Improve Defibrillation Efficacy Research Articles

A His bundle pacing protocol for suppressing ventricular arrhythmia maintenance and improving defibrillation efficacy

Background:The excitable gap (EG), defined as the excitable tissue between two subsequent wavefronts of depolarization, is critical for maintaining reentry that underlies deadly ventricular arrhythmias. EG in the His-Purkinje Network (HPN) plays an important role in the maintenance of electrical wave reentry that underlies these arrhythmias. Objective:To determine if rapid His bundle pacing (HBP) during reentry reduces the amount of EG in the HPN and ventricular myocardium to suppress reentry maintenance and/or improve defibrillation efficacy. Methods:In a virtual human biventricular model, reentry was initiated with rapid line pacing followed by HBP delivered for 3, 6, or 9 s at pacing cycle lengths (PCLs) ranging from 10 to 300 ms (n=30). EG was calculated independently for the HPN and myocardium over each PCL. Defibrillation efficacy was assessed for each PCL by stimulating myocardial surface EG with delays ranging from 0.25 to 9 s (increments of 0.25 s, n=36) after the start of HBP. Defibrillation was successful if reentry terminated within 1 s after EG stimulation. This defibrillation protocol was repeated without HBP. To test the approach under different pathological conditions, all protocols were repeated in the model with right (RBBB) or left (LBBB) bundle branch block. Results:Compared to without pacing, HBP for >3 seconds reduced average EG in the HPN and myocardium across a broad range of PCLs for the default, RBBB, and LBBB models. HBP >6 seconds terminated reentrant arrhythmia by converting HPN activation to a sinus rhythm behavior in the default (6/30 PCLs) and RBBB (7/30 PCLs) models. Myocardial EG stimulation during HBP increased the number of successful defibrillation attempts by 3%–19% for 30/30 PCLs in the default model, 3%–6% for 14/30 PCLs in the RBBB model, and 3%–11% for 27/30 PCLs in the LBBB model. Conclusion:HBP can reduce the amount of excitable gap and suppress reentry maintenance in the HPN and myocardium. HBP can also improve the efficacy of low-energy defibrillation approaches targeting excitable myocardium. HBP during reentrant arrhythmias is a promising anti-arrhythmic and defibrillation strategy.

Right ventricular insertion promotes reinitiation of ventricular fibrillation in defibrillation failure

Shocks near defibrillation threshold (nDFT) strength commonly extinguish all ventricular fibrillation (VF) wavefronts, but a train of rapid, well-organized postshock activations (PAs) typically appears before sinus rhythm ensues. If one of the PA waves undergoes partial propagation block (wavebreak), reentry may be induced, causing VF to reinitiate and the shock to fail. The purpose of this study was to determine whether wavebreak leading to VF reinititation following nDFT shocks occurs preferentially at the right ventricular insertion (RVI), which previous studies have identified as a key site for wavebreak. We used panoramic optical mapping to image the ventricular epicardium of 6 isolated swine hearts during nDFT defibrillation episodes. After each experiment, the hearts were fixed and their geometry scanned with magnetic resonance imaging (MRI). The MRI and mapping datasets were spatially coregistered. For failed shocks, we identified the site of the first wavebreak of a PA wave during VF reinitiation. We recorded 59 nDFT failures. In 31 of these, the first wavebreak event occurred within 1 cm of the RVI centerline, most commonly on the anterior side of the right ventricular insertion (aRVI) (23/31). The aRVI region occupies 16.8% ± 2.5% of the epicardial surface and would be expected to account for only 10 wavebreaks if they were uniformly distributed. By χ2 analysis, aRVI wavebreaks were significantly overrepresented. The anterior RVI is a key site in promoting nDFT failure. Targeting this site to prevent wavebreak could convert defibrillation failure to success and improve defibrillation efficacy.

