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European Heart Journal Advance Access published online on June 14, 2007

European Heart Journal, doi:10.1093/eurheartj/ehm211
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© The European Society of Cardiology 2007. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org

External cardioversion of atrial fibrillation in patients with implanted pacemaker or cardioverter-defibrillator systems: a randomized comparison of monophasic and biphasic shock energy application

Johannes C. Manegold{dagger}, Carsten W. Israel{dagger}, Joachim R. Ehrlich, Gabor Duray, Dmitri Pajitnev, Florian T. Wegener and Stefan H. Hohnloser*

Division of Cardiology, Department of Medicine, J. W. Goethe University Hospital, Theodor-Stern-Kai 7, 60590 Frankfurt, Germany

Received 18 January 2007; revised 17 April 2007; accepted 3 May 2007.

* Corresponding author. Tel: +49 69 6301 7404; fax: +49 69 6301 7017. E-mail address: hohnloser{at}em.uni-frankfurt.de


    Abstract
 Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Conclusions
 References
 
Aims: External cardioversion (ECV) of atrial fibrillation (AF) may damage implanted pacemaker and cardioverter-defibrillator (ICD) systems. This prospective study evaluated the safety and efficacy of ECV comparing mono- to biphasic shock waveforms in patients with implanted rhythm devices.

Methods and results: Patients with pacemaker or ICD systems and an indication for ECV were randomized to receive mono- or biphasic shocks. Systems were tested immediately before and after ECV, 1 h and 1 week later with respect to device and lead integrity. Forty-four patients (71 ± 10 years, 31 male; 29 pacemakers, 12 ICDs, three cardiac resynchronization systems) underwent ECV with antero-posterior paddle orientation (monophasic in 21 and biphasic in 23 patients). Pacing impedances were reduced immediately after ECV (atrial 402–392 ohm, P < 0.001; ventricular 517–496 ohm, P = 0.001) and returned to baseline values within 1 week. Ventricular sensing was reduced immediately after ECV (12.4–11.6 mV, P = 0.004). There was no device or lead dysfunction in any patient. ECV was successful in 42/44 patients (95%), cumulative energy was significantly lower for biphasic compared with monophasic shocks (P = 0.001).

Conclusion: ECV for AF seems to be safe and effective in patients with implanted rhythm devices.

Key Words: Cardioversion • Monophasic shocks • Biphasic shocks • Pacemaker • Implantable cardioverter-defibrillator • Atrial fibrillation


    Introduction
 Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Conclusions
 References
 
Atrial fibrillation (AF) occurs frequently in patients with implanted pacemaker and cardioverter-defibrillator systems (ICDs) with a prevalence of up to 25–50% within the first year after implantation.1,2 Besides the AF associated morbidity and mortality, the rhythm disturbance may also lead to adverse device reactions such as pacemaker mediated tachycardia, inappropriate shock therapy and reduction of the percentage of biventricular pacing. In many patients with an implanted device, termination of AF by means of external electrical cardioversion is therefore indicated. However, there are numerous case reports on device and lead failure following external cardioversion (ECV).38 In vitro studies indicate that measures protecting the device from high energy do not prevent or may even increase current shunting at the site of contact between electrode tip and myocardium.9,10 Unfortunately, no controlled clinical study has demonstrated the safety of external DC cardioversion in patients with an implanted rhythm device. Accordingly, the present prospective randomized trial aimed to evaluate the safety and efficacy of mono- vs. biphasic ECV of AF in patients with implanted rhythm devices.


