Atrial Pacing Therapies for Prevention of Atrial Fibrillation in Patients with Implantable Defibrillators

Atrial fibrillation (AF), atrial flutter and atrial tachycardia (AT) occur frequently in patients following implantation of an implantable cardioverter defibrillator (ICD) for the treatment of ventricular tachyarrhythmias. Some new generation ICDs have incorporated atrial antitachycardia pacing therapy (ATP) and atrial pacing algorithms designed specifically for the prevention of AF. In the GEM III AT clinical evaluation, atrial ATP efficacy for termination of AF and AT was assessed. Overall ATP efficacy for AF/AT, based on device classification, was 40% when adjusted using the Generalized Estimating Equations to account for correlated data that arises from utilizing multiple episodes in some patients. However, many episodes of AF/AT were noted to terminate within 10 minutes of onset. Applying a more conservative definition of efficacy, termination within 20 sec of delivery of the last atrial ATP, efficacy for termination of AF/AT was 26%. 50 Hz burst pacing was shown to have minimal efficacy for termination of AF and modest incremental benefit following ramp or burst pacing therapies for AT. These observations provide a more realistic expectation of the value of atrial ATP in the ICD population with AF. Atrial ATP terminates some episodes of AT but previously reported efficacy rates of 40-50% are exaggerated and in part reflect spontaneous terminations of some AF/AT episodes.     

Implantable Atrial Defibrillator and Detection of Atrial Flutter

The implantable atrial defibrillator (IAD) is designed to detect and treat atrial fibrillation (AF) with low energy synchronized shocks. A patient with a history of persistent AF was implanted with an IAD after ineffective treatment with procainamide and sotalol. Through four months of follow-up, the IAD performed appropriate detection and treatment of AF. During the fifth month, the patient was put on flecainide in an attempt to minimize the AF recurrence rate. On flecainide the patient experienced typical atrial flutter which required IAD reprogramming for appropriate detection and therapy delivery. This case report examines the optimization of the IAD to detect atrial flutter. Six months of follow-up after optimization the IAD has shown appropriate detection of both atrial flutter and AF. During the entire follow-up period the IAD had appropriate detection of sinus rhythm (no false positive detection, i.e. sinus rhythm as AF).     

A Novel Mechanism of Failure to Detect Atrial Arrhythmias by Pacemakers and Implantable Cardioverter Defibrillators

Failed Atrial Arrhythmia Detection by Pacemakers and ICDs. A 64‐year‐old man with complete heart block, status post‐Medtronic dual chamber pacemaker insertion, failed ablation for atrial tachycardia at an outside institution. Despite persistent palpitations and known unsuccessful ablation, pacemaker interrogation revealed no evidence of atrial arrhythmias. At electrophysiology study, burst pacing from the high right atrium and distal coronary sinus at 370 ms revealed bidirectional 2:1 interatrial conduction block. Left atrial burst pacing at 260 ms induced an atrial tachycardia (cycle length 340 ms) with 2:1 left to right atrial block and right atrial activation at 680 ms. The tachycardia was localized to the lateral left atrial roof. A series of ablation lesions from left to right superior pulmonary vein terminated the tachycardia. Left to right interatrial conduction block is a mechanism for underdetection of atrial arrhythmias with implantable devices not previously described. As the extent of atrial ablation increases, the incidence of this mechanism of underdetection may increase. Though devices are often considered ideal for atrial arrhythmia detection and are used in multiple trials, detection failures can occur despite appropriate device function. This case underscores the need for electrocardiographic monitoring in addition to device‐based electrogram monitoring. (J Cardiovasc Electrophysiol, Vol. 21, pp. 325–328, March 2010)     

Immediate Reinitiation of Atrial Fibrillation Following Internal Atrial Defibrillation

