Atrial pacing for suppression of early reinitiation of atrial fibrillation after successful internal cardioversion.

AIMS: To evaluate the efficacy of atrial pacing in the suppression of early reinitiation of atrial fibrillation after successful internal cardioversion. METHODS AND RESULTS: The efficacy of atrial pacing in suppressing early reinitiation of atrial fibrillation was studied in 12 of 45 (29%) patients with early reinitiation of atrial fibrillation after successful cardioversion. These patients were randomized to undergo either repeated defibrillation alone or repeated defibrillation followed by high right atrial pacing at 500 ms in a crossover fashion. In patients with persistent early reinitiation of atrial fibrillation despite atrial pacing at 500 ms and repeated defibrillation, atrial pacing at 300 ms was tested. Lastly, if early reinitiation of atrial fibrillation persisted, administration of intravenous sotalol (1.5 mg. kg(-1)) was tested. Atrial pacing at 500 ms after defibrillation prevented early reinitiation of atrial fibrillation in five of 12 (42%) patients, and was significantly more effective than repeated defibrillation (0/9 patients, 0%, P<0.05). During atrial pacing at 500 ms, the density of atrial premature depolarizations (APDs) was significantly decreased (2.4+/-2.4 APDs. min(-1)vs 16.4+/-9.8 APDs. min(-1), P<0. 05) and the coupling interval of atrial premature depolarization was significantly increased (420+/-32 ms vs 398+/-19 ms, P<0.05) as compared to no pacing. In the remaining seven (58%) patients, atrial pacing at 500 ms failed to prevent early reinitiation of atrial fibrillation, but significantly decreased the density of atrial premature depolarization (3.4+/-2.4 APDs. min(-1)vs 14.2+/-4.8 APDs. min(-1), P<0.05) and delayed the onset of early reinitiation of atrial fibrillation (33+/-17s vs 11+/-11 s, P<0.05). Atrial pacing at 300 ms decreased the coupling interval of atrial premature depolarization as compared to no pacing and during atrial pacing at 500 ms (P<0.05), but without early reinitiation of atrial fibrillation suppression. Administration of intravenous sotalol was effective in preventing early reinitiation of atrial fibrillation in five of seven (71%) patients where pacing failed to suppress early reinitiation of atrial fibrillation. CONCLUSION: The results of this study suggest that atrial pacing can be useful when combined with transvenous defibrillation in patients with early reinitiation of atrial fibrillation.     

Early Reinitiation of Atrial Fibrillation Following External Electrical Cardioversion in Amiodarone-Treated Patients

Early reinitiation of atrial fibrillation (ERAF) following external or internal electrical cardioversion is one of the factors determining unsuccessful electrical cardioversion. Prevention of ERAF has not been studied systematically in patients on amiodarone therapy. Methods and Results: 22 patients had ERAF within 1[emsp4 ]min after external electrical cardioversion of atrial fibrillation. 11 patients were on amiodarone therapy and 11 patients had no antiarrhythmic medication. The effect of atropine, post-shock atrial pacing and intravenous ajmaline on ERAF was consecutively tested in these patients. Administration of atropine before repeated defibrillation or post-shock atrial pacing prevented ERAF in 9 of the 11 patients (82%) on amiodarone therapy but in only 3 of 11 patients (27%) without amiodarone (p<0.05). In the remaining patients, intravenous ajmaline was effective in the suppression of ERAF in 5 patients without amiodarone and in 1 patient with amiodarone. The PP interval preceding the atrial premature beat reinitiating atrial fibrillation was nonsignificantly longer in amiodarone-treated patients (1127±419[emsp4 ]ms) in comparison to patients without amiodarone (896±271[emsp4 ]ms). 27% of patients without amiodarone at the time of electrical cardioversion and 55% of patients with amiodarone remained in sinus rhythm during the follow-up of 29±14 and 30±14 months, respectively. Conclusions: ERAF in patients on amiodarone can be treated by atropine or atrial pacing to prevent bradycardia-dependent ERAF. ERAF in amiodarone-treated patients does not apparently predict late recurrence of atrial fibrillation on continued amiodarone therapy.     

