Initiation Of Ventricular Fibrillation Research Articles

Can the Direct Cardiac Effects of the Electric Pulses Generated by the TASER X26 Cause Immediate or Delayed Sudden Cardiac Arrest in Normal Adults?

There is only a small amount of experimental data about whether the TASER X26, a nonlethal weapon that delivers a series of brief electrical pulses to cause involuntary muscular contraction to temporarily incapacitate an individual, can initiate ventricular fibrillation to cause sudden cardiac arrest either immediately or sometime after its use. Therefore, this paper uses the fundamental law of electrostimulation and experimental data from the literature to estimate the likelihood of such events. Because of the short duration of the TASER pulses, the large duration of the cardiac cell membrane time constant, the small fraction of current from electrodes on the body surface that passes through the heart, and the resultant high pacing threshold from the body surface, the fundamental law of electrostimulation predicts that the TASER pulses will not stimulate an ectopic beat in the large majority of normal adults. Since the immediate initiation of ventricular fibrillation in a normal heart requires a very premature stimulated ectopic beat and the threshold for such premature beats is higher than less premature beats, it is unlikely that TASER pulses can immediately initiate ventricular fibrillation in such individuals through the direct effect of the electric field generated through the heart by the TASER. In the absence of preexisting heart disease, the delayed development of ventricular fibrillation requires the electrical stimuli to cause electroporation or myocardial necrosis. However, the electrical thresholds for electroporation and necrosis are many times higher than that required to stimulate an ectopic beat. Therefore, it is highly unlikely that the TASER X26 can cause ventricular fibrillation minutes to hours after its use through direct cardiac effects of the electric field generated by the TASER.

Defibrillator Implantation Without Induction of Ventricular Fibrillation

An increasing number of cardiac electrophysiologists are fortunate not to have endured the challenges of implanting monophasic waveform cardioverter-defibrillators (ICDs). With early technology, ICDs were routinely tested during the implantation procedure and then again before discharge, with a not-infrequent need for system revisions. With transvenous, high-output devices and biphasic shocks, the number of patients who have an inadequate defibrillation safety margin (DSM) has become so small that questions have been raised about the need for testing at all. However, given the fact that ICDs are designed to be potentially lifesaving, it is incumbent on physicians to obtain a high level of assurance that the device will work as designed if needed. It also should be noted that all clinical trials of ICD therapy for the prevention of sudden cardiac death incorporated testing for the adequacy of the DSM. Article p 2382 Despite the fact that we usually call the sequence of induction of ventricular fibrillation (VF) and defibrillation at different energies in the electrophysiology laboratory “defibrillation threshold testing,” it is, in fact, usually a DSM that is determined.1 Particularly with the typical protocol of 2 defibrillations at a minimum of 10 J below the maximum output of the device, a true probability curve for defibrillation success cannot be constructed. Regardless, this protocol is well accepted in practice. An alternative approach is upper limit of vulnerability testing, which closely correlates with the defibrillation threshold.2 This method requires only 1 initiation of VF, but strictly performed, multiple shocks may need to be delivered before VF is induced and the energy corresponding to the upper limit of vulnerability is determined. In the present issue of Circulation , Day et al3 present the results of the Arrhythmia Single Shock Defibrillation Threshold Testing Versus Upper Limit of Vulnerability: Risk Reduction Evaluation (ASSURE) …

Precordial Thump in the Catheterization Laboratory Experimental Evidence for Commotio Cordis