    Methods
 Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Conclusions
 References
 
Patients
All patients with implanted rhythm devices referred for electrical cardioversion of AF to the Department of Cardiology at the J. W. Goethe University, Frankfurt, Germany, between December 2005 and September 2006 were considered for this study. AF was documented in the 12 lead ECG and by means of intracardiac recordings via the implanted atrial leads where available. There were no restrictions regarding the implanted devices or lead compositions (i.e. manufacturers, device model, device age, pacing mode, lead polarity, implantation site, etc.). However, patients with implanted systems with evidence of pre-existing technical problems (e.g. undersensing or exit block) not correctable by device reprogramming were excluded from participation. Further exclusion criteria were the presence of contraindications for ECV, pregnancy, and age <18 years. The study protocol complies with the declaration of Helsinki and was approved by the institutional review board; written informed consent was obtained from each patient.

Device interrogation and programming before cardioversion
Immediately before cardioversion, all devices were interrogated; sensing and pacing performance was checked including lead impedances and battery status. Device memory functions were interrogated and printed out, documenting the precise duration of the current AF episode by analysis of device-stored electrograms where possible. In patients with devices not capable of electrogram storage, AF duration was assessed by the time from the first ECG documentation. The underlying intrinsic rhythm was assessed and in patients without a sufficient intrinsic rhythm, devices were programmed to an atrial and ventricular output four times above the threshold value, otherwise output remained at twice the diastolic threshold. Pacing mode remained in DDD(R) or VVI(R), pacing was programmed to unipolar in all atrial and ventricular leads, sensing to bipolar where possible with an atrial sensitivity of 0.15–0.50 mV, and a ventricular sensitivity of 2.0–4.0 mV. Automatic capture control algorithms were not activated. In ICD systems, all tachycardia detection and therapy algorithms remained active.

Anticoagulation
According to current guidelines,11 patients had to be on oral anticoagulation (INR 2.0–3.0) for at least 3 weeks prior to cardioversion or—in case of lack of previous anticoagulation—underwent transoesophageal echocardiography to rule out the presence of atrial thrombi. In the latter patients, overlapping treatment with fractionated or unfractionated heparin was applied.12 After cardioversion, anticoagulation with oral vitamin K antagonists was continued for at least 4 weeks.

DC cardioversion
DC cardioversion was performed under sedation with intravenous administration of midazolame and etomidate with repeated drug administration as necessary in case of sequential shock delivery. Patients were randomized to cardioversion utilizing mono- or biphasic shock forms. Randomization was performed using an unblocked randomization scheme without stratification prepared by a computer program with sequentially numbered opaque sealed envelopes opened immediately before cardioversion. A damped sine monophasic waveform (cardioverter model CardioServ, GE Medical Systems, Milwaukee, WI, USA) was compared with a rectangular biphasic waveform (cardioverter model M Series Primary AED, Zoll Medical Corp., Chelmsford, MA, USA). To protect the implanted devices and lead systems against current shunt during shock application, a strict anterior–posterior cardioversion electrode position was obtained with the posterior paddle (circular, diameter 12 cm) placed left of the patient’s spine at the midscapular level and the anterior paddle (rectangular, 10 x 8.5 cm for biphasic and 11 x 7.5 cm for monophasic shocks) placed to the right of the sternum with its upper edge at the level of the fourth anterior intercostal space. In all patients, the distance between the anterior electrode and the implanted device had to be ≥8 cm. Special disposable wet polymer gel pads (11.4 x 15.2 cm, 3M Health Care, St Paul, MN, USA) were positioned between the electrodes and the patient’s skin for better current conduction and minimization of skin burns.

A maximum of four shocks at escalating doses was applied. Biphasic shocks were applied at 100, 150, 2 x 200 J, monophasic shocks at 200, 300, 2 x 360 J according to results of prior studies.13,14 In case of repeated shock applications, sequential shocks were delayed for at least 5 min to avoid overheating of the device itself or the implanted leads. All shocks were synchronized to the QRS complex of the surface ECG. An ECG was recorded immediately prior, during, and immediately after cardioversion as well as 1 h later. The device programmer remained at the bedside with respective system software activated to allow immediate telemetry whenever necessary to reprogram the device (e.g. in case of a threshold increase, undersensing, or spurious programming) and to verify sinus rhythm or persistence of AF via the atrial electrogram.

