Mechanisms of unpinning and termination of ventricular tachycardia

High-energy defibrillation shock is the only therapy for ventricular tachyarrhythmias. However, because of adverse side effects, lowering defibrillation energy is desirable. We investigated mechanisms of unpinning, destabilization, and termination of ventricular tachycardia (VT) by low-energy shocks in isolated rabbit right ventricular preparations (n = 22). Stable VT was initiated with burst pacing and was optically mapped. Monophasic "unpinning" shocks (10 ms) of different strengths were applied at various phases throughout the reentry cycle. In 8 of 22 preparations, antitachycardia pacing (ATP: 8-20 pulses, 50-105% of period, 0.8-10 mA) was also applied. Termination of reentry by ATP was achieved in only 5 of 8 preparations. Termination by unpinning occurred in all 22 preparations. Rayleigh's test showed a statistically significant unpinning phase window, during which reentry could be unpinned and subsequently terminated with E80 (magnitude at which 80% of reentries were unpinned) = 1.2 V/cm. All reentries were unpinned with field strengths < or = 2.4 V/cm. Unpinning was achieved by inducing virtual electrode polarization and secondary sources of excitation at the core of reentry. Optical mapping revealed the mechanisms of phase-dependent unpinning of reentry. These results suggest that a 20-fold reduction in energy could be achieved compared with conventional high-energy defibrillation and that the unpinning method may be more effective than ATP for terminating stable, pinned reentry in this experimental model.     

The mechanisms of the vulnerable window: the role of virtual electrodes and shock polarity

Vulnerability and defibrillation are mechanistically dependent upon shock strength, polarity, and timing. We have recently demonstrated that shock-induced virtual electrode polarization (VEP) may induce reentry. However, it remains unclear how the VEP mechanism may explain the vulnerable window and polarity dependence of vulnerability. We used a potentiometric dye and optical mapping to assess the anterior epicardial electrical activity of Langendorff-perfused rabbit hearts (n = 7) during monophasic shocks (+/-100 V and +/-200 V, duration of 8 ms) applied from a transvenous defibrillation lead at various coupling intervals. Arrhythmias were induced in a coupling interval and shock polarity dependent manner: (i) anodal and cathodal shocks induced arrhythmias in 33.2 +/- 30.1% and 53.1 +/- 39.3% cases (P < 0.01), respectively, and (ii) the vulnerable window was located near the T-wave. Optical maps revealed that VEP was also modulated by the coupling interval and shock polarity. Recovery of excitability produced by negative polarization, known as de-excitation, and the resulting reentry was more readily achieved during the relative refractory period than the absolute refractory period. Furthermore, anodal shocks produced wavefronts propagating in an inward direction with respect to the electrode, whereas cathodal shocks propagated in an outward direction. Wavefronts produced by anodal shocks were more likely to collide and annihilate each other than those caused by cathodal shocks. The probability of degeneration of the VEP-induced phase singularity into a sustained arrhythmia depends upon the gradient of VEP and the direction of the VEP-induced wavefront. The VEP gradient depends upon the coupling interval, while the direction depends upon shock polarity; these factors explain the vulnerable window and polarity-dependence of vulnerability, respectively.     

A physical approach to remove anatomical reentries: a bidomain study

Controlling cardiac chaos is often achieved by applying a large damaging electric shock-defibrillation. It removes all waves, without differentiating reentries and normal waves, anatomical and functional reentries. Anatomical reentries can be removed by anti-tachycardia pacing (ATP) as well. But ATP requires the knowledge of the position of the reentry, and an access to it with an invasive stimulating electrode. We show that the physics of electric field distribution between cardiac cells permits one to deliver an electric pulse exactly to the core of an anatomical reentry, without knowing its position and even to locations where access with a stimulating electrode is not possible. The energy needed is two orders of magnitude less than defibrillation energy. The results are insensitive to both a detailed ionic model and to the geometry of the fibers.     