Incidence and modes of onset of early reinitiation of atrial fibrillation after successful internal cardioversion, and its prevention by intravenous sotalol

OBJECTIVES—To study the incidence and mode of onset of early reinitiation of atrial fibrillation (ERAF) following successful internal cardioversion of chronic atrial fibrillation, and to determine the effects of sotalol in the prevention of ERAF.
DESIGN—The incidence and modes of onset of ERAF and the acute effects of intravenous sotalol in the prevention of ERAF were studied retrospectively.
SETTING—Electrophysiology laboratory at a university teaching hospital.
PATIENTS—64 patients, mean (SD) age 62 (10) years, who underwent internal cardioversion of chronic atrial fibrillation (mean duration of atrial fibrillation 31 (39) months).
MAIN OUTCOME MEASURES—ECGs and intracardiac electrograms recorded during the internal cardioversion of atrial fibrillation using 3/3 ms biphasic, R wave synchronised shocks.
RESULTS—52 patients (81%) had successful electrical cardioversion, and 20 (31%) of these had ERAF during the procedure. There was no clinical predictor for the occurrence of ERAF. Fifty eight episodes of ERAF were observed. Five ERAF episodes (9%) had preceding bradycardia and 53 (91%) of these were triggered by atrial premature beats with normal preceding heart rate. Atrial premature beats that reinitiated atrial fibrillation had a shorter coupling interval (333 (43) ms v 396 (100), p < 0.001) and a lower prematurity index (0.44 (0.11) v 0.55 (0.14), p < 0.001) than those that did not reinitiate atrial fibrillation. Repeated shock delivery and increasing the defibrillation energy did not prevent ERAF. Intravenous sotalol infusion decreased the numbers of atrial premature beats and prolonged their coupling interval, and prevented ERAF after repeated defibrillation in 83% of patients with ERAF.
CONCLUSIONS—ERAF is a significant clinical problem after successful internal cardioversion of chronic atrial fibrillation, and was observed in up to 31% of patients. In most episodes, ERAF was triggered by short coupling atrial premature beats with preceding normal heart rate. Intravenous sotalol was effective in preventing ERAF in most cases.


Keywords: atrial fibrillation; low energy cardioversion; sotalol     

Low-Energy Transvenous Cardioversion of Atrial Fibrillation Using a Single Atrial Lead System

Atrial Cardioversion Using a Single Atrial Lead System. Introduction: Clinical studies have shown that electrical conversion of atrial fibrillation (AF) is feasible with transvenous catheter electrodes at low energies. We developed a single atrial lead system that allows atrial pacing, sensing, and defibrillation to improve and facilitate this new therapeutic option. Methods and Results: The lead consists of a tripolar sensing, pacing, and defibrillation system. Two defibrillation coil electrodes are positioned on a stylet-guided lead. A ring electrode located between the two coils serves as the cathode for atrial sensing and pacing. We used this lead to cardiovert patients with acute or chronic AE. The distal coil was positioned in the coronary sinus, and the proximal coil and the ring electrode in the right atrium. R wave synchronized biphasic shocks were delivered between the two coils. Atrial signal detection and pacing were performed using the proximal coil and the ring electrode. Eight patients with acute AF (38 ± 9 min) and eight patients with chronic AF (6.6 ± 5 months) were included. The fluoroscopy time for lead placement was 3.5 ± 4.3 minutes. The atrial defibrillation threshold was 2.0 ± 1.4 J for patients with acute AE and 9.2 ± 5.9 J for patients with chronic AF (P < 0.01). The signal amplitude detected was 1.7 ± 1.1 mV during AF and 4.0 ± 2.9 mV after restoration of sinus rhythm (P < 0.001). Atrial pacing was feasible at a threshold of 4.4 ± 3.3 V (0.5-msec pulse width). Conclusions: Atrial signal detection, atrial pacing, and low-energy atrial defibrillation using this single atrial lead system is feasible in various clinical settings. Tbis system might lead to a simpler, less invasive approach for internal atrial cardioversion.     

