The contribution of artificial pacemaking to understanding the pathogenesis of arrhythmias

Right atrial or ventricular pacing was performed on 36 occasions in 26 patients in an attempt to terminate a variety of tachyarrhythmias. Of 16 episodes of atrial flutter, 13 were terminated successfully; in 9 of the 13, sinus rhythm or the patient's pre-flutter rhythm was restored immediately, whereas in 4 patients, intervening atrial fibrillation or unstable atrial flutter occurred. Pacing terminated paroxysmal atrioventricular junctional or paroxysmal atrial tachycardia on 3 occasions; in a fourth patient, this tachyarrhythmia terminated during catheter manipulation. Six episodes of pacemaker-induced ventricular tachycardia were abolished by ventricular pacing. In 2 patients, atrial tachycardia was only transiently suppressed, and in 1 of these patients, d-c cardioversion produced a similar effect. Atrial fibrillation, spontaneously converting to atrial flutter, resulted during pacing for atrial tachycardia with block; the latter arrhythmia returned when the atrial flutter was terminated. Atrial fibrillation in 7 patients remained unaffected by atrial pacing. Based on the different electrophysiologic mechanisms responsible for reentrant excitation and automatic pacemaker discharge, an attempt has been made to determine the pathogenesis of the tachyarrhythmia by its response to pacing.     

Efficacy of intravenous amiodarone in the management of paroxysmal or new atrial fibrillation with fast ventricular response

We tested the efficacy of intravenous amiodarone (5 mg/kg) in slowing ventricular response and/or restoring sinus rhythm in 26 patients with paroxysmal or new atrial fibrillation with fast ventricular response. There were 16 men and 10 women with ages ranging from 35 to 84 years, mean 63 years. Intravenous amiodarone initially slowed the ventricular response in all patients from 143 +/- 27 to 96 +/- 10 beats/min (P less than 0.001). Twelve patients (46%) reverted to sinus rhythm within the first 30 min (range 5 to 30 min, mean 14 +/- 9 min). One patient reverted to atrial flutter after 10 min and 40 min later to sinus rhythm. Six patients (23%) converted to sinus rhythm after 2 to 8 hr and in these 6 cases, the initial slowing in ventricular response obtained with amiodarone persisted until conversion. Seven patients (27%) did not convert to sinus rhythm following amiodarone administration and they required further medical therapy to slow the ventricular response and/or to convert to sinus rhythm. No serious side effects from drug administration were noted. Intravenous amiodarone appears as a highly effective medication in the conversion or control of new onset atrial fibrillation with fast ventricular response.     

Nutzen einer VDD-Defibrillationselektrode zur Aufzeichnung von atrialen Elektrogrammen bei Vorhofflimmern/-flattern

BACKGROUND: Monitoring of atrial signals improves the accuracy in identifying supraventricular tachyarrhythmias to prevent inappropriate therapies in patients with implantable cardioverter-defibrillators (ICD). Since complications due to the additional atrial lead were found in dual chamber ICD systems with 2 leads, we designed a single-pass VDD-lead for use with dual chamber ICDs. PATIENTS AND METHODS: After promising animal experiments in a German multicenter study a prototype VDD lead (single-coil defibrillation electrode with 2 additional fractally coated rings for bipolar sensing in the atrium) was temporarily used in 20 patients. Atrial and ventricular signals were recorded during sinus rhythm, atrial flutter, atrial fibrillation and ventricular tachycardia or ventricular fibrillation. Terminations of ventricular arrhythmias were performed by internal DC shock. RESULTS: The implantation of the electrode was successful in 18 of 20 patients. Mean atrial pacing threshold was 2.45 +/- 0.9 V/0.5 ms, mean atrial impedance was 215 +/- 31 Ohm. Atrial amplitudes were greater during sinus rhythm (2.7 +/- 1.6 mV) than during atrial flutter (1.36 +/- 0.28 mV, p < 0.05) or atrial fibrillation (0.92 +/- 0.29 mV, p < 0.01). During ventricular fibrillation atrial "sinus"-signals had significantly (p < 0.01) lower amplitudes than during sinus rhythm. Mean ventricular sensing was 13.3 +/- 7.9 mV, mean ventricular impedance was 577 +/- 64 Ohm. Defibrillation was successful with 20 J shock. 99.6% of P waves could be detected in sinus rhythm and 85 +/- 9.9% of flutter waves during atrial flutter. During atrial fibrillation 55% of atrial signals could be detected without modification of the signal amplifier. CONCLUSIONS: A new designed VDD dual chamber electrode provides stable detection of atrial and ventricular signals during sinus rhythm and atrial flutter. For reliable detection of atrial fibrillation modifications of the signal amplifier are necessary.     