HomeCirculationVol. 115, No. 11Precordial Thump in the Catheterization Laboratory Experimental Evidence for Commotio Cordis Free AccessReview ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessReview ArticlePDF/EPUBPrecordial Thump in the Catheterization Laboratory Experimental Evidence for Commotio Cordis Guillaume Cayla, MD, Jean Christophe Macia, MD and Jean Luc Pasquie, MD, PhD Guillaume CaylaGuillaume Cayla From the CHU Montpellier, Clinique du Cœur et Des Vaisseaux, Hôpital Arnaud de Villeneuve, Montpellier, France. Search for more papers by this author , Jean Christophe MaciaJean Christophe Macia From the CHU Montpellier, Clinique du Cœur et Des Vaisseaux, Hôpital Arnaud de Villeneuve, Montpellier, France. Search for more papers by this author and Jean Luc PasquieJean Luc Pasquie From the CHU Montpellier, Clinique du Cœur et Des Vaisseaux, Hôpital Arnaud de Villeneuve, Montpellier, France. Search for more papers by this author Originally published20 Mar 2007https://doi.org/10.1161/CIRCULATIONAHA.106.667725Circulation. 2007;115:e332A 57-year-old man was admitted to our institution for a diagnostic coronarography. During the right coronary injection (Iomeron 350, Altana Pharma, Le Mée sur Seine, France), complete atrioventricular block occurred for 3 seconds. A precordial thump was performed to restart cardiac activation. Unfortunately, the precordial thump occurred during repolarization of the first ventricular escape rhythm, resulting in ventricular fibrillation, which required external cardioversion. This is the first case documented of ventricular fibrillation initiation in a man by mild chest trauma. In commotio cordis—infrequent sudden death in young athletes caused by blunt chest trauma—ventricular fibrillation is induced by a light blow delivered at a wide range of velocities, as documented in an animal model.1 This tracing (Figure) is highly remarkable in that precordial thump, a common resuscitation maneuver, was responsible for commotio cordis, resulting in ventricular fibrillation that necessitated immediate cardioversion. Download figureDownload PowerPointDuring the RCA injection, the tracing exhibits blocked P waves followed by ventricular escape rhythm. The precordial thump resulted in a +30 mm Hg aortic pressure and incidentally occurred during the repolarization of the first beat of the escape rhythm in a phase of supervulnerability and induced ventricular fibrillation. P indicates p waves; ER, escape rhythm.DisclosuresNone.FootnotesCorrespondence to Jean Luc Pasquié, Clinique du Cœur et des Vaisseaux, Hôpital Arnaud de Villeneuve, Centre Hospitalier Universitaire, 34295 Montpellier Cedex 5, France. E-mail [email protected]Reference1 Link MS, Maron BJ, Wang PJ, VanderBrink BA, Zhu W, Estes NA 3rd. Upper and lower limits of vulnerability to sudden arrhythmic death with chest-wall impact (commotio cordis). J Am Coll Cardiol. 2003; 1: 99–104.Google Scholar Previous Back to top Next FiguresReferencesRelatedDetailsCited By Quinn T and Kohl P (2021) Cardiac Mechano-Electric Coupling: Acute Effects of Mechanical Stimulation on Heart Rate and Rhythm, Physiological Reviews, 10.1152/physrev.00036.2019, 101:1, (37-92), Online publication date: 1-Jan-2021. Quinn T and Kohl P (2016) Rabbit models of cardiac mechano-electric and mechano-mechanical coupling, Progress in Biophysics and Molecular Biology, 10.1016/j.pbiomolbio.2016.05.003, 121:2, (110-122), Online publication date: 1-Jul-2016. Quinn T (2013) The importance of non-uniformities in mechano-electric coupling for ventricular arrhythmias, Journal of Interventional Cardiac Electrophysiology, 10.1007/s10840-013-9852-0, 39:1, (25-35), Online publication date: 1-Jan-2014. Osorio J, Dosdall D, Tabereaux P, Robichaux R, Stephens S, Kerby J, Stickney R, Pogwizd S and Ideker R (2012) Effect of Chest Compressions on Ventricular Activation, The American Journal of Cardiology, 10.1016/j.amjcard.2011.10.024, 109:5, (670-674), Online publication date: 1-Mar-2012. Madias C, Maron B, Alsheikh-Ali A, Rajab M, Estes N and Link M (2009) Precordial thump for cardiac arrest is effective for asystole but not for ventricular fibrillation, Heart Rhythm, 10.1016/j.hrthm.2009.06.029, 6:10, (1495-1500), Online publication date: 1-Oct-2009. Nolan J and Soar J (2009) Defibrillation in clinical practice, Current Opinion in Critical Care, 10.1097/MCC.0b013e32832931cb, 15:3, (209-215), Online publication date: 1-Jun-2009. Osorio J, Dosdall D, Robichaux R, Tabereaux P and Ideker R (2008) In a Swine Model, Chest Compressions Cause Ventricular Capture and, By Means of a Long-Short Sequence, Ventricular Fibrillation, Circulation: Arrhythmia and Electrophysiology, 1:4, (282-289), Online publication date: 1-Oct-2008. March 20, 2007Vol 115, Issue 11 Advertisement Article InformationMetrics https://doi.org/10.1161/CIRCULATIONAHA.106.667725PMID: 17372182 Originally publishedMarch 20, 2007 PDF download Advertisement SubjectsArrhythmiasCardiopulmonary Resuscitation and Emergency Cardiac Care