How to enhance acute outcome of electrical cardioversion by drug therapy: importance of immediate reinitiation of atrial fibrillation

INTRODUCTION: In almost 20% of patients with persistent atrial fibrillation (AF), electrical cardioversion is unsuccessful because of shock failure (i.e., no single sinus beat) or immediate reinitiation of AF (IRAF; recurrence within 2 min). Relative prevalence of shock failure and IRAF are not well known because data on outcome of electrical cardioversion therapy mostly do not distinguish shock failure from IRAF. METHODS AND RESULTS: In this review, the role of pretreatment with antiarrhythmic drugs on prevention of shock failure and total outcome of the cardioversion procedure are investigated. Quinidine and propafenone seem to be effective in preventing IRAF. Verapamil given in addition to Class I or III drugs may strengthen the preventive effects of these drugs than if they were given alone. Ibutilide prevents shock failure, although neither ibutilide nor dofetilide seems to be effective in preventing IRAF. CONCLUSION: Pretreatment with antiarrhythmic drugs may enhance cardioversion outcome predominantly by preventing IRAF. Different antiarrhythmic drugs within the same Vaughan-Williams class have different effects on shock failure and IRAF.     

Implantable Atrial Defibrillators

Implantable Atrial Defibrillators. Due to the limited efficacy of antiarrhythmic drugs for atrial fibrillation, several nonpharmacologic therapeutic options have evolved. One of these is an implantable atrial defibrillator. Recent studies have shown that internal atrial defibrillation is feasible with relatively low energies. To date, the optimal electrode configuration involves large surface area catheters in the right atrium and coronary sinus. In humans, atrial defibrillation can generally be achieved with < 2 J using this electrode configuration and a biphasic shock waveform. For shocks < 5 J, there is no significant pathological damage to the atria or coronary sinus. Further investigation is needed to guarantee that atrial defibrillation shocks do not provoke ventricular arrhythmias. Preliminary data suggest that atrial defibrillation shocks synchronized to R waves that are not closely coupled are safe. In addition, the shocks are well tolerated if the shock energy is < 1.5 J. With additional studies to confirm the safety of implantable atrial defibrillators, further reduce shock energy, and improve patient tolerance, an implantable atrial defibrillator can become an acceptable therapy for patients with symptomatic, paroxysmal atrial fibrillation.     

Incidence of Atrial Fibrillation Following Ventricular Defibrillation with Transvenous Lead Systems in Man

Atrial Fibrillation After Ventricular Defibrillation. Introduction: The induction of atrial fibrillation (AF) following implantable defibrillator therapy of ventricular fibrillation carries multiple risks. The frequency of shock-induced AF may be more problematic in patients with transvenous defibrillators because current is often delivered through atrial tissue. Thus, the purpose of this study was to determine the incidence of AF following transvenous ventricular defibrillation. Methods and Results: Atrial electrograms were recorded before and after energy delivery in patients undergoing intraoperative testing of transvenous defibrillation lead systems. A total of 114 tracings were examined from 21 patients following ventricular defibrillation. Transvenous deflbrillation shock strength ranged between 200–800 volts (2–40 joules). Bipolar atrial electrograms were obtained from atrial electrodes with 1-cm interelectrode spacing located on one of the defibrillation catheters. The timing of the ventricular defibrillation shock was expressed as a percentage of the preceding sinus PP interval. Three of the 114 transvenous shocks (2.6%) generated AF. Each episode of AF occurred in a different patient. The shocks responsible for AF occurred at 21%, 43%, and 84% of the preceding sinus PP interval. No relation was found between AF induction and the timing of pulse delivery, pulse strength, or pulse number. Conclusion: We conclude that transvenous ventricular defibrillation infrequently causes AF and that timing shock delivery to the atrial cycle is likely to be of marginal or no benefit in the prevention of shock-induced AF. (J Cardiovasc Electrophysiol, Vol. 3, pp. 411–417, October 1992)     