Device interrogation after cardioversion
Immediately after cardioversion, devices were interrogated and the following parameters were specifically checked: telemetric ECG (including atrial and ventricular electrograms), programmed parameters, atrial and ventricular lead impedance, atrial and ventricular pacing threshold, P-wave and R-wave amplitude, and battery status including voltage and battery impedance if available. Sensing and pacing parameters were reprogrammed where applicable for sufficient safety margins to avoid exit block and undersensing. Complete interrogation was repeated 1 h later and 1 week after cardioversion.

Studied parameters
Cumulative energy applied during monophasic and biphasic cardioversion was recorded together with any adverse event. Particularly, any device or lead failure after cardioversion were recorded: Sensing problems, exit block, significant increase of the pacing threshold (defined as doubling of the threshold before cardioversion); suspicious lead impedance (<200 or >2000 ohm), lead dislodgement; physical dysfunction of the device, power-on-reset, spurious programming, battery problems (defined as elective replacement indication, end of service, reduction of voltage >0.1 V, or increase of battery impedance >0.1 kohm). Concurrently, any influence of class IC and class III antiarrhythmic drugs on pacing performance was analysed.

Statistical analysis
This was a prospective, randomized, single-blind trial to test the feasibility and safety of ECV in pacemaker and defibrillator patients, comparing mono- to biphasic shocks. Kolmogorov-Smirnov Z test was used to distinguish normal from non-normal distribution. The incidence of adverse events between the two shock forms was assessed using Fisher’s exact test. Changes in the entire patient group and in each subgroup before vs. after cardioversion were assessed using paired two-sided t-test (with Bonferoni correction for multiple comparisons), with Wilcoxon or Friedman test whichever applied when data were not normally distributed. Differences related to mono- vs. biphasic shock forms on studied parameters were analysed using unpaired t-test for parameters with normal distribution respectively with Mann–Whitney U test if asymmetric distribution was found. Statistical analyses were performed using the Statistical Package for Social Sciences (SPSS, version 12.0) and BIAS for Windows (Version 8.01). A two-sided P-value <0.05 was considered statistically significant.


    Results
 Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Conclusions
 References
 
Patients and implanted devices
Forty-four patients (31 male, mean age 70 ± 10 years) were included. All but one patient had cardiovascular disease; the mean body mass index was 27 ± 4 kg/m2 (Table 1). In 29 patients, AF had first been documented >12 months ago and in 15 patients the history of atrial tachyarrhythmia lasted <12 months. Thirty-seven patients (84%) received beta blocker treatment, 20 patients (45%) amiodarone, 20 patients (45%) digitalis glycosides, and 33 patients (75%) angiotensin inhibitors or angiotensin receptor blockers. Twenty-one patients were randomized to receive monophasic and 23 to receive biphasic shocks for cardioversion. In 29 patients, pacemaker systems were implanted for conventional bradycardia indications (complete pacemaker dependency in three patients); ICDs were implanted for primary or secondary prevention of sudden cardiac death in 15 patients. All pacemaker systems were dual-chamber devices, nine patients were fitted with dual-chamber ICDs, three with single-chamber, and three patients with a biventricular system (Tables 2 and 3). About 15 devices were implanted in the right, 29 in the left subclavian region. Thirty-nine of 40 atrial leads were bipolar, as were 39 of 44 ventricular leads, two left ventricular (LV) leads were unipolar and one was bipolar. Mean time since device implantation was 477 days. Before cardioversion, no device had an elective replacement indication; however, three pacemaker systems were implanted >5 years earlier (maximum 8.5 years).


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Table 1 Patient characteristics

 

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Table 2 Implanted pacemaker and cardioverter-defibrillator systems (devices)

 

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Table 3 Implanted pacemaker and cardioverter-defibrillator systems (leads)

 
Cardioversion success
AF had been present for a median of 21 (range 1–1359) days before the cardioversion attempt. All but two patients could be cardioverted to sinus or a paced rhythm; after 1 h 41 of 44 patients (93%) were still in sinus rhythm. There were no clinical complications during or after cardioversion.