Autonomic modulation of electrical restitution, alternans and ventricular fibrillation initiation in the isolated heart

Abnormal autonomic nerve activity is a strong prognostic marker for ventricular arrhythmias but the mechanisms underlying the autonomic modulation of ventricular fibrillation (VF) initiation are poorly understood. We examined the effects of direct sympathetic (SS) and vagus (VS) nerve stimulation on electrical restitution, alternans and VF threshold (VFT) in a novel isolated rabbit heart preparation with intact dual autonomic innervation. Monophasic Action Potentials (MAPs) were recorded from a left ventricular epicardial site on innervated, isolated rabbit hearts (n=16). Standard restitution, effective refractory period (ERP), electrical alternans and VFT were measured at baseline and during SS and VS separately. The restitution curve was shifted downwards and made steeper with SS whilst VS caused an upward shift and a flattening of the curve. The maximum slope of restitution was increased from 1.30+/-0.10 at baseline to 1.86+/-0.17 (by 45+/-12%, P<0.01) with SS and decreased to 0.69+/-0.10 (by 51+/-6%, P<0.001) with VS. ERP was decreased from 127.3+/-2.5 ms to 111.8+/-1.8 ms with SS (by 12+/-2%, P<0.001) and increased to 144.0+/-2.2 ms with VS (by 13+/-2%, P<0.001). VFT was decreased from 4.7+/-0.6 mA to 1.9+/-0.5 mA with SS (by 64+/-5%, P<0.001) and increased to 8.7+/-1.1 mA with VS (by 89+/-14%, P<0.0005). There was a significant inverse relationship between the maximum slope of restitution and VFT (r=-0.63, P<0.0001). When compared with baseline, SS caused electrical alternans at longer pacing cycle lengths (139.0+/-8.4 vs. 123.0+/-7.8 ms, P<0.01) with greater degree of alternans (32.5+/-9.9 vs. 15.4+/-3.2%, P<0.05). It also caused a wider range of cycle lengths where alternans occurred (53.0+/-6.2 vs. 41.0+/-7.0 ms, P<0.05) whilst vagus nerve stimulation shortened this range (33.0+/-7.3 ms, P<0.001). Sympathetic stimulation increased maximum slope of restitution and electrical alternans but decreased ERP and VF threshold whilst vagus nerve stimulation had opposite effects. The interaction between action potential duration and beat-to-beat interval may play an important role in the autonomic modulation of VF initiation.

The Microvolt T-Wave Alternans Test

Sudden cardiac death (SCD) still remains a major cause of mortality among patients with ischaemic and nonischaemic cardiomyopathy, and implantable cardioverter-defibrillator (ICD) therapy has been shown to improve survival in these patients. However, the use of a prophylactic ICD therapy in clinical practice needs accurate identification of patients likely to benefit from it, considering the high incidence of device-related complications, the psychological consequences of ICD implantation and social costs. Current risk stratification for SCD is mainly based on assessment of ejection fraction and it is strongly influenced by the largest clinical trials on primary prevention: the MADIT II and SCD-HeFT studies. In recent years, the microvolt T-wave alternans test (MTWA) is emerging as a powerful non-invasive tool for risk stratification of SCD. MWTA is a beat-to-beat alternation in the amplitude of the T wave on the order of microvolts, which can be assessed during an exercise test, pharmacological stress or atrial pacing. MTWA has been associated with unidirectional block, re-entry and initiation of ventricular fibrillation in animal studies. There is strong evidence that intracellular calcium cycling plays a key role in the mechanism of MTWA. Several large clinical trials have shown that MTWA is comparable or superior to other noninvasive markers and to electrophysiological study in risk stratification of SCD. The very high negative predictive value of MTWA may provide a better selection of patients who would be likely or not likely to benefit from ICD implantation. Broad evidence-based data suggest that non-invasive MTWA may improve the accuracy of primary prevention of SCD in patients with ischaemic and non-ischaemic cardiomyopathy. Further studies are needed to evaluate the role of MTWA testing as an integral part of risk stratification, in combination with additional risk markers.