A framework of current based defibrillation improves defibrillation efficacy of biphasic truncated exponential waveform in rabbits

Defibrillation is accomplished by the passage of sufficient current through the heart to terminate ventricular fibrillation (VF). Although current-based defibrillation has been shown to be superior to energy-based defibrillation with monophasic waveforms, defibrillators with biphasic waveforms still use energy as a therapeutic dosage. In the present study, we propose a novel framework of current-based, biphasic defibrillation grounded in transthoracic impedance (TTI) measurements: adjusting the charging voltage to deliver the desired current based on the energy setting and measured pre-shock TTI; and adjusting the pulse duration to deliver the desired energy based on the output current and intra-shock TTI. The defibrillation efficacy of current-based defibrillation was compared with that of energy-based defibrillation in a simulated high impedance rabbit model of VF. Cardiac arrest was induced by pacing the right ventricle for 60 s in 24 New Zealand rabbits (10 males). A defibrillatory shock was applied with one of the two defibrillators after 90 s of VF. The defibrillation thresholds (DFTs) at different pathway impedances were determined utilizing a 5-step up-and-down protocol. The procedure was repeated after an interval of 5 min. A total of 30 fibrillation events and defibrillation attempts were investigated for each animal. The pulse duration was significantly shorter, and the waveform tilt was much lower for the current-based defibrillator. Compared with energy-based defibrillation, the energy, peak voltage, and peak current DFT were markedly lower when the pathway impedance was > 120 Ω, but there were no differences in DFT values when the pathway impedance was between 80 and 120 Ω for current-based defibrillation. Additionally, peak voltage and the peak current DFT were significantly lower for current-based defibrillation when the pathway impedance was < 80 Ω. In sum, a framework of adjusting the charging voltage and shock duration to deliver constant energy for low impedance and constant current for high impedance via pre-shock and intra-shock impedance measurements, greatly improved the defibrillation efficacy of high impedance by lowering the energy DFT.

Real-Time Ventricular Fibrillation Amplitude-Spectral Area Analysis to Guide Timing of Shock Delivery Improves Defibrillation Efficacy During Cardiopulmonary Resuscitation in Swine.

BackgroundThe ventricular fibrillation amplitude spectral area (AMSA) predicts whether an electrical shock could terminate ventricular fibrillation and prompt return of spontaneous circulation. We hypothesized that AMSA can guide more precise timing for effective shock delivery during cardiopulmonary resuscitation.Methods and ResultsThree shock delivery protocols were compared in 12 pigs each after electrically induced ventricular fibrillation, with the duration of untreated ventricular fibrillation evenly stratified into 6, 9, and 12 minutes: AMSA‐Driven (AD), guided by an AMSA algorithm; Guidelines‐Driven (GD), according to cardiopulmonary resuscitation guidelines; and Guidelines‐Driven/AMSA‐Enabled (GDAE), as per GD but allowing earlier shocks upon exceeding an AMSA threshold. Shocks delivered using the AD, GD, and GDAE protocols were 21, 40, and 62, with GDAE delivering only 2 AMSA‐enabled shocks. The corresponding 240‐minute survival was 8/12, 6/12, and 2/12 (log‐rank test, P=0.035) with AD exceeding GDAE (P=0.026). The time to first shock (seconds) was (median [Q1–Q3]) 272 (161–356), 124 (124–125), and 125 (124–125) (P<0.001) with AD exceeding GD and GDAE (P<0.05); the average coronary perfusion pressure before first shock (mm Hg) was 16 (9–30), 10 (6–12), and 3 (−1 to 9) (P=0.002) with AD exceeding GDAE (P<0.05); and AMSA preceding the first shock (mV·Hz, mean±SD) was 13.3±2.2, 9.0±1.6, and 8.6±2.0 (P<0.001) with AD exceeding GD and GDAE (P<0.001). The AD protocol delivered fewer unsuccessful shocks (ie, less shock burden) yielding less postresuscitation myocardial dysfunction and higher 240‐minute survival.ConclusionsThe AD protocol improved the time precision for shock delivery, resulting in less shock burden and less postresuscitation myocardial dysfunction, potentially improving survival compared with time‐fixed, guidelines‐driven, shock delivery protocols.

Low level tragus nerve stimulation is a non-invasive approach for anti-atrial fibrillation via preventing the loss of connexins

