Pharmacological management of atrial fibrillation: an update

Therapy of atrial fibrillation remains difficult in many patients. There is increasing awareness that antiarrhythmic drug therapy instituted to maintain sinus rhythm after successful cardioversion of atrial fibrillation may pose a substantial risk to the patient. Therefore, results of prospective randomized trials are needed to allow a more evidence-based approach to the treatment of this common arrhythmia. Two recently published studies have shown superiority of amiodarone over conventional antiarrhythmic drugs in maintaining sinus rhythm. The largest such study published today, the Canadian Trial in Atrial Fibrillation (CTAF), has randomized 403 patients to amiodarone or to sotalol or propafenone. At the end of the observation period, amiodarone-treated patients were significantly more likely to remain in sinus rhythm than conventionally treated patients. A number of new antiarrhythmic drugs, mainly class III substances, are currently developed for the treatment of atrial fibrillation or atrial flutter. Ibutilide has recently been released for intravenous administration, attempting pharmacological cardioversion of atrial fibrillation/atrial flutter. It has been evaluated in a number of prospective trials, which showed a higher conversion rate in patients with atrial flutter. Dofetilide is another new compound developed mainly for maintenance of sinus rhythm after restoration of sinus rhythm. It has been evaluated in two prospective, randomized, placebo-controlled trials; moreover, analysis of the DIAMOND trials showed effectiveness of dofetilide in maintaining sinus rhythm in patients with depressed left ventricular function without increased mortality when compared with placebo. Finally, several ongoing studies compare the therapeutic strategy of controlling ventricular rate in atrial fibrillation compared with the strategy of maintaining sinus rhythm. These trials will help to optimize therapy in atrial fibrillation, the most commonly encountered arrhythmia.     

Termination of Spontaneous Atrial Flutter by Transesophageal Pacing

Transesophageal atrial pacing using the constant-rate technique was performed in 26 patients presenting with spontaneous atrial flutter (atrial cycle length between 180 and 270 ms). All but one patient had been treated with one or more antiarrhythmic agents (digoxin, quinidine, procainamide, propranolol, verapamil, diltiazem, and propafenone) within the previous 12 hours. Transesophageal atrial pacing at cycle lengths between 80 and 180 ms was successful in terminating atrial flutter in 22 patients: immediate reversion to sinus rhythm in 16, following transient sinus pause in one, following a brief period of atrial fibrillation in three, and following longer periods of atrial fibrillation in another two. No post-conversion ventricular arrhythmia and no other complications were observed. All patients experienced only a mild burning discomfort during the procedure. It is concluded that atrial pacing via the esophagus is a safe and noninvasive technique of terminating spontaneous atrial flutter. The effectiveness of this technique is comparable to endocardial or epicardial atrial pacing.     

Fetal arrhythmias: natural history and management

The aim was to delineate the significance and natural history of fetal arrhythmias and provide information about their management. A cohort of 114 infants with fetal arrhythmias detected during prenatal ultrasound (US) screening were studied. All subjects underwent echocardiography and were treated as clinically indicated. Postnatal outcome was obtained in 100% of infants until 1 year of age. The incidence of fetal arrhythmias was 0.3%. Among the 87 fetuses with atrial extrasystoles, 2.3% developed supraventricular tachycardia (SVT) in utero. Of the 10 SVT cases, only five required antiarrhythmic therapy in utero with digoxin and propafenone, which successfully restored sinus rhythm in 100% of fetuses, both nonhydropic and hydropic. Sinus bradycardia was associated with structural anomalies in 5 of 6 patients and only 2 of 4 fetuses with atrioventricular block survived. It is concluded that prognosis is good for most fetal tachyarrhythmias, whereas it is less favorable for bradyarrhythmias.     