Ventricular Fibrillation

Ventricular fibrillation (VF) is the leading cause of sudden cardiac death. This brief review addresses issues relevant to the dynamics of the rotors responsible for functional reentry and VF. It also makes an attempt to summarize present-day knowledge of the manner in which the dynamic interplay between inward and outward transmembrane currents and the heterogeneous cardiac structure establish a substrate for the initiation and maintenance of rotors and VF. The fragmentary nature of our current understanding of ionic VF mechanisms does not even allow an approach toward a "Theory of VF". Yet some hope is provided by recently obtained insight into the roles played in VF by some of the sarcolemmal ion channels that control the excitation-recovery process. For example, strong evidence supports the idea that the interplay between the rapid-inward sodium current and the inward-rectifier potassium current controls rotor formation, as well as rotor stability and frequency. Solid evidence also exists for an involvement of L-type calcium current in the control of rotor frequency and in determining VF-to-ventricular tachycardia conversion. Less clear, however, is whether or not time dependent outward currents through voltage-gated potassium channels affect the fibrillatory process. Hopefully, taking advantage of currently available approaches of structural, molecular and cellular biology, together with computational and imaging techniques, will afford us the opportunity to further advance knowledge on VF mechanisms.

Endocardial Electrograms From the Right Ventricular Outflow Tract After Induced Ventricular Fibrillation in Patients With Brugada Syndrome

The pathogenesis of Brugada syndrome (BS) is reported to be phase 2 reentry resulting from shortening of the action potential duration at the epicardial site of the right ventricular outflow tract (RVOT). However, several reports have shown a high incidence of ventricular late potentials (LPs) and a high rate of induction of ventricular fibrillation (VF) by programmed ventricular stimulation (PVS) among patients with BS. The aim of this study was to investigate the role of slow conduction for the initiation of VF by PVS in these patients. Endocardial mapping of the RVOT was conducted in 17 patients in whom VF was induced by PVS from the RV apex or RVOT; 11 patients had a positive LP. In 10 patients, RV mapping showed that low-amplitude fragmented and delayed potentials (DPs) were recorded at the RVOT below the pulmonary valve (PV) or between the PV and His bundle electrogram recording site. Electrograms recorded after PVS showed a high incidence of fractionated and disorganized DPs that lead to VF. Slow conduction at the RVOT may contribute to the induction of VF by PVS. However, the role of slow conduction in spontaneous VF remains controversial.

Influence of Drive Cycle Length on Initiation of Ventricular Fibrillation During Implantable Cardioverter Defibrillator Threshold Testing

Programmed electrical stimulation of the heart as a method to induce tachyarrhythmias has been described since the 1960s. To date, no study has examined optimal drive cycle length in the induction of ventricular fibrillation (VF) during defibrillation threshold testing after implantable cardioverter-defibrillator placement. We hypothesized that longer drive cycle length, by means of the longer action potential duration, would promote intramyocardial phase 2 reentry and facilitate induction of VF. Fifty consecutive implants were randomized in a prospective crossover format for this study. The group consisted of 40 men and 10 women, with each patient receiving either a 400 or 600 ms initial drive train prior to 1.2 J internal shock on the T wave with a goal to induce ventricular fibrillation. The timing of the T wave shock was determined by measuring the interval from the beginning of the QRS to the apex of the T wave in lead II. Successful inductions were defibrillated via the cardioverter defibrillator. Patients were then crossed over and the protocol repeated. Twenty of 23 (87%) patients were successfully induced into VF in the initial 400 ms drive train arm whereas 22 of 27 (81%) were successfully induced in the 600 ms arm. Thus, a total of 44 (88%) patients were successfully induced at 400 ms, 41 (82%) patients were successfully induced at 600 ms, and 2 (4%) patients were not inducible at either cycle length, but were inducible with 50 Hz ventricular stimulation. However, no significant difference was noted between the two groups. No investigation to date has questioned whether a relationship exists between drive cycle length and initiation of ventricular fibrillation. Our study addresses this question, though negative for difference between 400 and 600 ms drive trains. Further research into optimal strategies for inducing ventricular fibrillation will minimize patient sedation time and discomfort while undergoing defibrillator threshold testing.

