Shock Electrode Research Articles

Real-world experience with the insertion of a new implantable cardiac monitor

Abstract Funding Acknowledgements Type of funding sources: Private company. Main funding source(s): Biotronik SE & Co.KG OnBehalf BIO|CONCEPT.BIOMONITOR III study group, BIO|MASTER.BIOMONITOR III study group, BIO|STREAM-ICM study group Background Implantable Cardiac Monitors (ICM) provide continuous long-term heart rhythm monitoring. The new ICM BIOMONITOR III / IIIm (BM III) is provided with a single-step insertion tool. Purpose To report on the insertion procedure of the BM III in a large real-world patient population. Methods The BM III combines a low cross-section (4.5 x 8.5 mm) with an extended ICM length (77 mm, including flexible antenna). It is inserted into subcutaneous tissue with an ‘injection’ tool that forms the pocket and delivers the device in a single step. We report results of the insertion procedure from a pooled data set from the BIO|CONCEPT BM III (completed) and the BIO|MASTER BM III and BIO|STREAM-ICM (ongoing) studies. Results From 54 investigational sites in 11 countries, 455 insertions were reported (including 39 BM IIIm). The patients were 63 ± 16 years old, had a BMI of 27.6 ± 5.4, and 43% were women. The indications were syncope or pre-syncope (57%), cryptogenic stroke (23%), management of AF (11%) or other (9%). Insertions took 1.7 ± 1.8 minutes until removal of the insertion tool, 4.7 ± 3.4 minutes until wound closure, and 7.1 ± 5.6 minutes including wound cleaning. The wound was sutured (79%) or closed with staples (10%) or adhesive strips (10%). General anaesthesia was used in 8% of the patients and antibiotic prophylaxis in 50% (44% systemic and 6% local). Insertions took place in the catheter laboratory (62%), operating theatre (22%) or in a consultation room (16%) without specific precautional equipment. The insertion site was parallel to the heart"s long axis (56%), parasternal (39%), in the 2nd/3rd intercostal space (3.5%), axillary (0.9%) or at the clavicula (0.7%). The device was repositioned in one case (0.2%). 13 adverse events were reported in connection to the insertion procedure. 5 cases of device pocket bleeding or hematoma occurred. In 5 further cases, the device migrated, posing the risk of extrusion, or actually extruded. Three of these cases used only adhesive strips or no wound closure at all. In two cases, an incorrect usage of the incision tool and substantial subcutaneous fatty tissue may have contributed. One device was damaged by a 200 J defibrillation shock with a shock electrode placed over the device. One patient suffered from dyspnoea, possibly due to psychogenic hyperventilation. One patient had a vasovagal syncope due to pain after an insertion with insufficient local anaesthesia. No infections were reported until the day of analysis, which was more than 30 days after insertion in 92% of all cases. Conclusion The new BM III was inserted in typically less than 5 minutes until wound closure. A relevant number of insertions took place in a consultation room. Prophylactic antibiotics may be unnecessary, because no pocket infections were reported, although no antibiotic prophylaxis was used in one half of all cases (N = 229). In summary, the insertion with the new tool is fast and has a low risk of complications.

Uncommon inappropriate shock of subcutaneous defibrillator in early postoperative period due to air in close proximity of shock electrode is presented

Clinical case report of uncommon inappropriate shock of subcutaneous defibrillator in early postoperative period due to air in close proximity of shock electrode is presented.

Treatment of Ventricular Tachycardia Induced by Coil of Ventricular Lead of Implantable Cardioverter Defibrillator

Implantable cardioverter defibrillator (ICD) -DDD for arrhythmogenic heart disease of unknown etiology, with the induction of ventricular tachycardia by the right ventricle (RV) of the shock electrode. The arrhythmia generated by the ICD electrode itself was the cause of multiple episodes with appropriate anti-tachycardia pacing (ATP) and shock therapy. The etiology of the arrhythmia was confirmed by electrophysiological study and successful treatment was performed with ablation, without the need for surgical repositioning of the electrode.