Transesophageal pacemaker therapy in atrial flutter after procainamide pretreatment

Transesophageal atrial stimulation was applied in 56 patients to terminate atrial flutter. Extrastimulation and atrial burst techniques were applied using programmable stimulator (Medtronic 5328) and hexapolar esophageal electrode catheters. Thirty patients were randomized to receive digoxin pretreatment (group A), and 26 patients were randomized to receive procainamide pretreatment (group B). Efficacy of each pretreatment was evaluated by observing the change in the rhythm. In group A, transesophageal pacemaker therapy successfully converted atrial flutter to sinus rhythm in 13 patients and to atrial fibrillation in 14 patients, whereas the arrhythmia remained unchanged in the 3 remaining patients in the digitalized group. In group B, after procainamide pretreatment, sinus rhythm appeared in 19 and atrial fibrillation in 5, and no change was observed in the remaining 2 patients. Procainamide is more efficacious than digoxin (P < 0.05) in facilitating cardioversion by transesophageal stimulation.     

Efficacy of Type 1C Antiarrhythmic Agents for Treatment of Resistant Atrial Fibrillation

In order to determine the efficacy of type lC agents (flecainide, encainide, propafenone) in patients with atrial fibrillation who have failed to maintain sinus rhythm with type 1A agents (quinidine, procainamide, disopyramide), 147 patients, that were admitted into the John Dempsey Hospital with new or recurrent atrial fibrillation between 1987–1991, were studied retrospectively. Out of the total, 29 patients converted spontaneously to sinus rhythm, 14 patients were left in atrial fibrillation, and 104 patients were given a type 1A antiarrhythmic. Sixty-five of these patients remained in sinus rhythm (54% converted on drug alone, 46% required electrical cardioversion) for at least 6 months. Of the remaining 39 patients, 28 were given a type 1C antiarrhythmic; 13 were successfully converted (61% chemical, 39% electrical) to and remained in sinus rhythm for at least 6 months; the remaining 15 either failed to convert or reverted to atrial fibrillation. New onset atrial fibrillation had a significantly lower incidence of congestive heart failure (10%) than recurrent atrial fibrillation (33%; P < 0.01). No differences in digoxin, beta blocker use, or other clinical characteristics were seen either between type 1A or type 1C successes or failures. Similarly, echocardiographic dimensions did not predict success or failure with either class of agent. In conclusion, type lC antiarrhythmics for suppression of recurrent atrial fibrillation represent a reasonable therapeutic alternative for suppression of atrial fibrillation in patients who have failed type lA agents. Prognostic factors predicting success or failure remain undetermined.     

Fetal tachyarrhythmias: transplacental and direct treatment of the fetus-a report of 60 cases.

From 1981 to 1990, 60 fetuses with tachyarrhythmia (21-39 weeks of gestation) were treated in utero. Of these, 54 were cases of supraventricular tachycardia, and six of atrial flutter. Non-immune fetal hydrops was present in 21 cases with supraventricular tachycardia and in five cases with atrial flutter, a total of 26 cases.Transplacental treatment by maternally administered antiarrhythmic drugs (digoxin only or in combination with verapamil) produced good results in non-hydropic fetuses. In this group, all 34 fetuses survived. In fetuses with hydrops, 20 out of 26 survived.In 13 fetuses of the 26 with hydrops, direct fetal therapy was performed in addition to the transplacental therapy when the tachyarrhythmia was refractory to transplacental treatment. During the 9 years of this study, a variety of direct treatment regimes have been used consisting of intraperitoneal and/or umbilical intravenous administrations of different drugs. Since 1988, umbilical vein punctures have shown that the transplacental passage of digoxin (and amiodarone) is hampered in the presence of hydrops, and direct treatment may he necessary in these cases. Amiodarone seems to he the drug of choice for direct therapy. It is highly effective in supraventricular tachycardia and atrial flutter. The long elimination half-time of amiodarone reduces the number of umbilical cord punctures needed to maintain the therapeutic drug level in the fetus.     

Amplitude of Atrial Electrical Activity During Sinus Rhythm and During Atrial Flutter-Fibrillation

The onset of atrial flutter or fibrillation in a patient with a DDD pacemaker may result in sensing of the atrial arrhythmia and an inappropriate ventricular pacing response. In order to assess the potential of this problem, we evaluated the amplitude of atrial electrograms recorded from the right atrial appendage during sinus rhythm and during atrial flutter or fibrillation during 19 episodes in 18 patients. in 11 episodes of fibrillation and eight episodes of flutter, there was no difference in amplitude of either unipolar or bipolar atrial electrograms compared to that recorded during sinus rhythm (p > 0.05). In 14 of 19 episodes, the direction of depolarization of the bipolar electrogram did not change appreciably between sinus rhythm and the atrial arrhythmia. In summary, there is insufficient difference between amplitude of atrial depolarizations recorded during sinus rhythm and atrial flutter or fibrillation to be differentiated reliably by DDD pacemakers.     