Immediate Reinitiation of AF. Introduction: Although the recurrence rate of atrial fibrillation has been reported to be similar to that after external and internal cardioversion, little is known about immediate reinitiation of atrial fibrillation (IRAF) following internal cardioversion. Methods and Results: Thirty-eight patients (24 men; mean age 63 ± 13 years) underwent internal atrial defibrillation. Catheter-based defibrillation electrodes were positioned in the anterolateral right atrium and the coronary sinus. All patients were cardioverted at a mean threshold of 4.6 ± 3.4 J. Five of 38 patients (13%) had 1 to 4 episodes of IRAF. No difference in clinical and echocardiographic characteristics were observed when patients with and without IRAF were compared. Atrial fibrillation was always reinitiated by an atrial premature beat. When the earliest atrial endocardial activation time on the defibrillation catheters was analyzed, these atrial premature heats did not seem to originate from the defibrillation catheters. Twenty-one patients had atrial premature heats without IRAF. When the coupling intervals of the first atrial premature heat in patients without and with IRAF after conversion were compared, a significant difference was found (661 ± 229 vs 418 ± 79 msec, P < 0.05). IRAF was successfully treated with repeated shock delivery after the administration of atropine in 1 patient and intravenous flecainide in 2. Only repeated shock delivery was sufficient to treat IRAF in another 2 patients. Late recurrences of atrial fibrillation occurred in 3 of 5 with IRAK and in 19 of 33 patients without IRAF (P = NS). Conclusion: IRAF after internal atrial defibrillation occurred in 13% of patients, was always initiated by an atrial premature heat having a short coupling interval not originating from the defibrillation catheters, and was prevented by repeated shock delivery with or without preceding administration of pharmacologic agents. IRAF did not predict early recurrences of the arrhythmia after discharge from the hospital, emphasizing the necessity to treat immediate reinitiation promptly to achieve a successful cardioversion.     

Feasibility of Atrial Sensing Via a Free-Floating Single-Pass Defibrillation Lead for Dual-Chamber Defibrillators

Background: Detection and misclassification of rapidly conducted atrial fibrillation (AF) and marked sinus tachycardia by implantable cardioverter defibrillators (ICD) can result in the delivery of inappropriate therapies. Continuous atrial sensing may improve the differentiation between supraventricular and ventricular tachycardia. The present approach is to implant a separate atrial pacing lead connected to a dual-chamber defibrillator. We hypothesized that a free-floating single-pass defibrillation lead reliably senses the atrial electrical activity. The aim of the study was to assess during implantation the efficacy of a custom-built free-floating single-pass defibrillation lead and to record sinus rhythm (SR), induced AF, and atrial flutter (Afl). Methods: The free-floating single-pass defibrillation lead (Biotronik, Berlin, Germany) had an atrial bipole with 10 mm spacing and a distance between the atrial bipole and the electrode tip of 13.5, 15 or 17-cm. The lead was temporarily implanted in 15 patients during an ICD implantation. Fifteen seconds recordings were made during SR and after the induction of AF and Afl as well as during induced ventricular fibrillation. The amplitude and the time that the amplitude was less than 0.3 mV were assessed. Results: The amplitude during SR (2.1 ± 1.4 mV) was significantly higher compared with the amplitudes for Afl (1.3 ± 0.5 mV; p < 0.02) and AF (0.7 ± 0.5 mV; p < 0.001). Low amplitudes were not observed during SR and rarely during Afl (1.6 ± 3.1%), but they were observed 19.9 ± 15.9% of the time during AF (p < 0.05). The correlation coefficients between SR and AF amplitudes were r = 0.25, between SR and Afl amplitudes r = 0.31, and between AF and Afl amplitudes r = 0.41. During the ventricular fibrillation conversion test 9 patients were in continuous SR. The P-wave amplitude before the induction of ventricular fibrillation was 2.1 ± 1.4 mV. The signal during ventricular fibrillation decreased to 1.1 ± 0.7 mV and increased immediately after the termination of ventricular fibrillation to 1.6 ± 0.8 mV. Conclusions: The recorded unfiltered signals indicate that SR as well as AF and Afl can immediately be detected after the implantation of the new free-floating single-pass defibrillation lead. High signal amplitude during SR did not predict high amplitude during AF or Afl. During induced ventricular fibrillation the P-wave amplitude decreased intermittently.     

Upper Limit of Vulnerability Predicts Chronic Defibrillation Threshold for Transvenous Implantable Defibrillators

ULV Predicts Chronic DFT. Introduction: The upper limit of vulnerability (ULV) is the shock strength at or above which ventricular fibrillation cannot be induced when delivered in the vulnerable period. It correlates acutely with the acute defibrillation threshold (DFT) and can be determined with a single episode of fibrillation. The goal of this prospective study was to determine the relationship between the ULV and the chronic DFT.
Methods and Results: We studied 40 patients at, and 3 months after, implantation of transvenous cardioverter defibrillators. The ULV was defined as the weakest biphasic shock that failed to induce fibrillation when delivered 0,20, and 40 msec before the peak of the T wave. Patients were classified as clinically stable or unstable based on prospectively defined criteria. There were no significant differences between the group means for the acute and chronic determinations of ULV (13.5 ± 5.3 J vs 12.4 ± 6.8 J, P = 0.25) and DFT (10.1 ± 5.0 J vs 9.9 ± 5.7 J, P = 0.74). Five patients (15%) were classified as unstable. The strength of the correlation between acute ULV and acute DFT (r = 0.74, P < 0.001) was similar to that between the chronic ULV and chronic DFT (r = 0.82, P < 0.001). There was a correlation between the change in ULV from acute to chronic and the corresponding change in DFT (r = 0.67, P < 0.001). The chronic DFT was less than the acute ULV + 3 J in all 35 stable patients, but it was greater in 2 of 5 unstable patients (P = 0.04).
Conclusions: The strength of the correlation between the chronic ULV and the chronic DFT is comparable to that between the acute ULV and the acute DFT. Temporal changes in the ULV predict temporal changes in the DFT. In clinically stable patients, a defibrillation safety margin of 3 J above the acute ULV proved an adequate chronic safety margin.     