Mechanistic inquiry into decrease in probability of defibrillation success with increase in complexity of preshock reentrant activity

Energy requirements for successful antiarrhythmia shocks are arrhythmia specific. However, it remains unclear why the probability of shock success decreases with increasing arrhythmia complexity. The goal of this research was to determine whether a diminished probability of shock success results from an increased number of functional reentrant circuits in the myocardium, and if so, to identify the responsible mechanisms. To achieve this goal, we assessed shock efficacy in a bidomain defibrillation model of a 4-mm-thick slice of canine ventricles. Shocks were applied between a right ventricular cathode and a distant anode to terminate either a single scroll wave (SSW) or multiple scroll waves (MSWs). From the 160 simulations conducted, dose-response curves were constructed for shocks given to SSWs and MSWs. The shock strength that yielded a 50% probability of success (ED(50)) for SSWs was found to be 13% less than that for MSWs, which indicates that a larger number of functional reentries results in an increased defibrillation threshold. The results also demonstrate that an isoelectric window exists after both failed and successful shocks; however, shocks of strength near the ED(50) value that were given to SSWs resulted in 16.3% longer isoelectric window durations than the same shocks delivered to MSWs. Mechanistic inquiry into these findings reveals that the two main factors underlying the observed relationships are 1) smaller virtual electrode polarizations in the tissue depth, and 2) differences in preshock tissue state. As a result of these factors, intramural excitable pathways leading to delayed breakthrough on the surface were formed earlier after shocks given to MSWs compared with SSWs and thus resulted in a lower defibrillation threshold for shocks given to SSWs.     

Polarity reversal lowers activation time during diastolic field stimulation of the rabbit ventricles: insights into mechanisms

To fully characterize the mechanisms of defibrillation, it is necessary to understand the response, within the three-dimensional (3D) volume of the ventricles, to shocks given in diastole. Studies that have examined diastolic responses conducted measurements on the epicardium or on a transmural surface of the left ventricular (LV) wall only. The goal of this study was to use optical imaging experiments and 3D bidomain simulations, including a model of optical mapping, to ascertain the shock-induced virtual electrode and activation patterns throughout the rabbit ventricles following diastolic shocks. We tested the hypothesis that the locations of shock-induced regions of hyperpolarization govern the different diastolic activation patterns for shocks of reversed polarity. In model and experiment, uniform-field monophasic shocks of reversed polarities (cathode over the right ventricle is RV-, reverse polarity is LV-) were applied to the ventricles in diastole. Experiments and simulations revealed that RV- shocks resulted in longer activation times compared with LV- shocks of the same strength. 3D simulations demonstrated that RV- shocks induced a greater volume of hyperpolarization at shock end compared with LV- shocks; most of these hyperpolarized regions were located in the LV. The results of this study indicate that ventricular geometry plays an important role in both the location and size of the shock-induced virtual anodes that determine activation delay during the shock and subsequently affect shock-induced propagation. If regions of hyperpolarization that develop during the shock are sufficiently large, activation delay may persist until shock end.     

Effects of burst stimulation during ventricular fibrillation on cardiac function after defibrillation

The purpose of defibrillation is to rapidly restore blood flow and tissue perfusion following ventricular fibrillation (VF) and shock delivery. We tested the hypotheses that 1) a series of 1-ms pulses of various amplitudes delivered before the defibrillation shock can improve hemodynamics following the shock, and 2) this hemodynamic improvement is due to stimulation of cardiac or thoracic sympathetic nerves. Ten anesthetized pigs received a burst of either 15 or 30 1-ms pulses (0.1-10 A in strength) during VF, after which defibrillation was performed. ECG, arterial blood pressure, and left ventricular (LV) pressure were recorded. Defibrillation shocks and burst pulses were delivered from a right ventricular coil electrode to superior vena cava coil and left chest wall electrodes. Sympathetic blockade was induced with 1 mg/kg timolol and trials were repeated. The first half of this protocol was repeated in two animals that were pretreated with reserpine. Heart rate (HR) after 1-, 2-, 5-, and 10-A pulses was significantly higher than after control shocks without preceding pulse therapy. Mean and peak LV pressure measurements increased 38 and 72%, respectively, following shocks preceded by 5- and 10-A pulses compared with shocks preceded by no burst pulses. Mean and peak arterial pressures increased 36 and 43%, respectively, following shocks preceded by 5- and 10-A pulses compared with shocks preceded by no burst pulses. After beta-blockade, HR, mean and peak arterial pressures, and mean LV pressure were not significantly different after pulses of any strength compared with control shocks. LV peak pressure following the 10-A pulses was significantly higher than with no burst pulses but was significantly lower than the response to the 10-A pulses delivered without beta-blockade. HR, mean and peak arterial pressures, and mean and peak LV pressure responses after 15 or 30 5- or 10-A pulses were similar to the responses to the same pulses after beta-blockade. We conclude that a burst of 15-30 1-ms pulses delivered during VF can increase HR, arterial pressure, and LV pressure following defibrillation. beta-Blockade or reserpine pretreatment prevents most of this postshock increase in HR, arterial pressure, and LV pressure.     