Dofetilide: a new class III antiarrhythmic agent

Dofetilide is a relatively new class III antiarrhythmic agent that selectively blocks the rapid component of the cardiac ion channel delayed rectifier current. This results in an increase in the action potential duration and effective refractory period of the myocyte, thereby terminating reentrant tachyarrhythmias and preventing their re-induction. Oral dofetilide is effective in the conversion of atrial fibrillation and flutter to sinus rhythm and in the maintenance of sinus rhythm after conversion. It is generally well tolerated but like other antiarrhythmic agents in its class, torsades de pointes may be induced as a consequence of therapy. This risk is minimized by dosage adjustment according to creatinine clearance and QT(c) interval, by selecting patients without known risk factors for torsades and by initiating treatment in a monitored hospital setting for the first 3 days. Unlike other antiarrhythmic agents, oral dofetilide did not increase mortality in patients with a recent myocardial infarction or congestive heart failure, hence its importance as an alternative medication for the pharmacological conversion of atrial fibrillation and flutter, and maintenance of sinus rhythm after conversion in patients at high risk of sudden death.     

Termination of recent-onset atrial fibrillation/flutter in the emergency department: a sequential approach with intravenous ibutilide and external electrical cardioversion

Safety and effectiveness are the goals in treating patients with arrhythmias. In an open prospective study, we observed the efficacy and safety of up to 2 mg intravenous ibutilide, a new class III antiarrhythmic agent in haemodynamically stable patients presenting in the emergency department (ED) with symptoms of recent-onset (<48 h) atrial fibrillation/flutter. Arrhythmia termination within 90 min, haemodynamic parameters and proarrhythmic effects were assessed. Non-responders to the ibutilide infusion underwent external electrical cardioversion. We included 51 patients. In 31 patients therapeutic intervention with intravenous ibutilide was successful within 90 min (61%). In another seven patients conversion to sinus rhythm occurred after 90 min without any other intervention (14%). Blood pressure remained stable and no relevant proarrhythmic effects were observed. The 13 patients who did not respond to ibutilide treatment underwent successful external electrical cardioversion. The overall conversion rate was 100%. Forty-seven patients (92%) were discharged within a median of 9 h and managed as outpatients. In conclusion, in haemodynamically stable patients with recent-onset atrial fibrillation/flutter intravenous ibutilide and external electrical cardioversion for conversion to sinus rhythm turned out to be effective and safe. The short duration of admission makes this strategy attractive for use in the ED.     

Controlling Paroxysmal Atrial Fibrillation by a Combination of Amiodarone and Flecainide: Description of a Case With 15-Year Follow-up

A 77-year-old man with no known cardiac disease has had paroxysmal atrial fibrillation for 35 years with disabling symptoms and poor exercise tolerance when not in sinus rhythm, and he did not respond to conventional therapy. Fifteen years ago he was placed on amiodarone. His arrhythmia converted to atrial flutter with a flutter rate below 200 beats/min; DC cardioversion at 3 months led to transient sinus rhythm. At 5 months he converted spontaneously to sinus rhythm and had very few recurrences until 4 years later when he began to experience further frequent recurrences when the dose was reduced from 400 mg/day to 200 mg/day. Redosing at the higher dose led to skin discoloration; amiodarone was then replaced with sotalol, which the patient did not tolerate. After 9 months with efforts to rate control with various agents, amiodarone was reintroduced at 400 mg/day, which achieved full control, but to obviate the development of skin changes, flecainide was added at a dose of 100 mg twice a day, and the dose of amiodarone was gradually reduced to 200 mg/day. This combination regimen has produced no side effects or organ toxicity, although a degree of hypogonadism developed. It responded well to testosterone replacement. On the combination regimen, there have been no symptomatic arrhythmia recurrences over 8 years. Amiodarone and flecainide may have additive or synergistic effects in maintaining sinus rhythm in atrial fibrillation; the antiarrhythmic property of amiodarone is likely to minimize or nullify the proarryhthmic reactions of flecainide during combination therapy. This combination regimen may allow the extension of the use of flecainide in controlling refractory atrial flutter and fibrillation in patients with structural cardiac disease. The efficacy and safety of the combination regimen of the two drugs should be addressed in controlled clinical trials.     