Successful intracardiac electrical conversion of atrial flutter in patients with complex congenital heart disease

Sixteen patients presenting on 21 occasions with atrial flutter in association with complex congenital heart disease were treated by intracardiac stimulation techniques combined with activation mapping. Nineteen episodes of atrial flutter were successfully converted to sinus rhythm. In the remaining two episodes atrial fibrillation was induced with spontaneous conversion to sinus rhythm within 12 hours in one episode and immediate DC cardioversion to sinus rhythm in the other. Intracardiac stimulation techniques were highly successful in this group and allowed reliable conversion to sinus rhythm without general anaesthesia and high energy cardioversion. In patients with atrial flutter associated with congenital heart disease intracardiac stimulation techniques should be tried first.     

Successful intracardiac electrical conversion of atrial flutter in patients with complex congenital heart disease.

Sixteen patients presenting on 21 occasions with atrial flutter in association with complex congenital heart disease were treated by intracardiac stimulation techniques combined with activation mapping. Nineteen episodes of atrial flutter were successfully converted to sinus rhythm. In the remaining two episodes atrial fibrillation was induced with spontaneous conversion to sinus rhythm within 12 hours in one episode and immediate DC cardioversion to sinus rhythm in the other. Intracardiac stimulation techniques were highly successful in this group and allowed reliable conversion to sinus rhythm without general anaesthesia and high energy cardioversion. In patients with atrial flutter associated with congenital heart disease intracardiac stimulation techniques should be tried first.     

Direct conversion of atrial flutter to sinus rhythm with low-output,short-duration transesophageal atrial pacing

Background and hypothesis: Transesophageal atrial pacing (TAP) is useful for terminating paroxysmal non-selfterminating atrial flutter (RAF); however, high output pacing of long stimulus duration causes severe symptoms such as chest pain. The objective of this study was to investigate the effect of low-output, short-duration TAP on the conversion of PAF. Methods: We applied low-output (within 15 mA with a pulse duration of 10 ms), short-duration (within 4 s) TAP in 31 patients (50±19 years) with PAF. Transesophageal pacing was delivered with 10 pulses of burst pacing at intervals that were 20 ms shorter than those of the flutter wave length. When the conversion was unsuccessful, we delivered 20 pulses of burst pacing. Results: Sixteen patients (52%) were converted directly to sinus rhythm and 12 (38%) to atrial fibrillation. Transesophageal pacing was ineffective in 3 (10%) patients. The duration of atrial flutter, maximum flutter wave amplitude, effective pacing intervals, underlying heart diseases, and cardiac function were not different between patients who had direct conversion to sinus rhythm and those converted to atrial fibrillation. The patients who had direct conversion to sinus rhythm had longer flutter wave cycle lengths than those converted to atrial fibrillation (248 vs. 221 ms, p<0.005). No patient had complications and complained of any symptoms. Conclusion: Low-output, short-duration TAP was useful to convert PAF directly to sinus rhythm without side effects.     

Therapeutic value of trans-esophageal electrostimulation in tachycardic arrhythmias

We were able to terminate atrial flutter in 136 of 162 patients by transesophageal rapid atrial stimulation (conversion to sinus rhythm in 75 cases, induction of atrial fibrillation in 61 cases). Atrial tachycardias were interrupted in 17 of 23 patients (sinus rhythm in 11, atrial fibrillation in 6 cases), AV reciprocating resp. AV nodal supraventricular tachycardias were terminated in 32 of 33 patients (sinus rhythm in 28 cases, atrial fibrillation in 4 cases). By transesophageal rapid ventricular and/or atrial pacing, ventricular tachycardias could be terminated in 10 of 15 patients. The success rate of transesophageal pacing is influenced by the type of tachyarrhythmia, by the type of atrial flutter and by the stimulation rate. It is not influenced by the tachycardia's cycle length. Because the success rates are comparable with invasive technique and the procedure is simpler, the non-invasive transesophageal antitachycardia pacing represents a useful method for termination of tachycardic arrhythmias.     

Continuous rapid atrial pacing to control recurrent or sustained supraventricular tachycardias following open heart surgery.