Atrial fibrillation (AF) is the most common cardiac arrhythmia, but the mechanism of AF maintenance remains unclear. It has been found that gap junctional remodeling (connexin expression is downregulated and distributed) is closely associated with AF maintenance [ [1] Van der Velden H.M. Ausma J. Rook M.B. Hellemons A.J. van Veen T.A. Allessie M.A. Jongsma H.J. Gap junctional remodeling in relation to stabilization of atrial fibrillation in the goat. Cardiovasc. Res. 2000; 46: 476-486 Crossref PubMed Scopus (214) Google Scholar ]. Autonomic nervous system stimulation can exert anti-arrhythmia effects [ 2 Thunsiri K. Shinlapawittayatorn K. Chinda K. Palee S. Surinkaew S. Chattipakorn S.C. KenKnight B.H. Chattipakorn N. Application of vagus nerve stimulation from the onset of ventricular fibrillation to post-shock period improves defibrillation efficacy. Int. J. Cardiol. 2014; 176: 1030-1032 Abstract Full Text Full Text PDF PubMed Scopus (6) Google Scholar , 3 He B. Lu Z. He W. Huang B. Jiang H. Similar effects of vagus nerve stimulation and atrial ganglionated plexi stimulation on ventricular effective refractory period and action potential duration in canine. Int. J. Cardiol. 2013; 168: 5116-5118 Abstract Full Text Full Text PDF PubMed Scopus (4) Google Scholar ]. Recently, we reported that cervical low level vagal nerve stimulation (LL-VNS) could suppress AF induced high-frequency stimulation [ [4] Yu L. Scherlag B.J. Li S. Sheng X. Lu Z. Nakagawa H. Zhang Y. Jackman W.M. Lazzara R. Jiang H. Po S.S. Low-level vagosympathetic nerve stimulation inhibits atrial fibrillation inducibility: direct evidence by neural recordings from intrinsic cardiac ganglia. J. Cardiovasc. Electrophysiol. 2011; 22: 455-463 Crossref PubMed Scopus (104) Google Scholar ] and then we developed a non-invasive approach, low level tragus nerve stimulation (LL-TS), and found that it had the same effect on suppressing AF [ [5] Yu L. Scherlag B.J. Li S. Fan Y. Dyer J. Male S. Varma V. Sha Y. Stavrakis S. Po S.S. Low-level transcutaneous electrical stimulation of the auricular branch of the vagus nerve: a noninvasive approach to treat the initial phase of atrial fibrillation. Heart Rhythm. 2013; 10: 428-435 Abstract Full Text Full Text PDF PubMed Scopus (111) Google Scholar ]. However, whether LL-TS could regulate Cx40 and Cx43 to suppress AF remains unknown. We hypothesized that LL-TS exerted anti-atrial fibrillatory effect via the downregulation of atrial Cx40 and Cx43.

Application of vagus nerve stimulation from the onset of ventricular fibrillation to post-shock period improves defibrillation efficacy

Application of vagus nerve stimulation from the onset of ventricular fibrillation to post-shock period improves defibrillation efficacy

Phosphodiesterase-3 inhibitor (cilostazol) attenuates oxidative stress-induced mitochondrial dysfunction in the heart.

BackgroundCilostazol is a type 3 phosphodiesterase inhibitor which has been previously demonstrated to prevent the occurrence of tachyarrhythmia and improve defibrillation efficacy. However, the mechanism for this beneficial effect is still unclear. Since cardiac mitochondria have been shown to play a crucial role in fatal cardiac arrhythmias and that oxidative stress is one of the main contributors to arrhythmia generation, we tested the effects of cilostazol on cardiac mitochondria under severe oxidative stress.MethodsMitochondria were isolated from rat hearts and treated with H2O2 to induce oxidative stress. Cilostazol, at various concentrations, was used to study its protective effects. Pharmacological interventions, including a mitochondrial permeability transition pore (mPTP) blocker, cyclosporine A (CsA), and an inner membrane anion channel (IMAC) blocker, 4′-chlorodiazepam (CDP), were used to investigate the mechanistic role of cilostazol on cardiac mitochondria. Cardiac mitochondrial reactive oxygen species (ROS) production, mitochondrial membrane potential change and mitochondrial swelling were determined as indicators of cardiac mitochondrial function.ResultsCilostazol preserved cardiac mitochondrial function when exposed to oxidative stress by preventing mitochondrial depolarization, mitochondrial swelling, and decreasing ROS production.ConclusionsOur findings suggest that cardioprotective effects of cilostazol reported previously could be due to its prevention of cardiac mitochondrial dysfunction caused by severe oxidative stress.