Success and failure of biphasic shocks: results of bidomain simulations.

The mechanisms behind the superiority of optimal biphasic defibrillation shocks over monophasic are not fully understood. This simulation study examines how the shock polarity and second-phase magnitude of biphasic shocks influence the virtual electrode polarization (VEP) pattern, and thus the outcome of the shock in a bidomain model representation of ventricular myocardium. A single spiral wave is initiated in a two-dimensional sheet of myocardium that measures 2 x 2 cm(2). The model incorporates non-uniform fiber curvature, membrane kinetics suitable for high strength shocks, and electroporation. Line electrodes deliver a spatially uniform extracellular field. The shocks are biphasic, each phase lasting 10 ms. Two different polarities of biphasic shocks are examined as the first-phase configuration is held constant and the second-phase magnitude is varied between 1 and 10 V/cm. The results show that for each polarity, varying the second-phase magnitude reverses the VEP induced by the first phase in an asymmetric fashion. Further, the size of the post-shock excitable gap is dependent upon the second-phase magnitude and is a factor in determining the success or failure of the shock. The maximum size of a post-shock excitable gap that results in defibrillation success depends on the polarity of the shock, indicating that the refractoriness of the tissue surrounding the gap also contributes to the outcome of the shock.     

The effect of spatial scale of resistive inhomogeneity on defibrillation of cardiac tissue

Defibrillation of cardiac tissue can be viewed in the context of dynamical systems theory as the attempt to move a dynamical system from the basin of attraction of one attractor (fibrillation) to another (the uniform rest state) by applying a stimulus whose form is physically constrained. Here we give an introduction to the physical mechanism of cardiac defibrillation from this dynamical perspective and examine the role of resistive inhomogeneity on defibrillation efficacy. Using numerical simulations with rotating waves on a one-dimensional periodic ring, we study the role of the spatial scale of resistive inhomogeneity on defibrillation. For a rotating wave on a periodic ring there are three stable attractors, namely the uniform rest state, a wave traveling clockwise and a wave traveling counterclockwise. As a result, the application of a stimulus has the potential for three different outcomes, namely elimination of the wave, phase resetting of the wave, and reversal of the wave. The results presented here show that with resistive inhomogeneities of large spatial scale, all three of these transitions are possible with large amplitude shocks, so that the probability of defibrillation is bounded well below one, independent of stimulus amplitude. On the other hand, resistive inhomogeneities of small spatial scale produce a defibrillation threshold that is qualitatively consistent with that found experimentally, namely the probability of defibrillation success is an increasing function that approaches one for large enough stimulus amplitude. Extending these results to higher dimensions, we describe conditions for successful defibrillation of functional reentry with large scale spatial inhomogeneity, but find that elimination of anatomical reentry is quite difficult. With small spatial scale inhomogeneity, there are no similar restrictions.     

Resonant Drift of Spiral Waves in the Complex Ginzburg-Landau Equation

Weak periodic external perturbations of an autowave medium can cause large-distance directed motion of the spiral wave. This happens when the period of the perturbation coincides with, or is close to the rotation period of a spiral wave, or its multiple. Such motion is called resonant or parametric drift. It may be used for low-voltage defibrillation of heart tissue. Theory of the resonant drift exists, but so far was used only qualitatively. In this paper, we show good quantitative agreement of the theory with direct numerical simulations. This is done for Complex Ginzburg-Landau Equation, one of the simplest autowave models.     

A Model for Multi-site Pacing of Fibrillation Using Nonlinear Dynamics Feedback

Traditionally, cardiac defibrillation requires a strong electric shock. Many unwanted side effects of this shock could be eliminated if defibrillation were performed using weak stimuli applied to several locations throughout the heart. Such multi-site pacing algorithms have been shown to defibrillate both experimentally (Pak et al., Am J Physiol 285:H2704–H2711, 2003) and theoretically (Puwal and Roth, J Biol Systems 14:101–112, 2006). Gauthier et al. (Chaos, 12:952–961, 2002) proposed a method to pace the heart using an algorithm based on nonlinear dynamics feedback applied through a single electrode. Our study applies a related but simpler algorithm, which essentially configures each electrode as a demand pacemaker, to simulate the multi-site pacing of fibrillating cardiac tissue. We use the numerical model developed by Fenton et al. (Chaos, 12:852–892, 2002) as the reaction term in a reaction–diffusion equation that we solve over a two-dimensional sheet of tissue. The defibrillation rate after pacing for 3 s is about 30%, which is significantly higher than the spontaneous defibrillation rate and is higher than observed in previous experimental and theoretical studies. Tuning the algorithm period can increase this rate to 45%. Electronic supplementary material The online version of this article (doi:) contains supplementary material, which is available to authorized users.     