Comparison of Bipolar Atrial Electrogram Amplitude in Sinus Rhythm, Atrial Fibrillation, and Atrial Flutter

Automatic mode switching pacemakers revert to non-atrial tracking modes in response to sensed atrial tachyarrhythmias. It is unclear how atrial electrogram amplitudes in sinus rhythm compare to those during atrial tachyarrhythmias. In this study, peak-to-peak bipolar atrial electrogram amplitudes were measured during sinus rhythm and either atrial fibrillation or atrial flutter in 69 patients. The mean atrial electrogram amplitudes were 1,59 ± 1.36 m V during sinus rhythm and 0.77 ± 0,58 mV during atrial fibrillation (P < 0.0001) for 25 patients with atrial fibrillation and 1.81 ± 2.07 mV during sinus and 1.5 ± 1.81 mV(P < 0.0001) for 44 patients with atrial flutter. The mean electrogram amplitudes during both atrial fibrillation and flutter correlated significantly with amplitudes during sinus rhythm (R = 0.79, R = 0.94. respectively, both P < 0,0001). The coefficient of variance of individual electrogram amplitudes was greater in atrial fibrillation than sinus (P < 0.0001). By comparing 20th percentile electrogram amplitudes in atrial fibrillation and flutter to mean sinus amplitudes, intermittent very low electrogram amplitudes (< 0.3 mV) were more likely during atrial fibrillation and flutter if the mean sinus electrogram amplitudes were < 1.5 mV and < 0.5 mV, respectively (P < 0.01). Eightieth percentile electrogram amplitude values in atrial fibrillation and flutter were equally likely to exceed mean sinus amplitude values in respective patients, in conclusion, mean atrial electrogram amplitudes during atrial fibrillation and flutter are less than but correlated to sinus rhythm electrogram amplitudes. Very low amplitude individual electrograms during these atrial arrhythmias are associated with low mean sinus rhythm electrogram amplitudes. These findings may have implications for the programming of permanent dual chamber pacemakers in patients with paroxysmal atrial fibrillation and flutter.     

Successful treatment of atrial flutter with amiodarone in a premature neonate. Case report and literature review.

This case report describes a 30-week gestation neonate who presented at birth with hydrops fetalis due to atrial flutter. Digoxin and electric cardioversion were unsuccessful in maintaining a stable sinus rhythm. The infant continued with intractable atrial flutter and severe hemodynamic deterioration until intravenous loading of amiodarone achieved conversion to stable sinus rhythm. Amiodarone was continued for 45 days; there was no recurrence of atrial flutter. Of note, the infant developed severe chronic lung disease after mechanical ventilation for 28 days. A lung biopsy ruled out amiodarone-induced pulmonary toxicity. A table is provided reviewing the different forms of neonatal supraventricular tachycardias. Apart from the successful management of the tachycardia, the role of amiodarone as an effective antiarrhythmic agent and its potential side effects, such as pulmonary toxicity and transient hypothyroidism, are discussed.     

Flecainide in the intrauterine treatment of fetal supraventricular tachycardia.

OBJECTIVES: To assess the efficacy of flecainide in the intrauterine treatment of fetal supraventricular tachycardia (SVT) with 1 : 1 atrioventricular conduction. DESIGN: Twenty fetuses (21-35 weeks of gestation) with SVT ranging between 215 and 280 bpm were analyzed retrospectively. Fetuses received flecainide and digoxin as either first, second or third line therapy. Intracardiac blood flow, venous Doppler waveforms and cardiotocograms were evaluated before and after drug induced conversion to sinus rhythm. RESULTS: After initiation of combined flecainide and digoxin therapy, the median time interval until final conversion to sinus rhythm was 5 days (range, 0-14 days). The majority of fetuses (n = 15; 75%) converted to sinus rhythm within 7 days of treatment, whereas the remaining five (25%) showed initial reduction of the heart rate to 160-215 bpm over several days, with restoration of a triphasic venous blood flow pattern before late conversion within 7-14 days after initiation of flecainide treatment. One of these fetuses showed a decrease in fetal heart rate to 160-190 bpm without conversion to sinus rhythm but with resolution of hydrops. All fetuses survived. CONCLUSIONS: Flecainide is safe and highly effective in the intrauterine treatment of hydropic fetuses with supraventricular tachycardia. Conversion into sinus rhythm can be expected 72 h after initiation of therapy but may take up to 14 days. Therefore therapy should be continued beyond 72 h, especially when an initial decrease of fetal heart rate is observed which may represent an early therapeutic response.     