Low‐Tilt Monophasic and Biphasic Waveforms Compared with Standard Biphasic Waveforms in the Transvenous Defibrillation of Ventricular Fibrillation

Commercially available implantable defibrillators utilize a high-tilt waveform. Studies in atrial fibrillation and transthoracic defibrillation of ventricular fibrillation (VF) have shown improved defibrillation efficacy using low-tilt (LT) waveforms. We investigated the feasibility, efficacy, and safety of a LT waveform in the transvenous defibrillation of VF and hypothesized that it would be more efficacious than standard tilted biphasic (STB) waveforms. The investigation was performed in four phases in a porcine model: an efficacy study of LT monophasic waveforms (n= 9), an efficacy study of LT biphasic waveforms (n= 9), a comparison study between the most successful LT waveforms and clinically available STB waveforms (n= 15), and a safety study (n= 9). A total of 1,056 shocks were delivered (phase 1: 288, phase 2: 288, phase 3: 480). The LT biphasic 8/4-ms waveform was significantly more likely to successfully defibrillate than the LT monophasic and STB waveforms with an odds ratio of 122.3 (95% confidence interval: 32.5, 460.2, P< 0.001). The calculated defibrillation threshold (E50) for the LT 8/4-ms waveform was 12.7 J compared to 43.5 J and 45.5 J for STB waveforms 6/6 ms and 8/4 ms, respectively, and 47.7 J for LT 12-ms waveform. The LT 8/4-ms waveform had no lasting detrimental effect on cardiac function, and any transient hemodynamical or biochemical changes observed were comparable to those observed with STB waveforms. LT waveforms are effective and appear safe in transvenous defibrillation in a porcine model of VF. The LT biphasic 8/4-ms waveform is more efficacious than conventional waveforms.

Abstract 302: Transthoracic Impedance Is Poorly Predicted by Patient Characteristics but Significantly Reduced by Placement of Defibrillator Pads in the Anteroposterior Position

Introduction The American Heart Association Resuscitation Guidelines advocate four pad positions to achieve defibrillation success following cardiac arrest. Transthoracic impedance (TTI) reflects the electrode-skin interface and patient impedance and affects current amplitude, energy delivered and defibrillation efficacy. Modern defibrillators utilise an impedance compensated waveform to account for changes in TTI to improve defibrillation success. However the effect of electrode pad position and patient characteristics on TTI remains unclear. Objective To evaluate the effect of patient characteristics and pad position on Transthoracic impedance (TTI). Methods Patients undergoing diagnostic cardiac catheterisation were recruited for the study following regional ethical approval. Standard self-adhesive defibrillator electrodes were applied to patients in both the anterolateral and anteroposterior positions and connected to Heartsine Samaritan defibrillators. TTI was measured by applying a 30kHz sinusoidal signal through the chest. The voltage was then converted to digital samples using an 8-bit microprocessor. The digital samples were then stored on the secure digital card to be retrieved using custom-made download data recovery software. TTI was measured at 10 second intervals in both positions for the duration of the clinical procedure. Results 32 patients (mean age 63), (66% male), were recruited. TTI measured at 10 seconds was significantly higher in the anterolateral position (88.3ohms vs 68.5ohms, p &lt;0.001). Mean TTI reduction over 5 minutes was 2.4% in the anterolateral position and 1.9% in anteroposterior position. There was no significant correlation between TTI measured from either pad position and age, height, weight, body surface area and Haemoglobin (r&lt;0.4 for all parameters). Conclusion TTI is significantly reduced by placement of defibrillator pads in the anteroposterior position. Furthermore patient characteristics are poorly predictive of TTI from either pad position. Patients suffering failed defibrillation attempts from pads positioned in the anterolateral position may benefit from prompt relocation to the anteroposterior position to improve defibrillation efficacy.

Implantable Cardioverter Defibrillator

Implantable Cardioverter Defibrillator

Cilostazol attenuates ventricular arrhythmia induction and improves defibrillation efficacy in swine

Previous reports demonstrated that cilostazol, a phosphodiesterase 3 inhibitor, affected cellular electrophysiology and reduced episodes of ventricular fibrillation (VF) in patients with Brugada syndrome. However, its effects on VF induction and defibrillation efficacy have never been investigated. We tested the hypothesis that cilostazol increases the VF threshold (VFT) and decreases the upper limit of vulnerability (ULV) and the defibrillation threshold (DFT). A total of 48 pigs were randomly assigned to defibrillation and VF induction studies. The diastolic pacing threshold (DPT), VFT, ULV, DFT, and effective refractory period were determined before and after the infusion of cilostazol at 6 mg/kg, 3 mg/kg, or vehicle. The DPT was significantly increased after administration of 3 and 6 mg/kg cilostazol. The ULV and DFT were significantly decreased after administration of 6 mg/kg cilostazol only. The ULV in the 6 mg/kg group had 12% lower peak voltage and 25% lower total energy, and the DFT had 13% lower peak voltage and 25% lower total energy. The VFT was not altered in any experimental group. This study shows that cilostazol administration significantly increased the DPT, which was associated with significantly reduced DFT and ULV.