Low-Energy Internal Cardioversion for Atrial Fibrillation Resistant to External Cardioversion

Internal Cardioversion. introduction : This report describes the electrical conversion of atrial fibrillation in two morbidly obese patients refractory to external cardioversion at 360 J.
Methods and Results : The two patients were lightly sedated and underwent placement of decapolar catheters in the coronary sinus and right atrial appendage. All ten electrodes of each decapolar catheter were electrically coupled, and defibrillation was attempted at successively increasing levels using a biphasic decaying exponential waveform generated by an external defibrillator. Both patients were returned to normal sinus rhythm using <10 J without complication.
Conclusion : Internal cardioversion is effective in restoration of sinus rhythm in some patients refractory to conventional forms of therapy     

Effect of atrial fibrillation duration on probability of immediate recurrence after transthoracic cardioversion

INTRODUCTION: An immediate recurrence of atrial fibrillation (IRAF) appears to be more common after early restoration of sinus rhythm with an implantable atrial defibrillator than after elective transthoracic cardioversion, which suggests that the probability of IRAF may be related to the duration of AF. METHODS AND RESULTS: Transthoracic cardioversion was performed 85 +/- 187 days (range 7 minutes to 8 years) after the onset of atrial fibrillation in 315 patients (mean age 61 +/- 13 years). IRAF was defined as a recurrence of AF within 60 seconds after restoration of sinus rhythm. IRAF occurred in 56% of patients when cardioversion was performed within 1 hour of the onset of AF compared with 12% of patients when cardioversion was performed after 24 hours of AF (P < 0.001). The duration of AF was the only independent predictor of IRAF among the clinical variables of age, gender, structural heart disease, antiarrhythmic drug therapy, and cardioversion energy (P < 0.01). CONCLUSION: IRAF is more likely to occur when the duration of AF is <1 hour than when the duration is >24 hours. This observation has clinical implications for the most appropriate timing of cardioversion, particularly in patients who receive device therapy for AF.     

Time to Cardioversion of Recurrent Atrial Arrhythmias After Catheter Ablation of Atrial Fibrillation and Long‐Term Clinical Outcome

Introduction: It is unclear whether early restoration of sinus rhythm in patients with persistent atrial arrhythmias after catheter ablation of atrial fibrillation (AF) facilitates reverse atrial remodeling and promotes long‐term maintenance of sinus rhythm. The purpose of this study was to determine the relationship between the time to restoration of sinus rhythm after a recurrence of an atrial arrhythmia and long‐term maintenance of sinus rhythm after radiofrequency catheter ablation of AF. Methods and Results: Radiofrequency catheter ablation was performed in 384 consecutive patients (age 60 ± 9 years) for paroxysmal (215 patients) or persistent AF (169 patients). Transthoracic cardioversion was performed in all 93 patients (24%) who presented with a persistent atrial arrhythmia: AF (n = 74) or atrial flutter (n = 19) at a mean of 51 ± 53 days from the recurrence of atrial arrhythmia and 88 ± 72 days from the ablation procedure. At a mean of 16 ± 10 months after the ablation procedure, 25 of 93 patients (27%) who underwent cardioversion were in sinus rhythm without antiarrhythmic therapy. Among the 46 patients who underwent cardioversion at ≤30 days after the recurrence, 23 (50%) were in sinus rhythm without antiarrhythmic therapy. On multivariate analysis of clinical variables, time to cardioversion within 30 days after the onset of atrial arrhythmia was the only independent predictor of maintenance of sinus rhythm in the absence of antiarrhythmic drug therapy after a single ablation procedure (OR 22.5; 95% CI 4.87–103.88, P < 0.001). Conclusion: Freedom from AF/flutter is achieved in approximately 50% of patients who undergo cardioversion within 30 days of a persistent atrial arrhythmia after catheter ablation of AF.     