Tratamento de Taquicardia Ventricular Induzida por Mola de Choque de Eletrodo de Cardioversor Desfi brilador Implantável

Paciente portador de cardioversor desfi brilador implantável (CDI)-DDD por cardiopatia arritmogênica de etiologia desconhecida, com induçãode taquicardia ventricular pela mola de ventrículo direito (VD) do eletrodo dechoque. A arritmia gerada pelo próprio eletrodo do CDI foi causa de múltiplos episódios com terapia apropriada por anti-tachycardia pacing (ATP) e choque. Confi rmada a etiologia da arritmia por estudo eletrofi siológico erealizado tratamento bem-sucedido com ablação, sem necessidadede reposicionamento cirúrgico do eletrodo

Pacing electrode modeling and simulation of cardiac contractility modulation

Abstract Cardiac contractility modulation (CCM) is a device-based therapy for the treatment of systolic left ventricular chronic heart failure. Unlike other devicebased therapies for heart failure, CCM delivers nonexcitatory pacing signals to the myocardium. This leads to an extension of the action potential and to an improved contractility of the heart. The modeling and simulation was done with the electromagnetic simulation software CST. Three CCM electrodes were inserted into the Offenburg heart rhythm model and subsequently simulated the electric field propagation in CCM therapy. In addition, simulations of CCM have been performed with electrodes from other device-based therapies, such as cardiac resynchronization therapy (CRT) and implantable cardioverter./.defibrillator (ICD) therapy. At the same distance to the simulation electrode, the electric field is slightly stronger in CCM therapy than in CCM therapy with additionally implanted CRT or ICD electrodes. In addition, there is a change in the electric field propagation at the electrodes of the CRT and the shock electrode of the ICD. By simulating several different therapy procedures on the heart, it is possible to check how they affect their behavior during normal operation. CCM heart rhythm model simulation allows the evaluation the individual electrical pacing and sensing field during CCM.

Rule-based processes in generalisation and peak shift in human fear conditioning.

Two experiments explored the role of verbalisable rules in generalisation of human differential fear conditioning with electric shock as the aversive stimulus. Two circles of different sizes served as conditioned stimuli (CS+ and CS-), before testing with a range of circle sizes. In Experiment 1, shock expectancy ratings followed a peak-shifted unimodal gradient, with maximum ratings at a test value further along the dimension from CS+ in the opposite direction to CS-. However, differentiable gradients were observed when participants were divided on the basis of the rules they reported using during the task (linear and similarity). Experiment 2 was designed to counter the contradictory feedback arising from extinction testing by removing the shock electrodes during the test phase. A more linear overall gradient was observed, and sub-groups defined by self-reported rules showed distinct gradients that were congruent with their rules. These results indicate that rule-based processes are influential in generalisation of conditioned fear along simple stimulus dimensions, and may help explain generalisation phenomena that have traditionally been attributed to automatic, similarity-based processes.

Ablation of Myocardial Tissue With Nanosecond Pulsed Electric Fields

BackgroundAblation of cardiac tissue is an essential tool for the treatment of arrhythmias, particularly of atrial fibrillation, atrial flutter, and ventricular tachycardia. Current ablation technologies suffer from substantial recurrence rates, thermal side effects, and long procedure times. We demonstrate that ablation with nanosecond pulsed electric fields (nsPEFs) can potentially overcome these limitations.MethodsWe used optical mapping to monitor electrical activity in Langendorff-perfused New Zealand rabbit hearts (n = 12). We repeatedly inserted two shock electrodes, spaced 2–4 mm apart, into the ventricles (through the entire wall) and applied nanosecond pulsed electric fields (nsPEF) (5–20 kV/cm, 350 ns duration, at varying pulse numbers and frequencies) to create linear lesions of 12–18 mm length. Hearts were stained either with tetrazolium chloride (TTC) or propidium iodide (PI) to determine the extent of ablation. Some stained lesions were sectioned to obtain the three-dimensional geometry of the ablated volume.ResultsIn all animals (12/12), we were able to create nonconducting lesions with less than 2 seconds of nsPEF application per site and minimal heating (< 0.2°C) of the tissue. The geometry of the ablated volume was smoother and more uniform throughout the wall than typical for RF ablation. The width of the lesions could be controlled up to 6 mm via the electrode spacing and the shock parameters.ConclusionsAblation with nsPEFs is a promising alternative to radiofrequency (RF) ablation of AF. It may dramatically reduce procedure times and produce more consistent lesion thickness than RF ablation.

A potential pathway to the relapse of fear? Conditioned negative stimulus evaluation (but not physiological responding) resists instructed extinction

Relapse of fear after successful intervention is a major problem in clinical practice. However, little is known about how it is mediated. The current study investigated the effects of instructed extinction and removal of the shock electrode on electrodermal responding (Experiment 1), fear potentiated startle (Experiment 2), and a continuous self-report measure of conditional stimulus valence (Experiments 1 and 2) in human differential fear conditioning. Instructed extinction and removal of the shock electrode resulted in the immediate reduction of differential fear potentiated startle and second interval electrodermal responding, but did not affect self-reported conditional stimulus valence. A separate sample of participants (Experiment 3) who were provided with a detailed description of the experimental scenario predicted the inverse outcome, reduced differential stimulus evaluations and continued differential physiological responding, rendering it unlikely that the current results reflect on demand characteristics. These results suggest that the negative valence acquired during fear conditioning is less sensitive to cognitive interventions than are the physiological indices of human fear learning and that valence reduction requires extended exposure training. Persisting negative valence after cognitive intervention may contribute to fear relapse after successful treatment.