Brain tissue oxygen pressure and cerebral metabolism in an animal model of cardiac arrest and cardiopulmonary resuscitation

Direct measurement of brain tissue oxygenation (PbtO2) is established during spontaneous circulation, but values of PbtO2 during and after cardiopulmonary resuscitation (CPR) are unknown. The purpose of this study was to investigate: (1) the time-course of PbtO2 in an established model of CPR, and (2) the changes of cerebral venous lactate and S-100B. In 12 pigs (12-16 weeks, 35-45 kg), ventricular fibrillation (VF) was induced electrically during general anaesthesia. After 4 min of untreated VF, all animals were subjected to CPR (chest compression rate 100/min, FiO2 1.0) with vasopressor therapy after 7, 12, and 17 min (vasopressin 0.4, 0.4, and 0.8 U/kg, respectively). Defibrillation was performed after 22 min of cardiac arrest. After return of spontaneous circulation (ROSC), the pigs were observed for 1h. After initiation of VF, PbtO2 decreased compared to baseline (mean +/- SEM; 22 +/- 6 versus 2 +/- 1 mmHg after 4 min of VF; P < 0.05). During CPR, PbtO2 increased, and reached maximum values 8 min after start of CPR (25 +/- 7 mmHg; P < 0.05 versus no-flow). No further changes were seen until ROSC. Lactate, and S-100B increased during CPR compared to baseline (16 +/- 2 versus 85 +/- 8 mg/dl, and 0.46 +/- 0.05 versus 2.12 +/- 0.40 microg/l after 13 min of CPR, respectively; P < 0.001); lactate remained elevated, while S-100B returned to baseline after ROSC. Though PbtO2 returned to pre-arrest values during CPR, PbtO2 and cerebral lactate were lower than during post-arrest reperfusion with 100% oxygen, which reflected the cerebral low-flow state during CPR. The transient increase of S-100B may indicate a disturbance of the blood-brain-barrier.

Ventricular Fibrillation Induced by Stretch Pulse: Implications for Sudden Death Due to Commotio Cordis

Nonpenetrating chest wall impact (commotio cordis) may lead to sudden cardiac death due to the acute initiation of ventricular fibrillation (VF). VF may result from sudden stretch during a vulnerable window, which is determined by repolarization inhomogeneity. We examined action potential morphologies and VF inducibility in response to sudden myocardial stretch in the left ventricle (LV). In six Langendorff perfused rabbit hearts, the LV was instrumented with a fluid-filled balloon. Increasing volume and pressure pulses were applied at different times of the cardiac cycle. Monophasic action potentials (MAPs) were recorded simultaneously from five LV epicardial sites. Inter-site dispersion of repolarization was calculated in the time and voltage domains. Sudden balloon inflation induced VF when pressure pulses of 208-289 mmHg were applied within a window of 35-88 msec after MAP upstroke, a period of intrinsic increase in repolarization dispersion. During the pressure pulse, MAPs revealed an additional increase in repolarization dispersion (time domain) by 9 +/- 6 msec (P < 0.01). The maximal difference in repolarization levels (voltage domain) between sites increased from 19 +/- 3% to 26 +/- 3% (P < 0.05). Earliest stretch-induced activation was observed near a site with early repolarization, while sites with late repolarization showed delayed activation. Sudden myocardial stretch can elicit VF when it occurs during a vulnerable window that is based on repolarization inhomogeneity. Stretch pulses applied during this vulnerable window can lead to nonuniform activation. Repolarization dispersion might play a crucial role in the occurrence of fatal tachyarrhythmias during commotio cordis.