Ventricular Fibrillation Resulting from Synchronized Internal Atrial Defibrillation in a Patient with Ventricular Preexcitation

VF After Synchronized Internal Atrial Defibrillation. This case describes ventricular proarrhythmia as a result of a synchronized internal atrial defibrillation shock in a 29-year-old man with Ebstein's anomaly referred for radiofrequency ablation of a right posterior accessory pathway. During the electrophysiologic study, atrial fibrillation was induced and 3/3 msec shocks of various strengths were delivered between two decapolar defibrillation catheters in the coronary sinus and right atrial appendage. A 2.0-J biphasic shock synchronized to an R wave after a short-long-short ventricular cycle length pattern with a preshock coupling interval of 245 msec induced ventricular fibrillation, which was externally defibrillated with 200 J. This observation has implications for the development of implantable atrial defibrillators.     

Internal Cardioversion of Persistent Atrial Fibrillation Using Rectilinear Biphasic Waveform

Internal electrical cardioversion is currently used in patients with persistent atrial fibrillation resistant to external electrical cardioversion. In external cardioversion, biphasic waveforms have shown a greater efficacy than monomorphic waveforms. The present study aimed to test the safety and efficacy of rectilinear biphasic waveform in converting patients with persistent atrial fibrillation to sinus rhythm using internal electrical cardioversion, and to compare it with that of classical monophasic waveform. Twenty-seven consecutive patients with persistent AF received 31 internal cardioversions, using monophasic waveform in 11 (group I), and rectilinear biphasic waveform in 20 cases (group II). Baseline patients characteristics were similar in both groups. Multipolar catheters were positioned in the distal coronary sinus and in the high right atrium. Synchronised shocks were delivered using an escalating protocol of 2, 5, 10, 15, 20, 30, and 50 Joules. In group I, 1 patient was resistant to maximal energy (success rate 91%). The mean energy of the maximal shock was 18 ± 13 J. In group II, all patients were converted to sinus rhythm. The mean energy of the maximal shock was 9 ± 5 J (p < 0.01 vs. group I). No significant complications occurred. At 3 months follow-up, 45% of group I and 60% of group II patients remained in sinus rhythm (p = NS).We conclude that internal cardioversion using rectilinear biphasic waveform is feasible and safe, and requires less energy than classical monophasic waveforms.     

Favorable effects of flecainide in transvenous internal cardioversion of atrial fibrillation

ObjectivesThe aim of the study was to evaluate the effects of intravenous (IV) flecainide on defibrillation energy requirements in patients treated with low-energy internal atrial cardioversion.BackgroundInternal cardioversion of atrial fibrillation is becoming a more widely accepted therapy for acute episode termination and for implantable atrial defibrillators.MethodsTwenty-four patients with atrial fibrillation (19 persistent, 5 paroxysmal) underwent elective transvenous cardioversion according to a step-up protocol. After successful conversion in a drug-free state, atrial fibrillation was induced by atrial pacing; IV flecainide (2 mg/kg) was administered and a second threshold was determined. In patients in whom cardioversion in a drug-free state failed notwithstanding a 400- to 550-V shock, a threshold determination was attempted after flecainide.ResultsChronic persistent atrial fibrillation was converted in 13/19 (68%) patients at baseline and in 16/19 (84%) patients after flecainide. Paroxysmal atrial fibrillation was successfully cardioverted in all the patients. A favorable effect of flecainide was observed either in chronic persistent atrial fibrillation (13 patients) or in paroxysmal atrial fibrillation (5 patients) with significant reductions in energy requirements for effective defibrillation (persistent atrial fibrillation: 4.42 ± 1.37 to 3.50 ± 1.51 J, p < 0.005; paroxysmal atrial fibrillation: 1.68 ± 0.29 to 0.84 ± 0.26 J, p < 0.01). In 14 patients not requiring sedation, the favorable effects of flecainide on defibrillation threshold resulted in a significant reduction in the scores of shock-induced discomfort (3.71 ± 0.83 vs. 4.29 ± 0.61, p < 0.005). No ventricular proarrhythmia was observed for any shock.ConclusionsIntravenous flecainide reduces atrial defibrillation threshold in patients treated with low-energy internal atrial cardioversion. This reduction in threshold results in lower shock-induced discomfort. Additionally, flecainide may increase the procedure success rate in patients with chronic persistent atrial fibrillation.     

