Europace Advance Access originally published online on January 11, 2006
Europace 2006 8(2):113-117; doi:10.1093/europace/euj034
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
DEFIBRILLATION
Passive electrode effect reduces defibrillation threshold in bi-filament middle cardiac vein defibrillation
Wessex Cardiothoracic Centre Southampton University Hospitals, Southampton UK ; Ela Medical SA Paris France
Manuscript submitted 3 December 2004. Accepted after revision 18 October 2005.
Corresponding author: Mail Point 46, Southampton General Hospital, Tremona Road, Southampton SO16 6YD, UK. Tel: +44 2380 798676; fax: +44 2380 798942. E-mail address: johnpaisey{at}doctors.org.uk
| Abstract |
|---|
|
|
|---|
Aims To investigate whether a passive electrode effect decreases defibrillation threshold (DFT) in multi-filament middle cardiac vein (MCV) defibrillation.
Methods and results Twelve pigs underwent active housing (AH) insertion, with defibrillation coils placed transvenously in right ventricular apex and superior vena cava. The MCV was cannulated, and 1.12F, 50 mm coil electrodes (Ela Medical SA, France) were deployed in its right and left branches. Lead placement was possible in 11 of 12 animals. DFT (J, mean±SD) was determined by three-reversal binary search and compared between the MCV monofilament (single filament deployed) and the AH (25.9±10.9) and the MCV mono+passive filaments (both filaments deployed, one connected) and the AH (19.9±11.4); 24% DFT reduction P=0.008.
Conclusion A bystander electrode adjacent to a monofilament electrode in the MCV reduces DFT by 24% when compared with monofilament MCV alone. Microfilament electrodes decrease DFT as auxiliary anode but not as sole anode.
Key Words: Defibrillation threshold, Passive electrode, Cardiac vein, Bystander electrode, Implantable defibrillator
| Introduction |
|---|
|
|
|---|
The passive electrode effect is the influence of an electrode that is not connected to a circuit (a bystander electrode) on that configuration's defibrillation characteristics. It has been demonstrated that bystander epicardial patch electrodes increase defibrillation threshold (DFT), through a passive electrode effect, when shocking from transvenous systems.1
Implantable cardioverter defibrillators (ICD) are an accepted treatment for primary4
6
and secondary7
9
prevention of life-threatening ventricular arrhythmias.
Evaluation of factors leading to a decrease in DFT may yield advantages in the clinical application of ICDs: failure rate will be reduced through an increase in safety margin (the difference between DFT and maximum output of device), and device size and longevity will be improved through the benefits of a lower DFT on battery and capacitor design.
The middle cardiac vein (MCV) has the potential to offer low DFT when compared with conventional endocardial systems through its anatomical location.10
It has been evaluated in animal11
15
and human16
studies.
| Methods |
|---|
|
|
|---|
Aims
To investigate whether a passive electrode effect may decrease DFT in multi-filament MCV defibrillation using a novel microfilament electrode.
Ethical considerations
Approval was granted by the local regional Ethics Committee, and the British Government Home Office licensed the project and personnel.
Animal preparation
Twelve female pigs (weight 53.1±10.0 kg) were sedated with intramuscular benzodiazepines (Streznil® 0.2 mL/kg). After 1545 min, general anaesthesia was induced with intravenous Saffan® (0.15 mL/kg) and the animals intubated. Anaesthesia was maintained with inhalational isoflurane (2% via oxygen at 10 L/min), and buprenorphine (0.20.4 mg) was given as adjuvant analgesia. Cut down was performed to the right internal jugular vein to facilitate transvenous lead placement. Intravenous normal saline was infused at 75 mL/h. The surface ECG was monitored continuously on lead II. Systemic blood pressure was monitored through a femoral artery cannula.