Defibrillation efficacy of a subcutaneous array lead: A case report

We report a case of Brugada syndrome with a high defibrillation threshold (DFT) in whom a subcutaneous array lead was used to lower the DFT in combination with a transvenous right ventricular defibrillation lead. The patient had previously received pacemaker implantation due to sick sinus syndrome. An implantable cardioverter defibrillator (ICD) with a transvenous right ventricular defibrillation lead alone required a high DFT. A subcutaneous array lead improved defibrillation efficacy in combination with a right ventricular lead. These data suggest that a subcutaneous array lead facilitates implantation of an effective ICD lead system in patients requiring a high DFT.

Effects of garlic on the induction of ventricular fibrillation

Objective Previous studies have shown that oral and intravenous administrations of garlic provide a significant antiarrhythmic effect and improve defibrillation efficacy. We tested the hypothesis that garlic could decrease the inducibility of ventricular arrhythmia. Methods Twenty-one pigs (25–30 kg) were divided into three groups. In each group, the ventricular fibrillation threshold (VFT) and the upper limit of vulnerability (ULV) were determined. After the control VFT and ULV values were obtained, solutions containing 20 mg/kg (group 1, n = 7) and 40 mg/kg (group 2, n = 7) of garlic (1.3% allicin) were administered intravenously. The VFT and ULV were determined again at the end of garlic infusion. In group 3 ( n = 7), 100 mL of normal saline was administered instead of garlic. Results The VFT values in groups 1 and 2 were not different from the control VFT. The ULV in group 1 was not different from the control ULV. However, the ULV in group 2 (328 ± 58 V, 8 ± 3 J) was significantly lower than the control ULV (415 ± 24 V, 13 ± 2 J), thus accounting for the reduction of ∼21% by peak voltage and ∼38% by energy. The effective refractory period and diastolic pacing threshold were not altered after garlic infusion. Saline did not alter VFT or ULV. Conclusion Garlic cannot alter the VFT, but it significantly decreases the ULV in a dose-dependent pattern, indicating that it can reduce the range of the stimulation strength between the VFT and ULV (vulnerability window) during the vulnerable period of a cardiac cycle.

Post‐Shock Synchronized Pacing in Isolated Rabbit Left Ventricle: Evaluation of a Novel Defibrillation Strategy

A failed near-threshold defibrillation shock is followed by an isoelectric window (IEW) and rapid repetitive responses that reinitiate ventricular fibrillation (VF). We hypothesized that properly timed (synchronized) postshock pacing stimuli (SyncP) may capture the recovered tissues during the repetitive responses and prevent postshock reinitiation of VF, resulting in improved defibrillation efficacy. We explored the effect of postshock SyncP on defibrillation efficacy in isolated rabbit hearts (n = 12). Optical recording-guided real-time detection and electrical stimulation (5 mA) of recovered tissues in anterior/posterior left ventricle (LV) were performed following IEW. The IEW duration was found to be 69 +/- 13 ms. With the same shock strength, successful and failed defibrillation episodes were associated with 50% and 15% of the myocardium, respectively, captured by the SyncP (P < 0.001). Electrical stimulation from the posterior LV resulted in 75% of episodes capturing myocardium, as compared with anterior LV stimulation (55%; P < 0.01) and higher successful defibrillation rate (14%, posterior vs. 3%, anterior LV). The overall success in terminating VF by postshock SyncP was approximately 10%. The causes for failed myocardium capture by postshock SyncP included lack of IEW after low-strength shock (42.9%), incorrect locations of reference site (25.7%) and pacing electrodes (17.9%), and others, such as wave breakthroughs (13.5%). Postshock SyncP was feasible and the larger the myocardium captured area, the more likely was the successful defibrillation. Postshock SyncP delivered to the posterior LV was more effective than anterior LV to terminate VF.