Mechanisms of enhanced shock-induced arrhythmogenesis in the rabbit heart with healed myocardial infarction

Shock-induced vulnerability and defibrillation have been mostly studied in structurally normal hearts. However, defibrillation therapy is normally applied to patients with diseased hearts, frequently those with prior myocardial infarction (MI). Shock-induced vulnerability and defibrillation have not been well studied under this condition. We sought to examine the mechanisms of shock-induced arrhythmogenesis and arrhythmia maintenance in a rabbit model of healed MI (4 wk or more postinfarction). Ligation of the lateral division or posterolateral division of the left coronary artery at a level of 40-70% from the apex was performed 53 +/- 21 days before acute experiments. Shock-induced vulnerability was assessed in infarcted (n = 8) and structurally normal (n = 8) hearts by delivering internal monophasic shocks at different shock strengths and delivery phases. Electrical activities from the anterior epicardium during shock application and during shock-induced arrhythmias were optically recorded and quantitatively analyzed. Ligation resulted in a transmural left ventricular free wall infarction mainly located at the apical region with a consistent endocardial border zone (BZ) as confirmed by histological studies. There were significant increases in the incidence, severity, and duration of shock-induced arrhythmias in the infarcted hearts versus controls due to 1) postshock break-excitation wavefronts that frequently originated near the infarction BZ and 2) the existence of an infarction BZ that created an anatomic reentry pathway and facilitated arrhythmia maintenance. In conclusion, the infarction BZ contributes to both increased shock-induced arrhythmogenesis and arrhythmia maintenance in the rabbit model of healed MI.     

Differences between left and right ventricular anatomy determine the types of reentrant circuits induced by an external electric shock. A rabbit heart simulation study

Despite the fact that elucidating the mechanisms of cardiac vulnerability to electric shocks is crucial to understanding why defibrillation shocks fail, important aspects of cardiac vulnerability remain unknown. This research utilizes a novel anatomically based bidomain finite-element model of the rabbit ventricles to investigate the effect of shock polarity reversal on the reentrant activity induced by an external defibrillation-strength shock in the paced ventricles. The specific goal of the study is to examine how differences between left and right ventricular chamber anatomy result in differences in the types of reentrant circuits established by the shock. Truncated exponential monophasic shocks of duration 8 ms were delivered via two external electrodes at various timings. Vulnerability grids were constructed for shocks of reversed polarity (referred to as RV- or LV- when either the RV or the LV electrode is a cathode). Our results demonstrate that reversing electrode polarity from RV- to LV- changes the dominant type of post-shock reentry: it is figure-of-eight for RV- and quatrefoil for LV- shocks. Differences in secondary types of post-shock arrhythmia also occur following shock polarity reversal. These effects of polarity reversal are primarily due to the fact that the LV wall is thicker than the RV, resulting in a post-shock excitable gap that is predominantly within the LV wall for RV- shocks and in the septum for LV- shocks.     

Virtual electrode polarization in the far field: implications for external defibrillation

We recently suggested that failure of implantable defibrillation therapy may be explained by the virtual electrode-induced phase singularity mechanism. The goal of this study was to identify possible mechanisms of vulnerability and defibrillation by externally applied shocks in vitro. We used bidomain simulations of realistic rabbit heart fibrous geometry to predict the passive polarization throughout the heart induced by external shocks. We also used optical mapping to assess anterior epicardium electrical activity during shocks in Langendorff-perfused rabbit hearts (n = 7). Monophasic shocks of either polarity (10-260 V, 8 ms, 150 microF) were applied during the T wave from a pair of mesh electrodes. Postshock epicardial virtual electrode polarization was observed after all 162 applied shocks, with positive polarization facing the cathode and negative polarization facing the anode, as predicted by the bidomain simulations. During arrhythmogenesis, a new wave front was induced at the boundary between the two regions near the apex but not at the base. It spread across the negatively polarized area toward the base of the heart and reentered on the other side while simultaneously spreading into the depth of the wall. Thus a scroll wave with a ribbon-shaped filament was formed during external shock-induced arrhythmia. Fluorescent imaging and passive bidomain simulations demonstrated that virtual electrode polarization-induced scroll waves underlie mechanisms of shock-induced vulnerability and failure of external defibrillation.     