Defibrillation system configuration
A dual coil defibrillation lead (Sprint Quattro®, Medtronic, Minneapolis, MN, USA) advanced to the right ventricular (RV) apex. Thus, the coils were sited in RV and superior vena cava (SVC). The MCV was catheterized with an 8F MPA1 catheter cut to 58 cm. Custom-designed microfilament electrodes (1.12F with 50 mm length, 58 mm2 surface area coils, ELA medical SA, Montrouge, France), Fig. 1, were introduced into the left and right branches of the MCV. An active housing (AH) was inserted subcutaneously in the left pectoral area (Defender®, ELA medical). Electrodes were connected through a junction box to an external defibrillator (5358, Medtronic). Induction of VF was by 5 s 50 Hz AC current application, and defibrillation attempts were performed with a biphasic waveform with capacitive tilt.
|
DFT determination
DFT determinations were performed in two stages: the point of entry onto the final pathway was determined (Fig. 2) and the DFT was determined by a three-reversal binary search with increments determined by the programmability of the device (1 J increments up to 16 J and 2 J increments up to 1834 J). If an animal could not be defibrillated by a certain configuration, the DFT was considered to be 34 J (maximum output of device) for analysis.
|
Statistical analysis
Two configurations were compared to examine the passive electrode effect, a comparison between MCV (mono)
AH and MCV (mono+passive)
AH, Fig. 3.
|
In studies of DFT, it is conventional to compare values by a paired t-test. In this protocol, there were several instances of 34 J DFT values being allocated, because animals were not successfully defibrillated in the configuration concerned. The DFTs were not therefore normally distributed making parametric testing inappropriate. For this reason, the more rigorous non-parametric Wilcoxon signed rank test was used to assess significance. A two-sided P-value of 0.05 or less was considered significant.
| Results |
|---|
|
|
|---|
Placement of a bi-filament electrode was possible in 11 of 12 animals. In one animal, the MCV could not be selectively catheterized. Screening time for the procedure was 13.4±6.4 min. The DFTs and impedances of the configurations (Table 1 and Fig. 4) are shown.
|
|
DFT was 24% less in monofilament+passive than in mono alone to AH, P=0.008. The electrical properties of the microfilaments were atypical: at high energy outputs, their impedance increased substantially, preventing efficacious defibrillation in some animals for configurations involving microfilaments as sole cathode (Fig. 5).
|
Autopsy was performed at the end of the procedure. No macroscopic damage was seen in myocardium or pericardium.
| Discussion |
|---|
|
|
|---|
The anatomical site of electrodes alters the shocking vector and affects the DFT either by allowing inclusion of a critical mass of myocardium,17
Defibrillation configurations involving epicardial patch electrodes were superseded by transvenous systems because of the lower complication rate of the latter.21
This came at the cost of an increased DFT.20
An electrode placed transvenously but having the low DFT of the epicardial patch electrodes would combine the advantages of epicardial patch electrodes and transvenous systems.
Possible reasons for the lower DFT seen with epicardial patches are anatomical site (infero-septal), epicardial location, large electrode surface area, and broad area of myocardium in contact with the distal electrode.22
Defibrillation electrode placement in the MCV may decrease DFT13
because of its infero-septal epicardial location. Placement of multiple defibrillation filaments is feasible14
and gives further theoretical advantages by increasing the surface area of the electrode and broadening the amount of myocardium in contact with the distal electrode. Placement of multiple filaments increases complexity of implantation partly by necessitating multiple proximal connections: the passive electrode effect might be used to reduce this complexity.
After observations that bystander epicardial patches increase DFT through a passive electrode effect, but no equivalent influence on DFT is exerted by transvenous shocking coils or pacing leads, the phenomenon received no further research attention. We have shown that the passive electrode effect exerted by a bystander MCV coil in the radicle adjacent to an identical active coil decreases DFT by 24%.
The ability of a bystander electrode to exert a passive electrode effect is dependent on the proportion of current that is drawn through the alternative route. This is a function of the impedance of the intended configuration when compared with the impedance of the parallel circuit created by the bystander electrode and intervening tissue. Epicardial patches have lower impedance than transvenous coils, allowing current shunting and a passive electrode effect: two transvenous coils have similar impedance, minimizing current shunting. Furthermore, an electrical passive electrode effect may only influence DFT if it significantly alters shocking vector; in the case of bystander epicardial systems, current is drawn in the opposite direction from the anode: predictably DFT is increased. In transvenous systems, the intended and bystander coils occupy similar anatomical sites: the vector is not greatly altered even if a passive electrode effect exists on electrical properties.