Right Atrial Thrombi and Depressed Right Atrial Appendage Function After Cardioversion of Atrial Fibrillation

BACKGROUND: It has been shown that cardioversion of atrial fibrillation may result in left atrial chamber and appendage dysfunction and cause new thrombi in the left atrium. The aim of this prospective study was to investigate right atrial appendage function and assess the incidence of new right atrial thrombi after electrical cardioversion. METHODS: Transthoracic echocardiography was performed in 25 patients 4 h before and at 24 h and 7 days after electrical cardioversion to determine right and left atrial mechanical function (internal atrial defibrillation, n = 16; external electrical cardioversion, n = 9), as assessed by peak A wave velocities derived from the transtricuspid and transmitral velocity profiles. In addition, transesophageal echocardiography was performed 4 h before and 24 h after cardioversion to evaluate postcardioversion thrombus formation in the right and left atrial chambers and to assess right and left atrial appendage function. The degree of spontaneous echo contrast was noted, and peak emptying velocities of the appendages were measured before and after cardioversion. RESULTS: Peak emptying velocities of both the right atrial appendage (mean +/- SD, 0.23 +/- 0.1 vs 0.32 +/- 0.11 m/sec; P = 0.02) and the left atrial appendage (0.3 +/- 0.15 vs 0.4 +/- 0.15 m/sec; P = 0.01) were significantly lower 24 h after cardioversion compared with 4 h before cardioversion, respectively. The degree of spontaneous echo contrast increased in the left atrium after cardioversion from 1.0 +/- 1.2 to 1.9 +/- 2.1 (P = 0.02), and in the right atrium, it increased from 0.8 +/- 1.1 to 1.2 +/- 1.1 (P = 0.1) after cardioversion. Peak A wave transtricuspid velocity increased from 0.26 +/- 0.05 m/sec at 24 h to 0.38 +/- 0.06 m/sec (P = 0.001) after 7 days; respective values for transmitral peak A wave velocity were 0.39 +/- 0.15 and 0.54 +/- 0.16 m/sec (P = 0.009). No thrombi were found in either the right or left atrium before cardioversion. In two patients, new thrombi in the right atrium were detected 24 h after internal atrial defibrillation. Thrombi were located at the superior rim of the fossa ovalis in both patients with patent foramen ovale. Another patient had developed a thrombus in the left atrial appendage. CONCLUSIONS: Electrical cardioversion may not only cause left atrial chamber and appendage dysfunction and left atrial thrombi but also lead to depressed right atrial appendage function and the generation of new thrombi in the body of the right atrium.     

Maintenance of Sinus Rhythm after Cardioversion of Atrial Fibrillation in Patients with Lone Atrial Fibrillation and Patients with Hypertension

Background: The success rate and prognosis of cardioversion of atrial fibrillation (AF) in patients with organic heart disease is well known. In contrast, little data exist about cardioversion success and maintenance of sinus rhythm (SR) in patients with lone AF and in patients with hypertension as the only underlying cardiovascular disease. Methods: In a prospective cardioversion registry 148 of 181 patients (81.8%) with lone AF (age 58 ± 13 years, duration of AF 7.6 ± 19 weeks) and 120 of 148 patients (81.1%) with hypertension (age 62 ± 10 years, duration of AF 6.6 ± 21 weeks) had successful cardioversion and were followed for 7.7 ± 1.9 months. Results: At follow-up, 120 patients (81.1%) with lone AF were in SR, and 18 of these patients had had repeated cardioversion during follow-up (AF total recurrence rate 31.1%). In stepwise regression analysis, the number of previous cardioversions was predictive of rhythm at follow-up (P = 0.0453). Rhythm at follow-up did not differ between patients who were or were not on antiarrhythmic drugs. At follow-up 96 patients (80%) with hypertension were in SR, and 9 of these had had repeated cardioversion during follow-up (AF total recurrence rate 27.5%). As in lone AF, the recurrence rate of AF did not differ between patients with or without antiarrhythmic drug treatment, and in multivariate regression analysis, the number of previous cardioversions was the only clinical predictor of rhythm at follow-up (P = 0.0284). Conclusions: Even in patients with such benign conditions as lone AF or hypertension as the only underlying disease, the prognosis of cardioversion in terms of maintenance of SR is poor. Future studies of rhythm control versus rate control need to include not only patients with organic heart disease but also patients with lone AF and patients with hypertension, since the long-term benefits of these two strategies remain unclear even in these subsets of patients.     