Mechanisms of superiority of ascending ramp waveforms: new insights into mechanisms of shock-induced vulnerability and defibrillation

Monophasic ascending ramp (AR) and descending ramp (DR) waveforms are known to have significantly different defibrillation thresholds. We hypothesized that this difference arises due to differences in mechanisms of arrhythmia induction for the two waveforms. Rabbit hearts (n = 10) were Langendorff perfused, and AR and DR waveforms (7, 20, and 40 ms) were randomly delivered from two line electrodes placed 10 mm apart on the anterior ventricular epicardium. We optically mapped cellular responses to shocks of various strengths (5, 10, and 20 V/cm) and coupling intervals (CIs; 120, 180, and 300 ms). Optical mapping revealed that maximum virtual electrode polarization (VEP) was reached at significantly different times for AR and DR of the same duration (P < 0.05) for all tested CIs. As a result, VEP for AR were stronger than for DR at the end of the shock. Postshock break excitation resulting from AR generated faster propagation and typically could not form reentry. In contrast, partially dissipated VEP resulting from DR generated slower propagation; the wavefront was able to propagate into deexcited tissue and thus formed a shock-induced reentry circuit. Therefore, for the same delivered energy, AR was less proarrhythmic compared with DR. An active bidomain model was used to confirm the electrophysiological results. The VEP hypothesis explains differences in vulnerability associated with monophasic AR and DR waveforms and, by extension, the superior defibrillation efficacy of the AR waveform compared with the DR waveform.     

The topology of defibrillation

We describe how Art Winfree's ideas about phase singularities can be used to understand the response of cardiac tissue with a random preexisting pattern of reentrant waves (fibrillation) to a large brief current stimulus. This discussion is organized around spatial dimension, beginning with a discussion of reentry on a periodic ring, followed by reentry in a two-dimensional planar domain (spiral waves), and ending with consideration of three-dimensional reentrant patterns (scroll waves). In all cases, we show how reentrant activity is changed by the application of a shock, describing conditions under which defibrillation is successful or not. Using topological arguments we draw the general conclusion that with a generic placement of stimulating electrodes, large-scale virtual electrodes do not give an adequate explanation for the mechanism of defibrillation.     

Attenuation of Post-Shock Increases in Brain Natriuretic Peptide with Post Shock Overdrive Pacing

Background

Predischarge defibrillation threshold testing is often performed a few days after ICD implantation in order to validate defibrillation thresholds obtained at the time of implant. Ventricular fibrillation is induced with such testing and causes an increase in serum Brain Natriuretic Peptide (BNP) levels. BNP is an indicator for cardiac stress. We wanted to examine the feasibility to alter the trend of BNP after predischarge testing in VVI, DDD and CRT ICD''s.

Methods

We measured BNP before predischarge testing and 5, 10, 20 and 40 minutes after predischarge testing in 13 groups with each 20 patients. We evaluated patients without post shock pacing and patients with a post shock pacing frequency of 60, 70, 80, 90 and 100 bpm and a duration of 30 and 60 sec as well as a post shock pacing frequency of 80 and 90 bpm and a duration of 120 sec post shock pacing.

Results

Patients without post shock pacing showed the highest BNP during the follow-up. The percentage values of BNP increased consistent significantly after 5 minutes compared with BNP before predischarge testing. The percentage values of BNP trend was significantly lower with a post shock pacing of 90 bpm and duration of 60 sec. In addition, we excluded a cardiac necrosis by predischarge testing because of similar values of myoglobin, cardiac troponin I and creatine kinase during the follow-up.

Conclusions

Our results suggested that post shock pacing with 90 bpm and duration of 60 sec as the best optimized post shock pacing frequency and duration for VVI, DDD and CRT ICD''s. A reduction of cardiac stress is going to be achieved with the optimization of the post shock pacing frequency and duration.     