A technique is described to control recurrent or sustained supraventricular tachycardia associated with rapid ventricular rates following open heart surgery. The technique utilizes a pair of temporarily implanted atrial epicardial wire electrodes to pace the heart. In one group of patients with recurrent atrial flutter and 2:1 A-V conduction, continuous rapid atrial pacing at 450 beats/min produced and sustained atrial fibrillation. The ventricular response rate immediately slowed when compared to that during atrial flutter, and if further slowing was required, it was easily accomplished by the administration of digitalis. Another group of patients with different arrhythmias (recurrent paroxysmal atrial tachycardia, sustained ectopic atrial tachycardia, or sinus rhythm with premature atrial beats which precipitated runs of atrial fibrillation) was treated with continuous rapid atrial pacing to produce 2:1 A-V block. In all instances, the continuous rapid atrial pacing suppressed the supraventricular tachycardia and maintained the ventricular response rate in a therapeutically desirable range. It was demonstrated that the technique is safe, effective, and reliable.     

Failure of rapid atrial pacing in the conversion of atrial flutter

Rapid atrial pacing, at rates of 150 to 600/min with stimulus strength up to 15 ma, was attempted in 15 patients with atrial flutter. In 13 of the patients, atrial capture was achieved with changes in both atrial and ventricular rates. In 7 of these, flutter resumed upon cessation of pacing. In the other 6, rapid atrial pacing produced atrial fibrillation which persisted until cardioversion. In 2 patients, atrial capture could not be obtained because of increased atrial refractoriness secondary to flutter. Thus, rapid atrial pacing was ineffective in converting atrial flutter to normal sinus rhythm in all 15 patients. This was in contrast to direct-current cardioversion which was successful in 12 of the patients, in all of whom stable sinus rhythm developed. The 3 patients who did not undergo cardioversion subsequently experienced spontaneous conversion to sinus rhythm. These results suggest that rapid atrial pacing has little place in the management of atrial flutter.     

Incidence of arrhythmias after atrial or dual-chamber pacemaker implantation

The incidence of sustained atrial, pacemaker-mediated and ventricularrhythm disturbances was studied retrospectively in a consecutiveseries of112 patients without a history of preexisting atrialtachy arrhythmias, receiving an atrial or dual-chamber pacemaker. Early atrial fibrillation (during the first week) was recordedtwice. Late atrial fibrillation was seen in seven patients,flutter in one, yielding a total incidence of 8.9% for 22 months.There were no significant differences with respect to age, aetiology,electrocardiographic diagnosis, pacing history, or the measuredintracardiac P wave between the group with and the group withoutatrial fibrillation. Treatment with digoxin reverted three patientsto sinus rhythm, association of digoxin and amiodarone, sixpatients. One patient with congestive heart failure remainedin atrial fibrillation. Pacemaker-mediated tachycardia was not a major problem. Onepatient of a subgroup with known ventricular arrhythmia hada non-sustained ventricular tachycardia during programming atfollow-up; sustained ventricular tachycardia was not recorded.Reprogramming to VDD, DVI or VVI was done in 6/100patients. The incidence of atrial fibrillation or flutter in highly selectedpatients with dual-chamber or atrial pacing is moderately low.It is not possible to identify patients with a high risk fordevelopment of atrial fibrillation; when it occurs, it is easilycontrolled with drugs. DDD pacing seems to be safe in patients with a history of seriousventricular arrhythmias, treated with appropriate drugs.     

胺碘酮和毛花甙C转复阵发性心房颤动及 心房扑动疗效的比较

目的对比胺碘酮和毛花甙C治疗阵发性心房颤动(房颤)及心房扑动(房扑)的疗效。方法阵发性房颤及房扑发作1～72h,随机分为胺碘酮组(30例)和毛花甙C组(28例),毛花甙C组静脉注射毛花甙C0.4～0.8mg;胺碘酮组静脉注射胺碘酮150或225mg后改为静脉滴注150～450mg,观察其复律情况,心室率的变化,QT间期及药物副作用。结果毛花甙C组,阵发性房颤24例,复律成功11例,阵发性房扑4例,复律成功2例。胺碘酮组,阵发性房颤25例,复律成功19例,阵发性房扑5例,复律成功3例。两组未复律者心室率均有明显控制,QT间期及副作用差异无显著性意义;毛花甙C组复律平均时间3.5h,胺碘酮组平均复律时间6.5h。结论阵发性房颤及房扑的复律胺碘酮疗效高于毛花甙C,二者心室率的控制及副作用无显著性差别,复律时间毛花甙C短于胺碘酮。     