Effect of cardioversion on device and lead function
Repeated device interrogations immediately and 1 h after cardioversion as well as 1 week later demonstrated that there were no incidences of atrial or (right or left) ventricular loss of capture or events of atrial or ventricular undersensing. All devices could be interrogated and programmed after cardioversion; there were no instances of physical dysfunction of the device, spurious programming or electrical reset induced by the shock. Device battery voltage and impedance were unchanged in all devices that allowed interrogation of these parameters. This also refers to devices with a battery resistance before cardioversion that documented advanced age.

There were no instances of clinically relevant or suspicious lead problems immediately after cardioversion and over the course of 1 week. There was no increase of any pacing threshold by ≥100%, as pre-specified as a clinical event.

Changes in atrial or ventricular pacing thresholds, pacing impedances, and sensed intrinsic signals were similar in patients randomized to receive mono- or biphasic shocks. These lead-related parameters are therefore reported for the entire patient group. Median atrial thresholds (not measured immediately before cardioversion since patients were in AF) were 0.75 V (range 0.5–2.25 V) immediately after cardioversion, 0.75 V (range 0.5–2.5 V, P = 0.071) when measured 1 h later with the same impulse duration, and were not significantly changed after 1 week (median 0.85 V, range 0.5–2.0 V, P = 0.53 vs. results after 1 h, Figure 1A). Testing for multiple dependent variables revealed no significant changes of any of these measurements (P = 0.216). Median ventricular thresholds were 0.75 V (range 0.5–2.0 V) for all measurements before and after cardioversion with a trend towards higher values immediately after cardioversion (P = 0.088), returning to baseline values within 1 h (P = 0.071 vs. immediately after cardioversion) and were not significantly changed over 1 week (P = 1.00 vs. results after 1 h, Figure 1B). Patients with a high-pacing threshold at baseline showed no significant increase of the threshold after cardioversion. The three LV leads had identical pacing threshold values before and after cardioversion.


Figure 1
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Figure 1 Atrial (A) and ventricular (B) threshold values. Results are expressed in volt at individually constant impulse duration (e.g. 0.4 or 0.5 ms). Atrial thresholds before cardioversion are taken from the last device interrogation during sinus rhythm. Boxes: upper to lower quartile, bold line: median value, thin lines: range (minimal to maximal value, excluding outliers and extreme values). CV, cardioversion.

 
The median atrial and ventricular pacing impedance showed a small but statistically significant decrease immediately after cardioversion (atrial 397–388 ohm, P < 0.001; ventricular 492–480 ohm, P = 0.002), remained unchanged after 1 h in the atrium (median 382 ohm, P = 0.414) and slightly lower in the ventricle (465 ohm, P = 0.001). After 1 week, atrial impedance was not significantly different compared with initial values (400 ohm, P = 0.988), whereas ventricular impedance was slightly lower (489 ohm, P = 0.017; Figure 2). Specifically, patients with high-impedance leads (n = 3) demonstrated no significant change of pacing impedance. There was no event of an impedance change to <200 or >2000 ohm. None of the changes in atrial or ventricular pacing impedance were associated with any clinical sequelae.


Figure 2
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Figure 2 Atrial (left) and ventricular (right) pacing impedance. Boxes: upper to lower quartile, bold line: median value, thin lines: range (minimal to maximal value, excluding outliers and extreme values). CV, cardioversion.

 
Sensing performance was adequate at ECG recording immediately after cardioversion and at all measurements during the course of the study. There was no case of atrial or ventricular undersensing. The only statistically significant change refers to the comparison of the median sensed R-wave immediately before and after cardioversion (Figure 3) which showed a decrease from 12.0 to 11.0 mV (P = 0.004), again, without any clinical relevance. All other changes in atrial and ventricular sensing performance were not statistically significant. Of note, there was no case of delayed deterioration of lead function, i.e. in no patient, sensing or pacing parameters worsened between 1 h and 1 week after cardioversion.