Video-Assisted Thoracoscopic Implantation of Cardioverter-Defibrillator Systems

Implantation of cardioverter-defibrillators in patients with limited venous access due to recurrent infections, thrombosis, or congenital anomalies can be challenging. For this subset of patients, we performed a video-assisted thoracoscopic intrapericardial implantation using standard shock electrodes and epicardial leads. The pulse generator was placed in pectoral or subcostal position. Allpacing and sensing parameters and defibrillation thresholds were satisfactory and stable in time. No major complications were reported. Our limited experience suggests that this technique is a potential alternative inpatients where endocardial implantation should be avoided.

External defibrillation on an implantable defibrillator

To the Editor: Despite the best efforts of healthcare providers, guideline-conform treatment failure is expected to occur, particularly in real-world emergency situations [1]. In the case reported here, a 79-year-old man with a history of coronary artery disease and implantation of a cardioverter defibrillator (ICD) presented to the emergency room with recurrent ventricular tachycardia. The junior physician-incharge applied an external biphasic DC shock of 200 J to the patient, holding the paddle in one hand and placing it directly over the ICD (Electronic Supplementary Material Fig. 1)—but without success. Arrhythmic stability was finally achieved by multiple, appropriate ICD shocks and intravenous amiodarone. Subsequent device interrogation and defibrillation testing of the ICD showed no instance of device malfunction. Coronary angiography revealed arteries free of significant stenoses. Strong electromagnetic interference induced by transthoracic DC shocks may cause permanent damage or alter the operation of the implanted device [2]. When attempting external defibrillation, clinicians are advised to place the paddles/pads as far as possible from any pulse generator and to choose biphasic over monophasic shock waveforms. A less deleterious effect might be expected if the orientation of the applied electric field is perpendicular—and not parallel—to the device with its lead(s), whereas if the device is located in the left pectoral region, an anterior– apex paddle position may be also acceptable. With an anterior–posterior electrode orientation and a distance between device and hand-held shock electrode of [8 cm, Manegold et al. [3] did not observe any dysfunction in patients with rightor left-sided implanted pacemakers or ICDs treated with external cardioversion for atrial fibrillation.

Major depression is not associated with blunting of aversive responses; evidence for enhanced anxious anticipation.

According to the emotion-context insensitivity (ECI) hypothesis, major depressive disorder (MDD) is associated with a diminished ability to react emotionally to positive stimuli and with blunting of defensive responses to threat. That defensive responses are blunted in MDD seems inconsistent with the conceptualization and diagnostic nosology of MDD. The present study tested the ECI hypothesis in MDD using a threat of shock paradigm. Twenty-eight patients with MDD (35.5±10.4 years) were compared with 28 controls (35.1±7.4 years). Participants were exposed to three conditions: no shock, predictable shock, and unpredictable shock. Startle magnitude was used to assess defensive responses. Inconsistent with the ECI hypothesis, startle potentiation to predictable and unpredictable shock was not reduced in the MDD group. Rather, MDD patients showed elevated startle throughout testing as well as increased contextual anxiety during the placement of the shock electrodes and in the predictable condition. A regression analysis indicated that illness duration and Beck depression inventory scores explained 37% (p<.005) of the variance in patients’ startle reactivity. MDD is not associated with emotional blunting but rather enhanced defensive reactivity during anticipation of harm. These results do not support a strong version of the ECI hypothesis. Understanding the nature of stimuli or situations that lead to blunted or enhanced defensive reactivity will provide better insight into dysfunctional emotional experience in MDD.

Association between respiratory sinus arrhythmia and reductions in startle responding in three independent samples

Evidence suggests that respiratory sinus arrhythmia (RSA) may be an important indicator of physiological flexibility. However, few studies have examined the relation between RSA and defensive habituation, a process contingent on physiological flexibility. In three independent samples, habituation was defined as the time course of 9 startle responses. In Sample one and two, startle was recorded (1) while shock electrodes were attached to participants’ and (2) before a threat-of-shock task. In Sample three, startle was recorded without these two components. In the first two samples, startle magnitude significantly decreased over time but in Sample three, startle only decreased at a trend level. Further, low RSA was associated with less of a reduction in startle magnitude over time within the first two samples, but was unrelated to startle reduction in the third. This suggests that low RSA is associated with less habituation to contextual anxiety, which may reflect difficulties regulating anxiety.