The effects of class IA antiarrhythmic drug on the common type of atrial flutter in combination with pacing therapy

In 11 patients with common type of atrial flutter (common AF), rapid atrial pacing from the high right atrium was performed before and/or after class Ia antiarrhythmic drug administration, confirming transient entrainment by decreasing the pacing cycle length by 10 ms. In 10 patients before the drug administration, common AF was not interrupted although the pacing cycle length was decreased to 200 ms in 5 patients, accelerated atrial flutter or atrial fibrillation was induced in 4 patients, and common AF was converted into sinus rhythm in only 1 patient. After the drug administration common AF was converted into sinus rhythm in 5 out of 6 patients. The class Ia antiarrhythmic drug prolonged the common AF cycle length (255 +/- 12 ms vs. 298 +/- 37 ms, p less than 0.005) and widened the entrainment zone (64 +/- 7 ms vs. 90 +/- 20 ms, p less than 0.05). The widening of the entrainment zone and the prolongation of the common AF cycle length facilitate the successful conversion of common AF at a longer pacing cycle length, which would not precipitate atrial fibrillation or accelerated atrial flutter. The combination therapy of rapid atrial pacing and the class Ia antiarrhythmic drug is thought to be useful in the therapy of common AF.     

Facilitating influence of procainamide on conversion of atrial flutter by rapid atrial pacing

In a prospective, double-blind, randomized, placebocontrolledstudy we investigated the facilitating influence of intravenousprocainamide on conversion of atrial flutter by rapid atrialpacing. Fifty consecutive patients with spontaneous sustained atrialflutter were 1:1 randomized into two homogenous groups: groupA received 10 mg. kg^–1 procainamide intravenously, groupB placebo. After infusion there was a significant (P<0·01)lengthening of the flutter cycle with respect to baseline ingroup A, exceeding the flutter cycle length of the control group(P<0·05). The overall success rate of rapid atrialpacing in restoring sinus rhythm was significantly higher afterpre-treatment with procainamide compared to placebo (100% vs76% P<0·05): 20 patients of group A reverted immediatelyafter pacing to sinus rhythm, the remaining five after a briefepisode of atrial fibrillation. In the placebo group, 16 patientsshowed a prompt conversion to sinus rhythm and three after transientatrial fibrillation. In the remaining six patients, due to sustainedpacing-induced atrial fibrillation, direct current cardioversionwas necessary. After administration of procainamide a less aggressivestimulation protocol with significantly (P<0·01) longerpaced cycles to interrupt atrial flutter was achievable. In conclusion, intravenous procainamide augments the efficacyof atrial pacing to convert atrial flutter to sinus rhythm.     

Use of procainamide with rapid atrial pacing for successful conversion of atrial flutter to sinus rhythm

Rapid atrial pacing is a useful technique and often the therapy of choice to terminate atrial flutter in patients. However, interruption of atrial flutter by rapid atrial pacing may not always produce sinus rhythm, but rather may result in atrial fibrillation. Twelve patients with spontaneous atrial flutter that had been present for greater than 24 h were studied to assess the efficacy of atrial pacing, alone and in combination with procainamide, to convert atrial flutter to normal sinus rhythm. Rapid atrial pacing for greater than or equal to 15 s from selected atrial sites at selected pacing rates were performed during atrial flutter. The initial pacing rate was always at a cycle length 10 ms shorter than the atrial flutter cycle length. If atrial flutter persisted after cessation of pacing, it was repeated at progressively shorter cycle lengths until either a rate of 400 beats/min was achieved or atrial fibrillation was induced. In two patients, atrial flutter was converted to sinus rhythm with pacing alone. Three patients developed sustained atrial fibrillation as a result of the rapid atrial pacing, this rhythm ultimately reverting back to atrial flutter in two. Ten patients received procainamide and 9 of the 10 had lengthening of the atrial flutter cycle length by a mean of 68 ms (1 patient continued to have atrial fibrillation). Then, using the same atrial pacing protocol, high right atrial pacing alone at a mean cycle length of 227 ms interrupted atrial flutter in all these patients, returning their rhythm to sinus rhythm. It is concluded that intravenous procainamide effectively augments the efficacy of rapid atrial pacing to convert atrial flutter to sinus rhythm.     