Ibutilide versus amiodarone in atrial fibrillation: a double-blinded,randomized study

OBJECTIVE: Ibutilide, a class III antiarrhythmic drug, has been shown to convert atrial fibrillation to sinus rhythm more rapidly than procainamide or sotalol. Our objective was to compare the efficacy and safety of ibutilide and amiodarone in patients after cardiac surgery. DESIGN: Prospective, randomized, double-blinded study. SETTING: Intensive care unit of a university hospital. PATIENTS: Forty adults with an onset of atrial fibrillation within 3 hrs after admission. INTERVENTIONS: Before the administration of antiarrhythmic drugs, a 24-hr Holter electrocardiograph was attached. Patients in the ibutilide group received ibutilide 0.008 mg/kg body weight over 10 mins; treatment was repeated if atrial fibrillation or flutter persisted. If sinus rhythm was not achieved within 4 hrs, amiodarone 5 mg/kg was administered over 30 mins, followed by amiodarone 15 mg/kg over 24 hrs. Patients in the amiodarone group received amiodarone 5 mg/kg over 30 mins, followed by amiodarone 15 mg/kg over 24 hrs if atrial fibrillation or flutter continued. MEASUREMENTS AND MAIN RESULTS: Within the first 4 hrs, atrial fibrillation was converted in nine of 20 patients (45%) in group ibutilide and in ten of 20 patients (50%) in group amiodarone (not significant). Mean time for conversion overall was 385 mins in group ibutilide and 495 mins in group amiodarone (not significant). In group amiodarone, the protocol was discontinued in two patients because of severe arterial hypotension. Atrial fibrillation recurred in 11 of 20 patients (55%) in group ibutilide and in seven of 20 patients (35%) in group amiodarone (not significant). Ventricular arrhythmia did not occur during the first 24 hrs of the protocol. CONCLUSIONS: Ibutilide has no significant advantage over amiodarone for the conversion of atrial fibrillation to sinus rhythm in either time to conversion or conversion overall, but severe hypotension was not seen with ibutilide.     

Recognition of fetal arrhythmias by echocardiography

Fetal arrhythmias were detected in 33/198 high risk pregnancies from 21 weeks to term. Using the two-dimensional echocardiographic image of the fetal heart as a guide, the M-mode beam was directed to define the motion of the ventricular and atrial walls and atrioventricular valve or semilunar valves. Atrial contraction was defined either by the atrial wall motion or from the A-point of the atrioventricular valve. Ventricular contraction was defined by closure of the atrioventricular valve (C-point), the onset of ventricular wall contraction, or from the semilunar valve opening. Ladder diagrams of the sequence of atrial and ventricular activation were constructed to define the temporal sequence of these events. Premature atrial contractions were present in 12. In one fetus this arrhythmia converted into supraventricular tachycardia while in the other 11 fetuses the course was benign. Two fetuses had premature ventricular contractions. Supraventricular tachycardia was noted in five fetuses. One with hydrops at 29 weeks returned to sinus rhythm following maternal administration of procainamide. A second hydropic fetus with paroxysmal atrial tachycardia and hydrops failed to respond to digitalis, propranolol, procainamide, verapamil, or amiodarone, and died shortly after cesarean section. Two mature fetuses had tachycardia close to term and were treated after cesarean section. One fetus with runs of atrial tachycardia died in utero. Three fetuses had complete heart block, two of whom were from mothers with connective tissue diseases. In four fetuses, there was bradycardia of less than 100/minute lasting more than 30 seconds, but these episodes disappeared in 2 minutes.(ABSTRACT TRUNCATED AT 250 WORDS)     

Left atrial appendage dysfunction: a cause of thrombosis? Evidence by transesophageal echocardiography-Doppler studies.