Figure 3
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Figure 3 Atrial (A) and ventricular (B) sensing. Atrial sensing before cardioversion is only included if sinus rhythm had been recorded earlier. Boxes: upper to lower quartile, bold line: median value, thin lines: range (minimal to maximal value, excluding outliers and extreme values).

 
There was no difference in measured lead and device parameters between systems implanted in the left (n = 29) vs. right (n = 15) subclavian region.

Comparison between mono- and biphasic shocks
In both modes of high-energy application, there were no incidences of device failure. One patient randomized to receive biphasic and one patient randomized to monophasic shocks could not be converted to sinus/atrial paced rhythm rendering an acute cardioversion success of 95 and 96% in both groups (Table 4). The first monophasic shock of 200 J and the first biphasic shock of 100 J were sufficient to terminate AF in 15/21 patients (71%) randomized to receive monophasic, and 17/23 patients (74%) randomized to receive biphasic shocks. The median cumulative shock energy applied was higher for monophasic application (200 J, range 200–1220 J vs. 100 J, range 100–650 J, P = 0.001). There were no statistically significant differences between patients randomized to monophasic or biphasic shocks with regard to any device sensing or pacing parameter at any point in time.


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Table 4 Cardioversion data

 
Influence of concurrent antiarrhythmic drug therapy
No patient received class I antiarrhythmic drugs or sotalol, 20 patients were on chronic amiodarone treatment. Twelve of 24 patients (50%) without amiodarone received monophasic shocks vs. nine of 20 patients with amiodarone (45%, P = 1.0). Two patients on amiodarone could not be reverted to sinus rhythm (success rate 100% without and 90% with amiodarone, P = 1.0). Cumulative shock energy was not different [median 200 J (range 100–1220 J)] in patients without and in patients with amiodarone [median 200 J (range 110–1220 J)], P = 0.9. There were no significant differences in all measurements of sensing function, pacing impedance, and pacing threshold between patients on and off amiodarone.


    Discussion
 Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Conclusions
 References
 
Main study findings
In the present study, there was no evidence of device failure following ECV of AF utilizing mono- or biphasic shock wave forms. The cumulative shock energy required for AF termination was lower with biphasic shocks. This is the first study to prospectively demonstrate that ECV can be safely performed in patients with implanted pacemaker, ICD, and cardiac resynchronization therapy (CRT) systems using an anterior–posterior shock electrode orientation with a distance to the implanted device ≥8 cm. Whenever changes in pacing or sensing parameters developed after high-energy application, these were clinically irrelevant. In no patient, device sensing or pacing function deteriorated between 1 h and 1 week after cardioversion.

External cardioversion in patients with implanted devices
Numerous cases of interaction between pacemaker systems and ECV procedures have been reported resulting in device failure15,16 and even death of patients.4 Although the risk of damage to the device during ECV is reduced by diodes that shunt current away from device housing, and may be further minimized by maintaining maximal distance between shock electrodes and the device, leads may not be protected by these measures. In fact, diodes may even increase current density at the lead tip that serves as an antenna particularly with unipolar leads, leading to myocardial damage at the electrode–endocardial junction.9,16 This may result in local myocardial oedema and fibrosis, leading to a transiently (in case of edema) or permanently/progressively (in case of scar formation) increased pacing threshold and a deterioration of sensing function of the device.