The impedance characteristics of the microfilament electrodes used, Fig. 5, were unusual in that they were high and rose further with increasing current. This creates a situation where the actively connected electrode has a higher impedance than the bystander, favouring current shunting and a passive electrode effect. The placement of the two filaments, in the branches of the MCV adjacent to the septum, caused any current shunted to be to a site that is likely to improve current distribution (a virtual composite electrode, the connected and passive electrode, with a greater surface area and broader area of myocardium involved).
Placement of multiple filaments in the MCV radicles allows close mimicry of epicardial patch electrode: the anatomical equivalence of MCV with multiple filaments simulating the structure and current distribution. Using the passive electrode effect to avoid multiple proximal connections reduces the complexity of such a system.
For the passive electrode effect to be a clinically useful phenomenon, lead configurations taking advantage of it must be safe, stable, and transvenously deployed. It would be required either to reduce DFT by over 50% or significantly reduce the variability of DFT.
We have shown that the branching structure of coronary sinus tributaries, already widely used in pacing and validated in acute defibrillation studies,16
is a suitable site to explore the uses of the passive electrode effect in transvenous defibrillation. The electrical properties of the microfilaments made them unsuitable as sole anode as their impedance increased preventing effective defibrillation in certain individuals.
Limitations of the study
Two bystander electrodes present in this study were not examined for a passive electrode effect; the RV and SVC coils were left in place for configurations that did not involve them. They are less likely to exert a passive electrode effect given their distance from the active circuit and were constant in the MCV mono and mono+passive configurations.
The magnitude of the DFT reduction would not be clinically useful, and the configuration used was demonstrated not to be reliable for the reasons discussed.
It is not certain that findings from any animal study can be replicated in humans: discordance in findings between prior porcine and human MCV defibrillation studies13
,15
,16
(possibly explained by the anatomical difference in the mediastinal orientation between the species) has been seen.
In this case, however, the model, anatomical site, and magnitude of effect are secondary to the proof of concept: a passive electrode effect may reduce DFT.
| Conclusion |
|---|
|
|
|---|
In a porcine model, with transvenously placed coronary venous leads, a passive electrode effect decreases DFT and impedance when shocking to an AH.
| Acknowledgement |
|---|
|
|
|---|
J.R.P. receives research funding from Ela Medical SA, Montrouge, France.
| References |
|---|
|
|
|---|
[1] Callihan RL, Idriss SF, Dahl RW, Wolf PD, Smith WM, Ideker RE. Comparison of defibrillation probability of success curves for an endocardial lead configuration with and without an inactive epicardial patch. J Am Coll Cardiol 1995; 25: 13739.[Abstract]
[2] Fotuhi PC, Ideker RE, Idriss SF, Callihan RL, Walker RG, Alt EU. Influence of epicardial patches on defibrillation threshold with nonthoracotomy lead configurations. Circulation 1995; 92: 30828.
[3] Fotuhi PC, Kenknight BH, Melnick SB, Smith WM, Baumann GF, Ideker RE. Effect of a passive endocardial electrode on defibrillation efficacy of a nonthoracotomy lead system. J Am Coll Cardiol 1997; 29: 82530.[Abstract]
[4] Moss AJ, Hall WJ, Cannom DS, et al. Improved survival with an implanted defibrillator in patients with coronary disease at high risk for ventricular arrhythmia. N Engl J Med 1996; 335: 193340.
[5] Moss AJ, Zareba W, Hall WJ, Klein H, Wilber DJ, Cannom DS, et al. Prophylactic implantation of a defibrillator in patients with myocardial infarction and reduced ejection fraction. N Engl J Med 2002; 346: 87783.
[6] Buxton AE, Lee KL, Fisher JD, Josephson ME, Prystowsky EN, Hafley G. A randomized study of the prevention of sudden death in patients with coronary artery disease. Multicenter Unsustained Tachycardia Trial Investigators. N Engl J Med 1999; 341: 188290.
