be transient and self-terminating. This report presents the results of a prospective trial of transesophageal pacing for the termination of spontaneously occurring atria1 flutter that was persistent despite antiarrhyth- mic drug therapy in patients with a wide variety of cardiac disorders. PATIENTS AND METHODS All patients referred to the arrhythmia consultation service at the University of Alabama at Birmingham or the Birmingham Veterans Administration Hospi- tals because of atria1 flutter were prospectively evalu- ated. The patients’ age, sex, underlying structural heart disease, antiarrhythmic medications and plasma levels, duration of atria1 flutter, and prior history of atria1 fibrillation, hypertension, congestive heart fail- ure, chronic obstructive pulmonary disease, or diabe- tes mellitus were recorded. Patients with a history of cardiac surgery within the preceding six weeks or a reversible extracardiac condition that may precipitate atria1 flutter, such as hyperthyroidism, pericarditis, uncontrolled congestive heart failure, recent myocar- dial infarction, or acute pulmonary disease, were ex- cluded from the study. Patients previously receiving maintenance type 1 antiarrhythmic drugs (or amioda- rone) continued to take their prior medications. Pa- tients not receiving type 1 antiarrhythmic drugs were June 1989 The American Journal of Medicine Volume 86 663