To the best of our knowledge, only one study has analysed the safety of ECV in patients with implanted pacemaker systems.17 This study in 36 patients reported an incidence of transient (up to 30 min) loss of capture in 50% of patients, a six-fold overall increase of ventricular pacing thresholds, sensing failure in 41% of patients, and three cases of pacemaker malfunction of which two required generator replacement. The study concluded that ECV represents a serious hazard to patients with an implanted pacemaker. This study, however, differed from the present one in several important aspects: all patients had unipolar electrodes and pacemaker devices implanted in the right pectoral region, external shock electrodes were placed in an antero-lateral and not in an antero-posterior orientation, and only monophasic shocks were applied. Finally, device and lead technology cannot be compared with contemporary rhythm devices. Thus, our study is the only one to examine the safety and efficacy of ECV in patients with state-of-the-art rhythm devices.

Our study incorporated several measures to protect devices and leads. One problem associated with ECV relates to the antero-lateral orientation of cardioversion electrodes used in many institutions. These create an electrical field parallel particularly to the ventricular lead thus maximizing current shunting through uni- and bipolar leads.10 The use of an antero-posterior orientation of cardioversion electrodes aims to prevent this ‘antenna effect’ of the ventricular lead since it creates an electrical field typically perpendicular to its orientation. In fact, basically all reports on failure of implanted leads after ECV occurred after antero-lateral electrode placement. Furthermore, an antero-posterior orientation of cardioversion electrodes has been demonstrated to result in lower energy requirements for termination of AF.13,18 Using lower energy levels together with a sufficient distance to the implanted device (in our study ≥8 cm) may further protect implanted rhythm devices. Of note, these guidelines also apply to emergency situations of ventricular tachyarrhythmia in patients with implanted devices; thus, it is important to convey the information to the paramedical staff in emergency facilities that ECV is safe in patients with devices if the precautions outlined above are considered.

Previous studies have demonstrated that biphasic shocks are superior to monophasic shocks for cardioversion of AF.19,20 However, none of these studies have included patients with implanted rhythm devices. Accordingly, the results of our study extend those of prior ones in demonstrating the safety of this form of electrical cardioversion to patients with pacemakers or ICDs. In both groups, there were no clinically significant events following mono- and biphasic external shocks. In agreement to previous findings, energy requirements were significantly lower for bi- compared with monophasic shock waveforms, thus at least providing a theoretical advantage of biphasic shock application.

There was no instance of failure or transient abnormality of pacemaker, ICD, or CRT devices. This applies also to devices with a battery status indicating advanced period of service. Similarly, a physical reaction of the implanted electrodes was measured which was similar to acute endocardial energy application and led to a decrease in pacing impedance and sensed intrinsic signals together with an increase in pacing threshold immediately after cardioversion. However, in case of pacing threshold, this did not even reach the level of statistical significance. All changes in pacing impedance of atrial, right, and LV leads were transient returning to baseline latest within one week. All of these changes were without any clinical sequelae. This also applied to unipolar leads and leads with a small tip area (Table 3) where the shunted energy may be concentrated on a particularly small area of electrode–endocardial contact. However, as outlined above our findings cannot be translated to the use of the antero-lateral position of shock electrodes, which is most likely much less safe with regards to implanted devices and leads than the antero-posterior orientation.

The present study included a variety of devices and leads, however, with the advantage that findings were not limited to one or few device systems. Our study also included a small number of CRT systems which showed regular function following cardioversion. This information appears to be clinically important since the safety of ECV in CRT systems has never been reported despite the fact that AF requiring cardioversion is frequent in heart failure. Clearly, further studies are warranted to confirm the safety of ECV in CRT, using the methods applied in our study.

Amiodarone has been reported to increase acute and chronic pacing21 and ventricular defibrillation thresholds22,23 and may therefore have an effect on device performance after ECV. However, the present study neither demonstrated a difference in energy requirements for ECV of AF, nor for pacing and sensing function between patients with and without amiodarone. This is in agreement with recent findings from the OPTIC trial in which amiodarone did not affect ICD defibrillation thresholds in a clinically relevant way.24


    Conclusions
 Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Conclusions
 References
 
This is the first prospective study that suggests that ECV in patients with AF and implanted rhythm devices may be safe and effective, provided that an antero-posterior electrode orientation and a distance between device and shock electrode ≥8 cm is used. Biphasic shocks required less energy for AF termination and may thus be preferable in these patients.