[7] The Antiarrhythmics versus Implantable Defibrillators (AVID) Investigators. A comparison of antiarrhythmic-drug therapy with implantable defibrillators in patients resuscitated from near-fatal ventricular arrhythmias. N Engl J Med 1997; 337: 157684.
[8] Kuck KH, Cappato R, Siebels J, Ruppel R. Randomized comparison of antiarrhythmic drug therapy with implantable defibrillators in patients resuscitated from cardiac arrest: the Cardiac Arrest Study Hamburg (CASH). Circulation 2000; 102: 74854.
[9] Connolly SJ, Gent M, Roberts RS, Dorian P, Roy D, Sheldon RS, et al. Canadian implantable defibrillator study (CIDS): a randomized trial of the implantable cardioverter defibrillator against amiodarone. Circulation 2000; 101: 1297302.
[10] Singer I, Goldsmith J, Maldonado C. Transseptal defibrillation is superior for transvenous defibrillation. Pacing Clin Electrophysiol 1995; 18: 22932.[CrossRef][Medline]
[11] Roberts PR, Allen S, Smith DC, Urban JF, Euler DE, Dahl RW, et al. A systematic evaluation of conventional and novel transvenous pathways for defibrillation. J Interv Card Electrophysiol 1999; 3: 2318.[Medline]
[12] Paisey JR, Yue AM, Bessoule F, Allen S, Roberts PR, Morgan JM. Examination of a middle cardiac vein defibrillation coil as stand-alone anode, auxiliary anode, and bystander electrode in a transvenous defibrillation circuit. Pacing Clin Electrophysiol 2004; 27: 108993.[Medline]
[13] Roberts PR, Urban JF, Euler DE, Kallok MJ, Morgan JM. The middle cardiac veina novel pathway to reduce the defibrillation threshold. J Interv Card Electrophysiol 1999; 3: 5560.[Medline]
[14] Roberts PR, Allen S, Betts T, Urban JF, Euler DE, Crick S, et al. A multifilamented electrode in the middle cardiac vein reduces energy requirements for defibrillation in the pig. Heart 2000; 84: 42530.
[15] Roberts PR, Urban JF, Betts T, Allen S, Dietz A, Euler DE, et al. Reduction in defibrillation threshold using an auxiliary shock delivered in the middle cardiac vein. Pacing Clin Electrophysiol 2000; 23: 127882.[CrossRef][Medline]
[16] Roberts PR, Paisey JR, Betts TR, Allen S, Whitman T, Bonner M, et al. Comparison of coronary venous defibrillation with conventional transvenous internal defibrillation in man. J Interv Card Electrophysiol 2003; 8: 6570.[Medline]
[17] Zipes DP, Fischer J, King RM. Termination of ventricular fibrillation in dogs by depolarizing a critical amount of myocardium. Am J Cardiol 1975; 36: 3744.[CrossRef][ISI][Medline]
[18] Chen PS, Shibata N, Dixon EG. Activation during ventricular defibrillation in open-chest dogs. Evidence of complete cessation and regeneration of ventricular fibrillation after unsuccessful shocks. J Clin Invest 1986; 77: 81023.[ISI][Medline]
[19] Chen PS, Swerdlow CD, Hwang C. Current concepts of ventricular defibrillation. J Cardiovasc Electrophysiol 1998; 9: 55362.[ISI][Medline]
[20] Kallok MJ. Pathways for defibrillation current. In Kroll MW and Lehmann MH (Eds.). Implantable Cardioverter Defibrillator Therapy: The EngineeringClinical Interface 1993; Kluwer Academic Publishers pp. 1059.
[21] Yee R, Klein GJ, Leitch JW, Guiraudon GM, Guiraudon CM, Jones DL, et al. A permanent transvenous lead system for an implantable pacemaker cardioverter-defibrillator. Nonthoracotomy approach to implantation. Circulation 1992; 85: 196204.
[22] Kallok MJ, Bourland JD, Tacker WA, Jones DL, Klein GJ, Wessale JL. Optimization of epicardial electrode size and implant site for reduced sequential pulse defibrillation thresholds. Med Instrum 1986; 20: 369.[Medline]
![]()
CiteULike
Connotea
Del.icio.us What's this?
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||