Atrial defibrillation threshold in humans minutes after atrial fibrillation induction; "A stitch in time saves nine".

AIMS: To assess the effects of atrial fibrillation duration on the defibrillation threshold in atrial fibrillation patients seconds or minutes after initiation of the arrhythmia. METHODS AND RESULTS: Nineteen patients with recurrent symptomatic atrial fibrillation were evaluated. After programmed induction of atrial fibrillation, the defibrillation threshold was assessed after two sequential periods of arrhythmia in the same patient: an "ultrashort" period of 30 s duration and a "short" period, which lasted 10 min. After the specified period, internal cardioversion was attempted using a balloon-guided catheter that allows the delivery of biphasic shocks between one electrode array placed in the left pulmonary artery and a proximal electrode array on the lateral right atrial wall. The defibrillation threshold was assessed with energy steps of 0.5 J with a starting level of 0.5 J. Mean time from induction to successful defibrillation was 92+/-30 s after the "ultrashort" period of atrial fibrillation and 910+/-86 s after the short period. The defibrillation threshold was significantly greater after 10 min of atrial fibrillation than after 30 s of arrhythmia (2.32+/-0.61 J vs 1.31+/-0.66 J, P<0.001). Clinical data were not found to affect the defibrillation threshold. CONCLUSIONS: Prolongation of atrial fibrillation over minutes in patients with paroxysmal arrhythmia increases the energy requirements for successful defibrillation.     

Low Energy Intracardiac Cardioversion After Failed Conventional External Cardioversion of Atrial Fibrillation

Objectives. This study was designed to evaluate the efficacy of intracardiac cardioversion in patients with chronic atrial fibrillation after unsuccessful external cardioversion.Background. Previous studies in patients with atrial fibrillation undergoing intracardiac cardioversion have suggested that intracardiac cardioversion is highly effective and safe. However, the characteristics of patients who benefit most from this invasive technique are unknown.Methods. We prospectively studied 25 consecutive patients with chronic atrial fibrillation (11 ± 9 months). All patients had undergone at least three attempts at conventional external transthoracic cardioversion by means of paddles in an anteroposterolateral position applying energies up to 360 J without success. Intracardiac shocks were delivered by an external defibrillator through defibrillation electrodes placed in the right atrium and coronary sinus or in the right atrium and left pulmonary artery. After conversion, all patients were treated orally with sotalol (mean 194 ± 63 mg/day).Results. Internal cardioversion was successful in 22 of 25 patients at a mean defibrillation threshold of 6.5 ± 3.0 J. Mean lead impedance was 56.4 ± 7.4 Ω. No severe complications were observed. At a mean follow-up of 15 ± 12 months, 12 (55%) of the patients treated successfully remained in sinus rhythm.Conclusions. In patients with failed external cardioversion, internal cardioversion offers a new option for restoring sinus rhythm. Intracardiac cardioversion is an effective and safe method and can be easily performed in patients with minimal sedation.     