Fish oil does not improve defibrillation efficacy

Sudden cardiac death, caused mainly by ventricular fibrillation (VF), is the major cause of death in many nations around the world [1]. Despite the use of an implantable cardioverter-defibrillator (ICD), the therapeutic goal is still far from ideal. Investigators have been investigating the means that could lower the shock strength required to successfully defibrillate, thus minimizing cellular damage in VF patients [2]. In the past decades, fish oil has been shown to be antiarrhythmic and decreases cardiovascular mortality [3,4].

Improved defibrillation efficacy with an ascending ramp waveform in humans

The purpose of this study was to compare an ascending ramp waveform (RAMP) with a standard, clinically available biphasic truncated exponential waveform (BTE) for defibrillation in humans. In animal studies, RAMP had a lower defibrillation threshold (DFT) than BTE. We studied 63 patients at implantable cardioverter-defibrillator placement using a dual-coil lead and left pectoral active can. The subjects were divided into two groups, one with a 12-ms ascending first phase and one with a 7-ms ascending first phase. Phase 2 of RAMP for both groups was a truncated exponential decay with 65% tilt and reversed polarity. The BTE had a 50% tilt in each phase. DFT and upper limit of vulnerability (ULV) were measured for both waveforms using a binary search protocol. The patient population was 77% male, with a mean age of 63 +/- 10 years and ejection fraction of 33 +/- 13%. Delivered energy at DFT was lower with the 7-ms RAMP vs BTE (5.4 +/- 2.6 J vs 6.5 +/- 3.4 J; P < .01) but unchanged with the 12-ms RAMP (7.4 +/- 4.5 J vs 7.1 +/- 4.9 J). Maximal voltage at DFT was significantly lower with either RAMP compared to BTE (P < .01). There was a strong correlation between ULV and DFT for both RAMP and BTE (P < .01). The 7-ms ascending ramp waveform significantly reduced delivered energy (18%) and voltage (24%) at DFT, whereas the 12-ms RAMP reduced only DFT voltage. This is the first report of a waveform that is superior to a BTE for defibrillation in humans. ULV correlates with DFT for RAMP, supporting the use of ULV testing for implantation of devices.

Improved internal defibrillation success with shocks timed to the morphology electrogram.

A previous retrospective study by our group suggested that shocks timed to the upslope of the shocking lead electrogram improved defibrillation efficacy. The goal of this study was to prospectively determine whether defibrillation threshold could be reduced by use of an algorithm that timed shocks to the upslope of coarse ventricular fibrillation (test treatment) compared with shocks delivered asynchronously after 10 seconds of fibrillation (control treatment). Ten pigs were instrumented with a 3-lead system for internal defibrillation. Initial estimates of the energy required to achieve defibrillation E50 for both treatments were made by an up/down method. Subsequently, additional shocks at V50+/-10% and V50-20% were given for each treatment to obtain data points at higher and lower intensities. Probability-of-success curves were estimated for both treatments by the best-fit method. Energies required were significantly lower for the timed shocks than for the asynchronous shocks (P<0.00 1). E80 was reduced 15.5%, from 27.1+/-2.5 to 22.9+/-1.8 J (P<0.002). The width of the probability-of-success curve (E80-E20) for the test treatment was also significantly narrower than that for the control treatment (7.1+/-0.9 versus 10.8+/-1.7, P<0.01). Normalized curve width (E80-E20)/E50 was decreased from 51+/-5% of E50 for control shocks to 37+/-4% of E50 for synchronous shocks (P<0.02). In this model, defibrillation threshold is lower and more deterministic when shocks are timed to the upslope of the shocking lead electrogram. If a similar reduction is observed in humans, shock timing may lower defibrillation threshold and simplify programming of shock intensity.

Additional lead improves defibrillation efficacy with an abdominal 'hot can' electrode system.