Electroporation induced by internal defibrillation shock with and without recovery in intact rabbit hearts

Defibrillation shocks from implantable cardioverter defibrillators can be lifesaving but can also damage cardiac tissues via electroporation. This study characterizes the spatial distribution and extent of defibrillation shock-induced electroporation with and without a 45-min postshock period for cell membranes to recover. Langendorff-perfused rabbit hearts (n = 31) with and without a chronic left ventricular (LV) myocardial infarction (MI) were studied. Mean defibrillation threshold (DFT) was determined to be 161.4 ± 17.1 V and 1.65 ± 0.44 J in MI hearts for internally delivered 8-ms monophasic truncated exponential (MTE) shocks during sustained ventricular fibrillation (>20 s, SVF). A single 300-V MTE shock (twice determined DFT voltage) was used to terminate SVF. Shock-induced electroporation was assessed by propidium iodide (PI) uptake. Ventricular PI staining was quantified by fluorescent imaging. Histological analysis was performed using Masson's Trichrome staining. Results showed PI staining concentrated near the shock electrode in all hearts. Without recovery, PI staining was similar between normal and MI groups around the shock electrode and over the whole ventricles. However, MI hearts had greater total PI uptake in anterior (P < 0.01) and posterior (P < 0.01) LV epicardial regions. Postrecovery, PI staining was reduced substantially, but residual staining remained significant with similar spacial distributions. PI staining under SVF was similar to previously studied paced hearts. In conclusion, electroporation was spatially correlated with the active region of the shock electrode. Additional electroporation occurred in the LV epicardium of MI hearts, in the infarct border zone. Recovery of membrane integrity postelectroporation is likely a prolonged process. Short periods of SVF did not affect electroporation injury.

On the resistance to extinction of fear conditioned to angry faces

The present study investigated whether, like fear conditioned to pictures of snakes and spiders, fear conditioned to angry faces resists extinction even after verbal instruction and removal of the shock electrode. Participants were trained in a differential Pavlovian fear conditioning procedure with angry face or happy face conditional stimuli (CSs). Prior to extinction, half the participants in each group were informed that no more unconditional stimuli would be presented and the shock electrode was removed. In the absence of this manipulation, participants showed resistance to extinction after training with angry face CSs, but not after training with happy face CSs. Instructed extinction and electrode removal abolished fear conditioning regardless of the emotion expressed by the CS faces. This finding suggests that fear conditioned to angry faces, like fear conditioned to racial out-group faces, is more malleable than fear conditioned to snakes and spiders.

A rare association of long QT syndrome and syndactyly: Timothy Syndrome (LQT 8)

A rare association of long QT syndrome and syndactyly: Timothy Syndrome (LQT 8)

Probing Field-Induced Tissue Polarization Using Transillumination Fluorescent Imaging

Despite major successes of biophysical theories in predicting the effects of electrical shocks within the heart, recent optical mapping studies have revealed two major discrepancies between theory and experiment: 1), the presence of negative bulk polarization recorded during strong shocks; and 2), the unexpectedly small surface polarization under shock electrodes. There is little consensus as to whether these differences result from deficiencies of experimental techniques, artifacts of tissue damage, or deficiencies of existing theories. Here, we take advantage of recently developed near-infrared voltage-sensitive dyes and transillumination optical imaging to perform, for the first time that we know of, noninvasive probing of field effects deep inside the intact ventricular wall. This technique removes some of the limitations encountered in previous experimental studies. We explicitly demonstrate that deep inside intact myocardial tissue preparations, strong electrical shocks do produce considerable negative bulk polarization previously inferred from surface recordings. We also demonstrate that near-threshold diastolic field stimulation produces activation of deep myocardial layers 2–6 mm away from the cathodal surface, contrary to theory. Using bidomain simulations we explore factors that may improve the agreement between theory and experiment. We show that the inclusion of negative asymmetric current can qualitatively explain negative bulk polarization in a discontinuous bidomain model.