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     

Is the Automatic Atrial Defibrillator a Promising Approach?

Automatic Atrial Defibrillator. Atrial fibrillation is a common arrhythmia, accounting for more consumption of medical resources than any other arrhythmia. The impact of the disease results from the combination of a loss of atrial contraction, and atrial control over cardiac rate. Studies in animals demonstrated the basic feasibility of atrial defibrillation using electrodes passed intravenously. Subsequent studies in patients confirmed that low-energy shocks were effective in converting atrial fibrillation and were safe if delivered synchronous to the R wave in the absence of a short preceding RR interval. Preliminary experience suggests that a small implanted device might provide beneficial therapy for patients with recurring episodes of persistent, drug-refractory, 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.     

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.     

Pharmacological Atrial Defibrillation via Temporarily Occluded Coronary Sinus: First clinical experience and implications for an implantable device

The aim of this paper is to report the first experience of pharmacological atrial defibrillation in humans via a temporarily occluded coronary sinus.Patients and methods: In 6 patients (3 women, 3 men; mean age 57.8y, min 31, max 71), with clinical recurrences of atrial fibrillation, an occlusive coronary venogram was carried out in order to establish the origin of the Vein of Marshall. Atrial fibrillation was then induced by atrial pacing in all the patients and after an adequate waiting period to assure that the atrial fibrillation episode was persistent and stable, a bolus of a very low dose of an antiarrhythmic drug was delivered in 3–4 seconds into the temporarily balloon occluded coronary sinus near the orifice of the vein of Marshall. For both the venogram and the pharmacological test a Baim-Turi (USCI-Bard, Billerica MA) or a Vueport (Cardima, Fremont CA) catheter was used.Results and comments: In five patients a single dose of 7mg of propafenone was immediately effective in restoring the sinus rhythm. In the remaining patient 2 doses of 7mg of propafenone failed to interrupt the arrhythmia, which was subsequently interrupted by a bolus of 0.1mg of ibutilide fumarate given after a waiting period of 20 minutes. Retroperfusion of the left atrium could account for these results; in fact the Vein of Marshall has no valvular apparatus in contrast with other coronary sinus tributary veins which are equipped with an uni- or bicuspidal valve.Conclusions: Pharmacological atrial defibrillation with a minimal dose of an antiarrhythmic drug delivered near the orifice of the Vein of Marshall via the temporarily occluded coronary sinus is feasible and effective. This new pharmacological atrial defibrillation can offer interesting opportunities in developing an implantable pharmacological atrial defibrillator.     

The Circadian Variation of Atrial Defibrillation Thresholds

BACKGROUND: A circadian variation exists for ventricular defibrillation thresholds (DFTs) with a morning peak and a corresponding decrease in therapy success rates from implantable cardioverter defibrillators. Such a variation in atrial DFTs may have implications for the timing of internal cardioversion of atrial arrhythmias. The aim of this study was therefore to determine the circadian variation of atrial DFTs in patents with recurrent atrial fibrillation (AF). METHODS AND RESULTS: Data were collected as part of the worldwide Jewel AF-only study. Patients had recurrent persistent AF and no history of ventricular arrhythmias. The atrial DFT was assessed at device implantation using a step-up protocol and was recorded for 100 patients (age 63.0 +/- 11.7, 74% male, ejection fraction 49.6 +/- 17.8%, left atrial diameter 46 +/- 9 mm). The mean atrial DFT was 6.3 +/- 4.3 J. For the most commonly tested lead configuration (right atrium to coronary sinus in 56 patients), the atrial DFT for patients implanted in the morning (3.3 +/- 1.5 J) was significantly lower than for both the DFT measured in the afternoon (5.8 +/- 3.4 J, p < 0.01) and the DFT measured in the evening (7.4 +/- 5.9 J, p < 0.01). CONCLUSION: There may be a significant variation in measured atrial DFT for the right atrium to coronary sinus configuration, with a nadir in the morning. This is the converse to measurements of ventricular DFTs suggesting different regulatory electrophysiological mechanisms. Further investigation of this possible variation is warranted.     