Although the left prepectoral site is preferred for "hot can" placement, this site is unavailable in some patients. We evaluated the influence of electrode location on defibrillation thresholds with alternative hot can and transvenous lead configurations. Three interrelated studies were performed. In group 1, the importance of hot can location was investigated by pairing a right ventricular lead to five different hot can placement sites in seven pigs. The defibrillation energies for right pectoral, left pectoral, left subaxillary, and right and left abdominal hot can sites were 20.3+/-2.7,* 15.9+/-3.8, 14.9+/-2.5, 32.0+/-3.4,* and 30.0+/-3.4 J,* respectively (*P<.005 versus left pectoral and left subaxillary sites). In group 2, the value of a three-electrode configuration with an abdominal hot can placement was investigated by adding a subclavian vein lead to the pectoral or abdominal hot can configurations in seven pigs. The defibrillation energies for left pectoral and abdominal sites were 18.6+/-4.2 and 29.0+/-5.8 J (P=.0001), respectively. The addition of a right or left subclavian vein lead with an abdominal hot can reduced the threshold to 19.3+/-4.2* or 18.8+/-3.2,* respectively (*P=.0001 versus abdominal site). In group 3, the contribution of the abdominal hot can electrode to the three-electrode configuration was tested by a comparison with two purely transvenous two-electrode configurations in six pigs. The defibrillation energy (19.9+/-3.2 J) for the abdominal hot can with a subclavian vein lead was lower than the transvenous lead configurations with a subclavian vein (29.0+/-2.5 J, P=.0001) or a superior vena cava lead (30.7+/-3.7 J, P=.0001). The right ventricular lead was the sole cathode during the first phase of the biphasic shock in all experiments. Defibrillation energy depends on the hot can placement site. The addition of a subclavian vein lead with an abdominal hot can improves defibrillation efficacy to the level of the pectoral placement and is better than a purely transvenous lead configuration.

Iridium oxide-coated defibrillation electrode: reduced shock polarization and improved defibrillation efficacy.

Transvenous implantable cardioverter-defibrillator (ICD) leads are designed to deliver electric shocks to the heart for termination of ventricular dysrhythmias. However, the efficiency of different lead materials has not been well studied. This study compares an ICD lead coated with iridium oxide (IROX), a material that reduces shock-induced polarization, with an otherwise identical, uncoated lead. The defibrillation threshold (DFT) was determined in 13 swine with both IROX-coated and uncoated ICD leads paired with an uncoated "can" electrode. The leads were exchanged through a Teflon sheath to reproduce the intracardiac position. The delivered energy DFT of the IROX-coated lead was 15.9+/-5.4 J and was significantly lower than the delivered energy DFT of the uncoated lead (19.1+/-5.1 J; P<.006). The initial lead impedance was equivalent in both leads (IROX, 41.7+/-5.8 omega; uncoated, 41.3+/-4.7 omega; P=NS) at DFT. However, the impedance rose by 7.3+/-2.0 omega during the first phase and by 3.7+/-2 omega during the second phase with the uncoated lead, whereas the corresponding impedance change was 1.0+/-0.3 omega during phase 1 and 1.6+/-0.5 omega during phase 2 (P<.01 each phase) when the IROX-coated lead was used. This study shows that an IROX coating of this lead system significantly lowers the DFT energy in the swine model. The blunting of the impedance rise by the IROX coating that is seen is consistent with a reduction in electrode polarization.

Can a Class III Antiarrhythmic Drug Improve Electrical Defibrillation Efficacy During Ventricular Fibrillation?

Objectives. We tested whether a new class III drug (MS-551) administered during ventricular fibrillation (VF) could decrease the defibrillation threshold (DFT) in anesthetized canine hearts.Background. Pretreatment with class III antiarrhythmic agents is known to enhance electrical defibrillation efficacy.Methods. In a preliminary study (n = 10), we ascertained the validity of DFT determination by a sequence of incremental defibrillation shocks in a single fibrillation/defibrillation episode. We then compared the DFTs after 130 s of VF with and without administration of MS-551 (2 mg/kg body weight) at 10 s after the onset of VF in 12 open chest dogs and 8 closed chest dogs.Results. MS-551 decreased the DFT in both experimental models (open chest [mean ±SD]: from 416 ± 106 to 318 ± 92 V, p < 0.05; closed chest: from 714 ± 75 to 615 ± 112 V, p < 0.05). The change (Δ) in DFT in each heart was inversely correlated with the drug-induced prolongation of VF cycle length before the defibrillation attempt (ΔDFT vs. ΔVF cycle length 10 s before the first discharge: r = −0.58 and −0.81, p < 0.05).Conclusions. MS-551 given after the induction of VF improved defibrillation efficacy. Class III antiarrhythmic agents deserve consideration when VF is resistant to electrical defibrillation during cardiopulmonary resuscitation.(J Am Coll Cardiol 1997;29:688–92)