The blood flow velocity patterns within the left atrial appendage were studied by transesophageal color flow imaging and pulsed Doppler in 84 patients. At the time of the study, 57 of the patients were in sinus rhythm, 25 were in atrial fibrillation, and two were in atrial flutter. The relationships between atrial rhythm, blood flow pattern and the presence/absence of spontaneous echocardiographic contrast or thrombus within the appendage were investigated. Transesophageal echocardiography allowed recording of blood flow velocities in 81 of the 84 patients studied. In 51 of the 55 patients in sinus rhythm the pulsed Doppler study showed a biphasic blood flow pattern, whereas a multiphasic pattern was found in the two patients with atrial flutter and in 14 patients with atrial fibrillation. In four patients with sinus rhythm and 10 patients with atrial fibrillation, no significant blood flow velocity could be detected. Thrombus or spontaneous echocardiographic contrast were found within the left atrial appendage in 20 patients, and in all these patients blood flow was either absent or significantly reduced. Our findings indicate that an absent or low blood flow velocity within the left atrial appendage represents a predisposing factor for thrombosis. Isolated left atrial appendage dysfunction has been documented in four patients during sinus rhythm, which may lead to thrombosis. This observation may offer an explanation for cardioembolic events that occur occasionally in patients without apparent heart disease and sinus rhythm.     

Verapamil in atrial fibrillation and atrial flutter.

A double-blind randomized study was performed to compare the efficacy of intravenous verapamil with saline in 28 patients with a rapid ventricular rate and atrial fibrillation or atrial flutter. Conversion of atrial fibrillation to sinus rhythm occurred in none of 14 patients after saline and in 3 of 20 patients (15%) 7 to 160 min after verapamil. The ventricular rate in atrial fibrillation was slowed greater than or equal to 15% in 2 of 14 patients (14%) by saline, in 17 of 20 patients (85%) by 1 dose of verapamil (p less than 0.001), and in 19 of 20 patients (95%) by 1 or 2 doses of verapamil (p less than 0.001). Conversion of atrial flutter to sinus rhythm occurred in none of 4 patients after saline and in 1 of 7 patients (14%) 105 min after verapamil. The ventricular rate in atrial flutter was slowed greater than or equal to 15% in none of 4 patients by saline, in 4 of 7 patients (57%) by 1 dose of verapamil, and in 7 of 7 patients (100%) by 1 or 2 doses of verapamil (p less than 0.001).     

Electrocardiographic and electrophysiological characteristics of atrial fibrillation organized into atrial flutter by oral administration of class I antiarrhythmic agents

The aim of this study was to evaluate the electrocardiographic (ECG) and electrophysiological characteristics of atrial fibrillation (AF) that organized into atrial flutter during oral administration of class I antiarrhythmic agents. The former clinical study included 72 consecutive patients (58 paroxysmal AF, 14 persistent AF) in whom class I antiarrhythmic agents were orally administered in the outpatient clinic for termination or prophylaxis of AF. The clinical background and ECG variables were compared between the patients with and without atrial flutter during class I antiarrhythmic agents therapy. An electrophysiological study was performed in ten patients with paroxysmal AF (five with [group A] and five without atrial flutter [group B] during oral class I antiarrhythmic agents therapy. Local electrograms from five different atrial sites (high and low right free wall, high and low septum, and distal coronary sinus) were analyzed during induced AF. The activation pattern of the right free wall during AF was also analyzed using a Halo catheter. Atrial flutter was documented during class I antiarrhythmic agents therapy in 14 (24%) patients with paroxysmal AF, whereas in none with persistent AF. The mean cycle length (f-f interval) and amplitude of the fibrillation waves in leads II and V1 from the surface ECG were significantly greater in the patients with than in those without atrial flutter. In the electrophysiological study, the mean cycle lengths for the low and high right free wall were significantly longer in group A than in group B, whereas those for the low septums and distal coronary sinus did not differ between the two groups. During the induced AF, the ratio of time exhibiting a consistent activation pattern (cranio-caudal, caudo-cranial, or undetermined) along the right free wall was significantly greater in group A than in group B. Atrial flutter newly developed during class I antiarrhythmic agents therapy in patients with coarse AF on the surface ECG and a relatively organized activation in the right atrial free wall. The observation of these findings may facilitate the identification of candidates for hybrid pharmacologic and ablative therapies.     