Conflict of interest: There was no financial support from any sponsor.


    Footnotes
 
{dagger} Both authors contributed equally to this study. Back


    References
 Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Conclusions
 References
 

  1. Israel CW, Neubauer H, Olbrich HG, Hartung W, Treusch S, Hohnloser SH. Incidence of Atrial tachyarrhythmias in pacemaker patients: results from the balanced evaluation of atrial tachyarrhythmias in stimulated patients (BEATS) study. Pacing Clin Electrophysiol (2006) 29:582–588.[CrossRef][Medline]
  2. Wilkoff BL, Hess M, Young J, Abraham WT. Differences in tachyarrhythmia detection and implantable cardioverter defibrillatior therapy by primary or secondary prevention indication in cardiac resynchronization therapy patients. J Cardiovasc Electrophysiol (2004) 15:1002–1009.[CrossRef][Web of Science][Medline]
  3. Giedwoyn JO. Pacemaker failure following external defibrillation. Circulation (1971) 44:293.[Free Full Text]
  4. Aylward P, Blood R, Tonkin A. Complications of defibrillation with permanent pacemaker in situ. Pacing Clin Electrophysiol (1979) 2:462–464.[CrossRef][Medline]
  5. Das G, Eaton J. Pacemaker malfunction following transthoracic countershock. Pacing Clin Electrophysiol (1981) 4:487–490.[CrossRef][Medline]
  6. Gould L, Patel S, Gomes GI, Chokshi AB. Pacemaker failure following external defibrillation. Pacing Clin Electrophysiol (1981) 4:575–577.[CrossRef][Medline]
  7. Levine PA, Barold SS, Fletcher RD, Talbot P. Adverse acute and chronic effects of electrical defibrillation and cardioversion on implanted unipolar cardiac pacing systems. J Am Coll Cardiol (1983) 1:1413–1422.[Abstract]
  8. Waller C, Callies F, Langenfeld H. Adverse effects of direct current cardioversion on cardiac pacemakers and electrodes: is external cardioversion contraindicated in patients with permanent pacing systems? Europace (2004) 6:165–168.[Abstract/Free Full Text]
  9. Lau FYK, Bilitch M, Wintroub HJ. Protection of implanted pacemakers from excessive electrical energy of DC shock. Am J Cardiol (1969) 23:244–249.[CrossRef][Web of Science][Medline]
  10. Das G, Staffanson DB. Selective dysfunction of ventricular electrode–endocardial junction following DC cardioversion in a patient with dual chamber pacemaker. Pacing Clin Electrophysiol (1997) 20:364–365.[CrossRef][Medline]
  11. Fuster V, Rydén LE, Cannom DS, Crijns HJ, Curtis AB, Ellenbogen KA, Halperin JL, Le Heuzey JY, Kay GN, Lowe JE, Olsson SB, Prystowsky EN, Tamargo JL, Wann S. ACC/AHA/ESC 2006 guidelines for the management of patients with atrial fibrillation – executive summary. Circulation (2006) 114:700–752.[Free Full Text]
  12. Stellbrink C, Nixdorff U, Hofmann T, Lehmacher W, Daniel WG, Hanrath P, Geller C, Mügge A, Sehnert W, Schmidt-Lucke C. Safety and efficacy of enoxaparin compared with unfractionated heparin and oral anticoagulants for prevention of thromboembolic complications in cardioversion of nonvalvular atrial fibrillation. Circulation (2004) 109:997–1003.[Abstract/Free Full Text]