Effect of the Implantable Atrial Defibrillator on the Natural History of Atrial Fibrillation

INTRODUCTION: The purpose of our study was to evaluate the effect of repeated cardioversion with an implantable atrial defibrillator on the clinical outcome of patients with atrial fibrillation. METHODS AND RESULTS: The effects of the implantable atrial defibrillator on the total duration of atrial fibrillation, number of atrial fibrillation recurrences, and left atrial size were evaluated prospectively in 16 patients with atrial fibrillation (13 men and 3 women; mean age 58 +/- 11 years). Seven patients had no cardiovascular disease, 5 patients had hypertension, 3 patients had coronary heart disease, and 1 patient had congenital heart disease. Eight patients had paroxysmal atrial fibrillation for a mean duration of 80 +/- 61 months, and eight patients had persistent atrial fibrillation for a mean duration of 68 +/- 119 months. Except for one patient who received digoxin throughout the study, all patients received the same Class I or III antiarrhythmic agent throughout the study. The implantable atrial defibrillator successfully converted 50 (93%) of 54 spontaneous episodes of atrial fibrillation in 12 patients. During the initial 3 months of clinical follow-up, the atrial defibrillator documented 261 +/- 270 hours of atrial fibrillation compared with 126 +/- 172 hours (P = 0.01) during the subsequent 3 months. The left atrial size decreased from 4.4 +/- 0.7 cm at the time of atrial defibrillator implantation to 4.1 +/- 0.6 cm (P = 0.02) 6 months later. The number of atrial fibrillation recurrences did not change. These findings were observed in the absence of changes in drug therapy. No complications were observed. CONCLUSION: Restoration and maintenance of sinus rhythm in patients with atrial fibrillation by repeated cardioversion with an implantable atrial defibrillator was associated with a reduction in the total arrhythmia duration and a reduction in left atrial size. These results suggest that maintenance of sinus rhythm with the atrial defibrillator may reverse the remodeling process associated with atrial fibrillation.     

Atrial Fibrillation/Flutter Induced by Implantable Ventricular Defibrillator Shocks:

Atrial Fibrillation/Flutter Induced by Defibrillator Shocks. Introduction : We evaluated the incidence and energy dependence of atrial fibrillation/flutter (AF) induced by implantable ventricular defibrillator shocks in 63 patients tested in the operating room or electrophysiology laboratory.
Methods and Results : Defibrillator shocks were epicardial monophasic in 32 patients, and through an Endotak® lead endocardial monophasic in 19 and biphasic in 12 patients. The epicardial and endocardial patient groups had similar clinical characteristics. A total of 517 defibrillator shocks were given. The epicardial group received 336 total defibrillator shocks and 10 ± 6 shocks (mean ± SD) per patient compared with the endocardial group, which received 181 total shocks and 6 ± 4 defibrillator shocks per patient (P = 0.004). In the epicardial group, AF occurred in 13 (41 %) patients and in 17 (5%) of the 336 shocks. No AF was induced with endocardial defibrillator shocks. The epicardial mean energy was 16 ± 9 J, lower than the endocardial mean energy of 20 ± 9 J (P < 0.004). In the epicardial monophasic group, energy correlated with AF induction. Each patient received 7 ± 6 defibrillator shocks < 15 J and 4 ± 2 shocks ≥ 15 J, yet AF occurred in only 2.3% versus 9.6% (P < 0.05) of defibrillator shocks < 15 J and ≥ 15 J, respectively. Of note, AF was not induced with energy < 4 J or > 31 J.
Conclusions : In the epicardial configuration, AF induction is energy dependent, with an apparent lower and upper limit of vulnerability. AF induction by defibrillator shocks delivered through an Endotak lead is very rare, possibly related to an apparent upper limit of vulnerability of less energy, avoidance of thoracotomy, or different energy field distribution.     