持续性心房颤动药物复律后心房收缩功能恢复的观察

目的　观察持续性心房颤动药物复律后心房收缩功能的恢复过程。方法　5 3例持续性心房颤动患者在药物复律后第1、1 4、2 8天运用超声心动图检测舒张期跨二尖瓣血流。结果　复律后A峰、A波积分逐步升高(0 . 3 5±0 . 1 0cm/s至0 . 62±0 . 1 1cm/s、4 .43±1 . 3 6cm/s2至6. 0 2±1. 5 0cm/s2 ) ,A波积分占总积分比例由2 6±7%上升至3 4±8%。结论　持续性心房颤动经药物复律后心房收缩功能逐步缓慢恢复。     

Atrial fibrillation in patients with a dual defibrillator: characteristics of spontaneous and induced episodes and effect of ventricular tachyarrhythmia induction

BACKGROUND: The pattern of FF intervals during atrial fibrillation (AF) has been analyzed in induced and spontaneous AF episodes, after the induction of ventricular fibrillation (VF) and after atrial shock, in order to suggest practical considerations for AF management in patients implanted with antitachycardia devices. METHODS: In 13 patients implanted with a dual-chamber defibrillator, FF intervals were analyzed during two separate induced AF episodes, before and after VF induction over AF, as well as during spontaneous AF episodes and after unsuccessful atrial shocks. The following parameters were considered: mean atrial cycle length (CL), atrial CL stability, and standard deviation of the atrial cycle. RESULTS: The AF pattern had comparable characteristics considering two separate inductions of AF, as well as spontaneous AF episodes. Ventricular tachyarrhythmia induction resulted in a shortening of atrial CL (P < 0.02) and in a less organized AF pattern (P < 0.005). Changes in the FF interval after ineffective shock therapy showed a shortening of AF cycles after shocks with energies far below the defibrillation threshold. CONCLUSIONS: (a) The AF pattern is reproducible in separate inductions of sustained AF and in spontaneous episodes, (b) dynamic changes involving a shortening of the AF cycle and an evolution to a less homogeneous pattern occur after VF induction, revealing a complex interplay between AF and VF, and (c) FF interval analysis after ineffective shock delivery may allow the relationship between delivered shock energy and effective defibrillation energy to be estimated, thereby providing practical suggestions for step-up protocols in atrial cardioversion.     

Is There Any Indication for an Intracardiac Defibrillator for the Treatment of Atrial Fibrillation?

ICD for Treatment of AF. The experience gained using intracardiac cardioverter defibrillators for the treatment of ventricular arrhythmias has prompted the development of an automatic atrial defibrillator capable of detecting and automatically terminating atrial fibrillation (AF). Experimental studies in sheep have shown that it is possible to terminate AF with energies ranging from < 1 to 7 joules [J], using biphasic shocks. The best electrode configuration using intracardiac catheters and/or a subcutaneous patch was two catheters, one in the right atrium and the other in the coronary sinus. Current studies in man focus on the answers to three questions. First, can the experimental results of atrial defibrillation derived from healthy anesthetized sheep without spontaneous AF be extrapolated to AF in man with areas of fibrosis within the atria and/or underlying heart disease in 80% of cases? Preliminary studies in man suggest that cardioversion of AF of short duration is feasible using a mean energy of 2 J. Second, are these energies well tolerated in an awake nonsedated patient? Energies < 1 J were well tolerated, but pain resulting from higher energies needs further investigation. Third, is low-energy atrial defibrillation safe, i.e., is there a risk of ventricular arrhythmias induced by an atrial shock? Experimental results in sheep have shown that the risk of R wave synchronized shock to induce ventricular arrhythmias was only present when the preceding RR interval was shorter than 300 msec. The risk of proarrhythmia in man is undergoing evaluation and must be sufficiently low (< 0.1) before sanctioning implantation of a stand-alone (without associated ventricular defibrillator) automatic atrial defibrillator. Preliminary data on 1212 shocks showed no proarrhythmia. There is definitely a significant group of patients with attacks of AF (Class IIIB or IIIC) that are resistant to antiar-rhythmic therapy. Another group of symptomatic patients may have infrequent attacks, or poorly tolerated (syncope or heart failure) or long-lasting attacks requiring medical intervention and/or hospitalization (Class IB, IIB), for whom an automatic atrial defibrillator may be a valuable option. The alternative therapies could be either catheter ablation of the AV node with implantation of a pacemaker or selective surgery. Most of the technical problems related to AF detection and reliable atrial defibrillation have been solved. However, clinical investigations are needed to evaluate the efficacy and safety of this new and exciting therapeutic modality.