  13. Kirchhof P, Eckhardt L, Loh P, Weber K, Fischer RJ, Seidl KH, Böcker D, Breithardt G, Haverkamp W, Borggrefe M. Anterior–posterior versus anterior–lateral electrode positions for external cardioversion of atrial fibrillation: a randomised trial. Lancet (2002) 360:1275–1279.[CrossRef][Web of Science][Medline]
  14. Joglar JA, Hamdan MH, Ramaswamy K, Zagrodzky JD, Sheehan CJ, Nelson LL, Andrews TC, Page RL. Initial energy for elective external cardioversion of persistent atrial fibrillation. Am J Cardiol (2000) 86:348–350.[CrossRef][Web of Science][Medline]
  15. Barold SS, Falkoff MD, Ong LS, Heinle RA. Interference in cardiac pacemakers: exogenous sources. In: Cardiac Pacing and Electrophysiology—El-Sherif N, Samet P, eds. (1991) Philadelphia, WB: Saunders. 608–633.
  16. Levine PA. Effect of cardioversion and defibrillation on implanted cardiac pacemakers. In: Modern Cardiac Pacing—Barold SS, ed. (1985) Mount Kisco, NY: Futura Publ. Co. 875–886. NY.
  17. Altamura G, Bianconi L, Lo Bianco F, Toscano L, Ammirati F, Pandozi C, Castro C, Cardinale M, Mennuni M, Santini M. Transthoracic DC shock may represent a serious hazard in pacemaker dependent patients. Pacing Clin Electrophysiol (1995) 18:194–198.[CrossRef][Medline]
  18. Botto GL, Politi A, Bonini W, Broffoni T, Bonatti R. External cardioversion of atrial fibrillation: role of paddle position on technical efficacy and energy requirements. Heart (1999) 82:726–730.[Abstract/Free Full Text]
  19. Mittal S, Ayati S, Stein KM, Schwartzman D, Cavlovich D, Tchou PJ, Markowitz SM, Slotwiner DJ, Scheiner MA, Lerman BB. Transthoracic cardioversion of atrial fibrillation: comparison of rectilinear biphasic versus damped sine wave monophasic shocks. Circulation (2000) 101:1282–1287.[Abstract/Free Full Text]
  20. Page RL, Kerber RE, Russell JK, Trouton T, Waktare J, Gallik D, Olgin JE, Ricard P, Dalzell GW, Reddy R, Lazzara R, Lee K, Carlson M, Halperin B, Bardy GH. Biphasic versus monophasic shock waveform for conversion of atrial fibrillation: the results of an international randomized, double-blind multicenter trial. J Am Coll Cardiol (2002) 39:1956–1963.[Abstract/Free Full Text]
  21. Israel CW, Ehrlich JR, Barold SS, Hohnloser SH. Treatment of atrial tachyarrhythmias with pacing and antiarrhythmic drugs. In: Advances in the Treatment of Atrial Tachyarrhythmia. Pacing, Cardioversion and Defibrillation—Israel CW, Barold SS, eds. (2002) Armonk, NY: Futura Publishing Co. Inc. 305–323.
  22. Jung W, Manz M, Pizulli L, Pfeiffer D, Lüderitz B. Effects of chronic amiodarone therapy on defibrillation threshold. Am J Cardiol (1992) 70:1023–1027.[CrossRef][Web of Science][Medline]
  23. Pelosi F Jr, Oral H, Kim MH, Sticherling C, Horwood I, Knight BP, Michaud GF, Morady F, Strickberger SA. Effects of chronic amiodarone therapy on defibrillation energy requirements in humans. J Cardiovasc Electrophysiol (2000) 11:736–740.[Web of Science][Medline]
  24. Hohnloser SH, Dorian P, Roberts R, Gent M, Israel CW, Fain E, Champagne J, Connolly SJ. Effect of amiodarone and sotalol on ventricular defibrillation threshold. The Optimal Pharmacological Therapy in Cardioverter Defibrillator Patients (OPTIC) Trial. Circulation (2006) 114:104–109.[Abstract/Free Full Text]

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