Intravenous Propafenone for Conversion of Atrial Fibrillation or Flutter to Sinus Rhythm: A Randomized, Placebo-controlled, Crossover Study

BACKGROUND: Propafenone has been claimed to be effective in converting atrial fibrillation and flutter to sinus rhythm; however, controlled clinical trials have reported variable results, and data about the safety of propafenone in the setting of heart failure are lacking. The aim of the present study was to evaluate the efficacy and safety of intravenous propafenone in converting atrial fibrillation and flutter to sinus rhythm. METHODS: Sixty patients with acute (<72 h) or chronic atrial fibrillation or flutter were included in a randomized, placebo-controlled, conditional cross-over study. Twenty eight patients, of whom 12 were in New York Heart Association class III and IV, had heart failure. Patients received intravenous propafenone (2 mg/kg in 10 minutes) and placebo subsequently at 1 hour intervals if sinus rhythm was not achieved. The patients' rhythms were continuously monitored for 1 hour and a 12-lead electrocardiogram, a 1-minute continuous rhythm strip and vital signs were recorded at baseline and at 15, 30, 45, and 60 minutes after the administration of each drug. RESULTS: Twenty of teh 59 patients (34%) treated with propafenone converted to sinus rhythm, while only 4 of the 50 patients (8%) treated with placebo converted (P <.001). Propafenone was more effective in patients with acute (<72 h) atrial fibrillation (64.5%). The conversion rate with propafenone was not significantly different from placebo in patients with atrial flutter and chronic atrial fibrillation (>72 h). Propafenone significantly decreased (P <.005 vs placebo) mean ventricular rate in nonresponders with a baseline heart rate of more than 100 beats/min. No clinically significant adverse effect occurred. CONCLUSIONS: We conclude that intravenous propafenone treatment is effective for converting acute atrial fibrillation; however, it seems unlikely to be beneficial in atrial flutter and chronic atrial fibrillation. Propafenone decreases ventricular rate in nonresponders, and a single dose of propafenone is relatively safe even in moderate-to-severe heart failure.     

Relation Between Left Atrial Size and Secondary Atrial Arrhythmias After Successful Catheter Ablation of Common Atrial Flutter

Catheter ablation ptovides an effective cure for patients with typical atrial flutter. However, these patients may have the potential to develop atrial tachyarrhythmias other than common atrial flutter. This study examines clinical and echocardiographic predictors for the occurrence of uncommon atrial flutter or atrial fibrillation after abolition of common atrial flutter. The study population comprised 17 patients (12 men, 5 women, age 32–74 years) who underwent successful radiofrequency catheter ablation of common atrial flutter. Common atrial flutter did not recur in any patient during a median follow-up time of 8 (range 1–25) months. Within a median of 7 (range 1–223) days, however, symptomatic atrial tachyarrhythmias occurred in 8 of 17 patients (47%): uncommon atrial flutter (n = 4); atrial fibrillation (n = 3); and both uncommon atrial flutter and atrial fibrillation in one patient. Preablation left atrial volume was significantly larger in patients who developed secondary arrhythmias compared with patients who remained in sinus rhythm (57.9 ± 15.6 vs 43.7 ± 16.4 cm³, P < 0.05). Enlarged left atrial volume dichotomized at 51 cm³ independently predicted postablation atrial arrhythmias (x²=5.11, rel. risk = 5.3, P < 0.05). On Kaplan-Meier analysis, time to occurrence of postablation atrial arrhythmias was significantly shorter in patietits with enlarged left atrium (P < 0.02). In conclusion, symptomatic uncommon atrial flutter and atrial fibrillation develops in a substantial proportion of patients after successful ablation of common atrial flutter. Out of a series of clinical and echocardiographic parameters, preablation left atrial size is the best predictor for the occurrence of these postablation atrial arrhythmias.