Radiofrequency ablation in auricular flutter. Predictive factors of primary success and medium term results

Ninety-one consecutive patients underwent radiofrequency ablation of chronic or paroxysmal atrial flutter. The average age of the patients was 66. There was a previous history of atrial fibrillation in 38% of cases and of cardiac surgery in 14.3% of cases. The primary success rate was 79% (92% in cases of common flutter). The predictive factors of success were the type of flutter (p < 0.001), left ventricular (p < 0.01) and left atrial dimensions (p < 0.01) at echocardiography. The length of the cavo-tricuspid isthmus measured by echocardiography had no influence on the initial result but, in primary success, did affect the parameters of the procedure (duration and number of applications of radiofrequency energy). After an average of 11 +/- 2 months, sinus rhythm was maintained in 67% of patients. There were recurrences of flutter in 27.5% of cases and of atrial fibrillation in 5.5% of cases: 85% of these episodes occurred during the first six months after ablation. A second procedure was carried out in 12 patients for recurrence of flutter (92% primary success rate). After an average follow-up of 8.4 months, 4 patients had a recurrence and required a third procedure (100% success rate). In cases of failure of ablation, the rhythm was converted by a shock or atrial pacing: 47.3% of these patients remained in sinus rhythm with antiarrhythmic therapy with a 12 month follow-up. Radiofrequency ablation of atrial flutter is, therefore, a safe method, the difficulty of which is mainly related to anatomical factors: the medium-term results are better than those of other therapeutic methods.     

Efficacy of rapid atrial pacing for conversion of atrial flutter in medically treated patients

To determine factors affecting the success rate of rapid atrial pacing in converting atrial flutter to sinus rhythm in medically treated patients, we prospectively used this technique for 120 consecutive episodes in a total of 110 patients (94 male, 16 female, mean age 63 ± 14 years). Structural heart disease was present in 77%, and all patients were receiving antiarrhythmic drugs at the time of the procedure. Atrial flutter type I was present in 92 of 110 patients (84%), and atrial flutter type II in 18 of 110 (16%). Primary success rate (return to sinus rhythm either immediately or after < 10 min of atrial fibrillation) was 70% (71/102) for flutter type I, and 6% ( 1/18) for flutter type II (p < 0.001). Delayed success (conversion to sinus rhythm in > 10 min but < 24 h) was observed in 15 additional episodes of flutter type I (15%) and in 1 additional episode of flutter type II (6%). The only clinical factors predicting primary success were (a) characteristics of flutter waves on the 12-lead surface electrocardiogram, (b) duration of flutter (primary success rate of 81 % if flutter < 1 month vs. 57% if > 1 month, p< 0.05), and (c) flutter rate (primary success rate of 78% if < 260/min vs. 56% if > 260/min, p< 0.05). In 6/71 episodes of flutter type I (8%), prolonged sinus pauses or severe bradyarrhythmias occurred after conversion to sinus rhythm. It was concluded that overdrive atrial pacing is an effective procedure to convert atrial flutter type I in sinus rhythm in medically treated patients; the primary success rate of the procedure depends on flutter type, duration, and rate. Because severe bradyarrhythmias are not uncommon at the time of conversion and because it does not require general anesthesia, this technique can be considered as a first-step therapy in this particular population.     

Atrial pacing for conversion of atrial flutter

Fifty-seven episodes of atrial flutter in 46 consecutive medically treated patients (aged 60 +/- 17 years) were treated by rapid atrial pacing. Thirty-three patients (72%) had structural heart disease. Most pacing trials were conducted in patients receiving digoxin (88%) and antiarrhythmic drugs (77%). In 51 of 57 trials (89%), patients were successfully converted to normal sinus rhythm. Multivariate analysis revealed that patients who had congestive heart failure and who were older were more likely to be refractory to pacing. Left atrial size did not influence outcome. Confirmation of local atrial capture with a bipolar atrial electrogram and use of multiple atrial pacing sites enhanced the success rate. Eight patients (17%) demonstrated sinus node suppression after atrial pacing; sinus node disease was previously unsuspected in 4 of these patients. These bradyarrhythmias were easily managed because a pacing catheter was already in place. The only significant complication was femoral vein thrombosis in 1 patient. It is concluded that atrial pacing is an effective, safe and convenient method for the elective conversion of atrial flutter in the general population of medically treated patients. This technique is an attractive alternative to transthoracic cardioversion, and may be preferable in many patients.     

Response of atrial flutter to overdrive atrial pacing and intravenous disopyramide phosphate, singly and in combination.