The future of electrical defibrillators for the heart]

The aim of electric defibrillation of the heart is to salvage a greater percentage of victims of cardiac arrest in the future. An initial decisive pathway towards this goal is to get a defibrillator to the victim as quickly as possible and apply an electric shock. This has now been implemented on a large scale--by means of the widespread propagation of (semi-)automatic external defibrillators (AED) and their PAD (Public Access Defibrillator) variant for use by laypersons. This is an initial necessary prerequisite which, however, is not sufficient to have a real impact on saving lives. For experience has shown that, despite the early use of AEDs, an appreciable proportion of the victims cannot be saved. The intention is to improve this situation by increasing the efficacy and reducing the harmful downside of the defibrillation waveforms applied. The solution is optimally dimensioned biphasic waveforms with high efficacy at low energy levels. In this connection, it is shown that the efficacy of high-energy defibrillation shocks is exceeded by their injurious effects, thus thwarting life-saving defibrillation. Examples of new waveforms of particularly high efficacy are presented. It is shown how such impulses should be physiologically dimensioned, and clinical results of cardioversion (atrial defibrillation) and initial out-of-hospital results of emergency defibrillation are discussed. In addition, new approaches for future waveforms enabling pulsed pulse-pause-modulated biphasic shocks are described. In this way, waveforms with a physiologically optimal effect on the heart can be produced which were previously impossible with portable defibrillators. Waveforms that have already been tested or are still in the research stage, justify hopes that improved survival of cardiac arrest victims may be expected. These new waveforms may also be of benefit in other types of defibrillators (e.g. cardioversion or implanted defibrillators).     

Dynamical effects of diffusive cell coupling on cardiac excitation and propagation: a simulation study

Cell coupling is considered to be important for cardiac action potential propagation and arrhythmogenesis. We carried out computer simulations to investigate the effects of stimulation strength and cell-to-cell coupling on action potential duration (APD) restitution, APD alternans, and stability of reentry in models of isolated cell, one-dimensional cable, and two-dimensional tissue. Phase I formulation of the Luo and Rudy action potential model was used. We found that stronger stimulation resulted in a shallower APD restitution curve and onset of APD alternans at a faster pacing rate. Reducing diffusive coupling between cells prolonged APD. Weaker diffusive currents along the direction of propagation steepened APD restitution and caused APD alternans to occur at a slower pacing rate in tissue. Diffusive current due to curvature changed APD but had little effect on APD restitution slope and onset of instability. Heterogeneous cell coupling caused APD inhomogeneities in space. Reduction in coupling strength either uniformly or randomly had little effect on the rotation period and stability of a reentry, but random cell decoupling slowed the rotation period and, thus, stabilized the reentry, preventing it from breaking up into multiple waves. Therefore, in addition to its effects on action potential conduction velocity, diffusive cell coupling also affects APD in a rate-dependent manner, causes electrophysiological heterogeneities, and thus modulates the dynamics of cardiac excitation. These effects are brought about by the modulation of ionic current activation and inactivation.     

Virtual electrode effects in defibrillation

This modeling study demonstrates that a re-entrant activity in a sheet of myocardium can be extinguished by a defibrillation shock delivered via extracellular point-source electrodes which establish spatially non-uniform applied field. The tissue is represented as a homogeneous bidomain with unequal anisotropy ratios in the cardiac conductivities. Spiral wave re-entry is initiated in the bidomain sheet following an S1-S2 stimulation protocol. The results indicate that the point-source defibrillation shock establishes large-scale changes in transmembrane potential in the tissue (virtual electrodes) that are ‘superimposed’ over regions of various degrees of membrane refractoriness in the myocardium. The close proximity of large-scale shock-induced regions of alternating membrane polarity is central to the ability of the shock to terminate the spiral wave. The new wavefronts generated following anode/cathode break phenomena restrict the spiral wave and render the tissue too refractory to further maintain the re-entry. In contrast, shocks delivered via line electrodes establish, in close proximity to the electrode, changes in transmembrane potential that are of same-sign polarity. These shocks are incapable of terminating the re-entrant activation.     

Termination of Ventricular Tachycardia with Antitachycardia Pacing after Ineffective Shock Therapy in an ICD Recipient with Hypertrophic Cardiomyopathy

Implantable Cardioverter Defibrillator (ICD) implantation is the only established therapy for primary or secondary prevention of sudden cardiac death in patients with Hypertrophic Cardiomyopathy (HCM). Ineffectiveness of shock therapy for the termination of potentially fatal ventricular arrhythmias in ICD recipients is rare in the presence of appropriate arrhythmia detection by the device. We report the case of a 48-year-old woman with HCM and a single chamber ICD, who received five inefficient high-energy (35 Joules) shocks for the termination of an appropriately detected episode of Ventricular Tachycardia (VT). The episode was safely terminated with a subsequent application of Antitachycardia Pacing (ATP) by the device. At the following ICD control, an acceptable defibrillation threshold was detected.