Effect of Atrial Natriuretic Peptide on Electrical Defibrillation Efficacy

ANP and Defibrillation. Introduction : In vitro studies have suggested that human atrial natriuretic peptide (ANP) modulates the electrophysiologic properties of myocardial cells. This study assessed whether ANP could influence defibrillation efficacy.
Methods and Results : In 35 anesthetized dogs, the transcardiac defibrillation threshold (DFT) as well as hemodynamic and electrophysiologic variables were determined before and during treatment with ANP (n = 11), hydralazine (n = 11), or saline (n = 13). ANP (1.5 μg/kg + 0.2 μg/kg per min) increased the plasma concentration of cyclic GMP (a second messenger for ANP) and significantly decreased aortic blood pressure (mean 100 ± 11 mmHg to 83 ± 15 mmHg). ANP also prolonged ventricular repolarization (effective refractory period 157 ± 7 msec to 165 ± 11 msec) and markedly reduced DFT (5.4 ± 1.2 J to 3.8 ± 0.7 J [P < 0.01]) without changing pulmonary artery pressure or sinus cycle length. Neither saline nor hydralazine (1.5 mg/kg) had a significant effect on DFT (saline 4.7 ± 2.1 J to 4.6 ± 2.4 J; hydralazine 4.3 ± 2.0 J to 4.2 ± 1.9 J), although hydralazine caused pronounced hypotension (mean aortic pressure 103 ± 9 mmHg to 74 ± 13 mmHg).
Conclusion : These results suggest that ANP increases defibrillation efficacy, and that this effect is not necessarily shared by other vasodilating agents.     

Optimization of Shocking Lead Configuration for Transvenous Atrial Defibrillation

Optimum Electrodes for Atrial Defibrillation. Introduction : High atrial defibrillation energy requirements (ADER) in patients with chronic atrial fibrillation (AF) may limit the acceptance of transvenous atrial defibrillation. We evaluated an optimized defibrillation electrode configuration that could help to reduce the ADKR in patients with AF.
Methods and Results : We tested ten different configurations in nine dogs with AF (3.33 ± 2.92 days) induced by rapid atrial pacing. The configurations were: right atrial (RA) appendage as anode und coronary sinus (CS) as cathode; RA and innominate vein (I) as anode to CS (cathode); RA-CS (anode) to I (cathode); I-CS (anode) to RA (cathode); RA and left lateral subcutaneous patch (P) as anode to CS (cathode); RA-CS (anode) to P (cathode); P-CS (anode) to RA (cathode); superior vena cava (SVC) and CS (anode) to RA (cathode); RA-CS (anode) to SVC (cathode); and RA-SVC (anode) to CS (cathode). ADER was defined as the voltage needed to defibrillate the atria in 10% to 90% of 20 consecutive shocks. Three lead systems had ADER lower than the RA (anode) to CS (cathode) configuration, which required a mean of 143 ± 58 volts. These three were: RA-SVC (anode) to CS (cathode) 103 ± 29 V; I-CS (anode) to RA (cathode) 129 ± 39 V; and P-CS (anode) to RA (cathode) 130 ± 38 V. The remaining configurations had ADER higher than the RA (anode) to CS (cathode) configuration.
Conclusion : Adding an additional shocking electrode may reduce ADER when compared with the RA (anode) to CS (cathode) configuration. This concept could he incorporated into future implantable atrial defibrillators or used for refractory patients undergoing temporary transvenous cardioversion.     

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.     

Clinical Experience with a Dual-Chamber Implantable Cardioverter Defibrillator to Treat Atrial Tachyarrhythmias

INTRODUCTION: This study evaluated the safety and efficacy of a new dual-chamber implantable cardioverter defibrillator (ICD) to detect and treat atrial tachyarrhythmias in patients with drug-refractory atrial fibrillation (AF) and no indication for a ventricular ICD. METHODS AND RESULTS: A dual-chamber ICD (Medtronic 7250 Jewel AF) was implanted in 144 of 146 patients. The device discriminates atrial tachycardia from AF based on cycle length and regularity, and uses atrial overdrive pacing as well as shocks to terminate tachyarrhythmia episodes. Patients were followed for an average of 12.6+/-6.2 months. Use of antiarrhythmic drugs was 63% at baseline and did not change over time. Kaplan-Meier estimates of 12-month complication-free survival, device therapy survival, and patient survival were 85%, 91%, and 98%, respectively. Positive predictive accuracy of spontaneous atrial tachyarrhythmia detection was 99%, while atrial overdrive pacing and shocks terminated 40% and 87% of treated episodes, respectively. Median duration of successfully treated episodes was 8.9 minutes versus 144 minutes for the therapy failures. There was no reduction in the use of patient-activated shock therapy over time; at the 12-month follow-up evaluation, 94% of patients were in sinus rhythm. Ventricular tachyarrhythmias (67 episodes) were detected and appropriately treated in 7.6% of patients. CONCLUSION: This dual-chamber ICD appears to be safe and well tolerated in patients with drug-refractory symptomatic atrial tachyarrhythmias. The device, used in combination with drugs, effectively treats atrial tachyarrhythmias with pacing and/or shock therapies and decreases the median episode duration. In addition, the device protects from ventricular tachyarrhythmias in patients with AF and structural heart disease.