Effective Cardioverter Defibrillator Implantation in Children Without Thoracotomy: A Valid Alternative

The implantation method for a cardioverter defibrillator in children is poorly standardized because of obvious features related to size and predisposing cardiac disease in children presenting with malignant ventricular arrhythmia. We propose an alternative method of implanting a cardioverter defibrillator without the need for associated thoracotomy, based on the subxiphoidal insertion of an epicardial bipolar ventricular pacing and sensing lead, an active can placed in the abdomen, and a subcutaneous array tunneled along the left thoracic wall as a shock electrode. This technique offers the advantage of an effective and minimally invasive implantable cardioverter defibrillator with wide applicability for children, independent of their size and cardiac status.

Stimulatory Current at the Edge of an Inactive Conductor in an Electric Field: Role of Nonlinear Interfacial Current&amp;#x2013;Voltage Relationship

Cardiac electric field stimulation is critical for the mechanism of defibrillation. The presence of certain inactive epicardial conductors in the field during defibrillation can decrease the defibrillation threshold. We hypothesized this decrease is due to stimulatory effects of current across the interface between the inactive conductor and the heart during field stimulation. To examine this current and its possible stimulatory effects, we imaged transmittance of indium-tin-oxide (ITO) conductors, tested for indium with X-ray diffraction, created a computer model containing realistic ITO interfacial properties, and optically mapped excitation of rabbit heart during electric field stimulation in the presence of an ITO conductor. Reduction of indium decreased transmittance at the edge facing the anodal shock electrode when trans-interfacial voltage exceeded standard reduction potential. The interfacial current-voltage relationship was nonlinear, producing larger conductances at higher currents. This nonlinearity concentrated the interfacial current near edges in images and in a computer model. The edge current was stimulatory, producing early postshock excitation of rabbit ventricles. Thus, darkening of ITO indicates interfacial current by indium reduction. Interfacial nonlinearity concentrates current near the edge where it can excite the heart. Stimulatory current at edges may account for the reported decrease in defibrillation threshold by inactive conductors.

Epicardial Conductors Can Lower the Defibrillation Threshold in Rabbit Hearts

During a defibrillation shock, epicardial conductors can introduce antistimulatory effects due to lowering of the voltage gradient in myocardial tissue under the conductor and stimulatory effects due to membrane polarization near edges. We hypothesized that increasing the area of conductors increases the defibrillation threshold (DFT), while increasing the amount of stimulatory edge of conductors decreases the DFT. To test this, we measured the DFT in excised rabbit hearts with and without sets of rectangular conductors having 250 or 500 mm(2) area and 100, 200, or 400 mm length of edges perpendicular to the line intersecting the shock electrodes. Unlike previous reports in which conductors increased or did not change DFT, present results indicate a conductor geometry having area of 250 mm (2) and edge of 200 mm decreases the DFT. This result is consistent with the hypothesis that stimulatory effects of the edge of a conductor can enhance defibrillation shock efficacy.

Panoramic imaging reveals basic mechanisms of induction and termination of ventricular tachycardia in rabbit heart with chronic infarction: Implications for low-voltage cardioversion

Sudden cardiac death due to arrhythmia in the settings of chronic myocardial infarction (MI) is an important clinical problem. Arrhythmic risk post-MI continues indefinitely even if heart failure and acute ischemia are not present due to the anatomic substrate of the scar and border zone (BZ) tissue. The purpose of this study was to determine mechanisms of arrhythmia initiation and termination in a rabbit model of chronic MI. Ligation of the lateral division of the left circumflex artery was performed 72 +/- 29 days before acute experiments (n = 11). Flecainide (2.13 +/- 0.64 microM) was administered to promote sustained arrhythmias, which were induced with burst pacing or a multiple shock protocol (four pulses, 140-200 ms coupling interval). Panoramic optical mapping with blebbistatin (5 microM) revealed monomorphic ventricular tachycardia (VT) maintained by a single mother rotor (cycle length [CL] = 174.7 +/- 38.4 ms) as the primary mechanism of arrhythmia. Mother rotors were anchored to the scar or BZ for 16 of the 19 rotor locations recorded. Cardioversion thresholds (CVTs) were determined at various phases throughout the VT CL from external shock electrodes. CVTs were found to be phase dependent, and the maximum versus minimum CVT was 7.8 +/- 1.9 vs. 4.1 +/- 1.6 V/cm, respectively (P = .005). Antitachycardia pacing was found to be effective in only 2.7% of cases in this model. These results indicate that scar and BZ tissue heterogeneity provide the substrate for VT by attracting and stabilizing rotors. Additionally, a significant reduction in CVT may be achieved by appropriately timed shocks in which the shock-induced virtual electrode polarization interacts with the rotor to destabilize VT.