Ten patients who suffered spontaneous paroxysms of atrial flutter were investigated by electrophysiological techniques. Two had overt Wolff-Parkinson-White syndrome; three Lown-Ganong-Levine syndrome; and one a concealed accessory atrioventricular connection. Atrial flutter was initiated, at study, by right atrial pacing and electrograms from the right atrium and coronary sinus were observed for at least five minutes to ensure stable flutter in both atria. Atrial flutter was terminated by 2.5 s or 5 s bursts of atrial pacing at rates 10, 50, or 100 beats/min faster than the intrinsic flutter rate in only two patients. Atrial flutter, which was reinitiated in two patients, was then treated with intravenous disopyramide phosphate, 2 mg/kg body weight, infused over five minutes. In all 10 patients the atrial rate slowed from a mean of 310 +/- 39 beats/min to 217 +/- 27 beats/min and atrial flutter terminated in one case. Though the mean ventricular rate fell from 161 +/- 52 beats/min to 156 +/- 45 beats/min the atrioventricular conduction ratio fell from 2.17 +/- 0.86 to 1.55 +/- 0.59 and four patients were left with symptomatically significant increases of ventricular rate. In seven of nine patients overdrive atrial pacing, repeated after disopryamide, resulted in the conversion of atrial flutter to sinus rhythm. In this study, overdrive atrial pacing and intravenous disopyramide, singly and in combination, terminated atrial flutter in nine of the 10 patients and it is suggested that this method may provide an effective alternative to direct current cardioversion.     

Randomized placebo-controlled trial of propafenone for treatment of atrial tachyarrhythmias after cardiac surgery

Fourteen patients with atrial fibrillation or flutter and a ventricular rate of greater than or equal to 120 beats/min occurring after cardiac surgery entered a double-blind placebo-controlled conditional crossover trial of intravenous propafenone. Patients randomly received either propafenone (2 mg/kg body weight) or placebo during a 10 minute intravenous infusion. If 20 minutes after the initiation of this infusion there was no conversion to sinus rhythm, the patient received a second intravenous infusion over 10 minutes (either propafenone or placebo, whichever was not given first). The electrocardiogram was recorded continuously throughout the study. Fourteen patients received propafenone and 10 received placebo. No patient's rhythm converted to sinus rhythm after placebo. In six patients (43%) (p less than 0.001), the arrhythmia converted to sinus rhythm between 5 and 10 minutes after the end of the propafenone infusion. After propafenone, the ventricular response to atrial fibrillation or flutter decreased significantly from 141.6 +/- 15.2 to 116.0 +/- 15.5 beats/min. Ventricular rate did not change after placebo. The mean propafenone plasma concentration was 3.46 +/- 2.17 mg/liter. The only side effect of propafenone noted was a decrease in systolic blood pressure of 9 +/- 9 mm Hg. Propafenone was useful for management of atrial fibrillation after cardiac surgery both for control of rapid ventricular response and for conversion to sinus rhythm.     

Digoxin for converting recent-onset atrial fibrillation to sinus rhythm. A randomized, double-blinded trial

Study Objective: to determine whether digoxin is effective in converting atrial fibrillation of recent onset to normal sinus rhythm. Design: randomized, double-blinded, placebo-controlled trial with a maximum 18-hour treatment period. Setting: emergency room and medical floors of a non-referral city hospital. Patients: consecutive sample of 36 patients with atrial fibrillation of 7 days' duration or less, not on digitalis glycoside or anti-arrhythmic agents, with ventricular rate between 85 to 175 beats/min, without evidence of heart failure, acute myocardial infarction, unstable angina, preexcitation syndrome, thyrotoxicosis, hypokalemia, renal impairment, or severe metabolic disturbances. Interventions: digoxin solution in capsules or identical placebo, given in doses of 0.6, 0.4, 0.2, and 0.2 mg, at 0, 4, 8, and 14 hours, respectively, or until conversion to sinus rhythm, whichever occurred first. Continuous electrocardiographic recording by Holter monitor. Measurements and Main Results: nine of eighteen patients receiving digoxin and 8 of 18 receiving placebo had a return to sinus rhythm within 18 hours of study entry (95% confidence interval for the difference in proportions, -11% to 22%). Mean time to conversion was 5.1 hours in the digoxin group and 3.3 in the placebo group (95% Cl, -3.6 to 7.0 hours). Conclusions: spontaneous reversion to sinus rhythm is common in patients with atrial fibrillation of recent onset. Digitalization was not shown to affect the likelihood of reversion to sinus rhythm, and thus cannot be recommended for this purpose in patients with atrial fibrillation.