Outcomes of In-Hospital Ventricular Fibrillation in Children

Ventricular fibrillation and ventricular tachycardia are less common causes of cardiac arrest in children than in adults. These tachyarrhythmias can also begin during cardiopulmonary resuscitation (CPR), presumably as reperfusion arrhythmias. We determined whether the outcome is better for initial than for subsequent ventricular fibrillation or tachycardia. All cardiac arrests in persons under 18 years of age were identified from a large, multicenter, in-hospital cardiac-arrest registry. The results from children with initial ventricular fibrillation or tachycardia, children in whom ventricular fibrillation or tachycardia developed during CPR, and children with no ventricular fibrillation or tachycardia were compared by chi-square and multivariable logistic-regression analysis. Of 1005 index patients with in-hospital cardiac arrest, 272 (27 percent) had documented ventricular fibrillation or tachycardia during the arrest. In 104 patients (10 percent), ventricular fibrillation or tachycardia was the initial pulseless rhythm; in 149 patients (15 percent), it developed during the arrest. The time of initiation of ventricular fibrillation or tachycardia was not documented in 19 patients. Thirty-five percent of patients with initial ventricular fibrillation or tachycardia survived to hospital discharge, as compared with 11 percent of patients with subsequent ventricular fibrillation or tachycardia (odds ratio, 2.6; 95 percent confidence interval, 1.2 to 5.8). Twenty-seven percent of patients with no ventricular fibrillation or tachycardia survived to hospital discharge, as compared with 11 percent of patients with subsequent ventricular fibrillation or tachycardia (odds ratio, 3.8; 95 percent confidence interval, 1.8 to 7.6). In pediatric patients with in-hospital cardiac arrests, survival outcomes were highest among patients in whom ventricular fibrillation or tachycardia was present initially than among those in whom it developed subsequently. The outcomes for patients with subsequent ventricular fibrillation or tachycardia were substantially worse than those for patients with asystole or pulseless electrical activity.

P5-26: A novel approach to study the ionic mechanism of action potential duration restitution and its memory effect

The adaptation of action potential duration (APD) during fast pacing and rate changes plays a critical role in the development of ventricular fibrillation (VF). APD restitution slope has been used to explain the initiation and maintenance of VF via alternans. However, different pacing protocols result in different APD restitution curves, a phenomenon known as APD memory. The ionic mechanism of APD rate dependency (APD restitution and its memory effect), as well as the contribution of gating variables and ion concentrations to APD rate dependency, are still not clear.

Catheter Ablation of Ventricular Fibrillation Storm in Patients with Infiltrative Amyloidosis of the Heart

Recent studies have demonstrated that premature ventricular contractions (PVCs) originating from the Purkinje system are responsible for initiation of ventricular fibrillation (VF) in patients with and without structural heart disease. Ablation of the PVCs has been shown to be feasible. We report 2 patients with repetitive VF associated with cardiac amyloidosis. Each episode of ventricular arrhythmia was preceded by monomorphic PVC. The electrical storms were drug resistant. Electrophysiological testing was performed and the sites of earliest activation were localized within the left ventricle in the absence of significant scar tissue. After ablation, PVCs subsided and there were no further VF recurrences.

Diurnal Variation in QT Dispersion in Patients With Chronic Heart Failure

QT dispersion is defined as the difference in QT interval among the different leads of the standard 12-lead electrocardiogram and reflects inhomogeneity of myocardial repolarization. Dispersion of repolarization is an important electrophysiologic feature that is considered fundamental for the initiation of ventricular fibrillation. However, no data exist regarding the diurnal variation of QT dispersion measured from simultaneous 12-lead recording in chronic heart failure patients. The aim of this study was to identify diurnal variation in QT dispersion in patients with chronic heart failure. QT dispersion was measured in the 12-lead standard electrocardiogram in 11 patients with chronic heart failure. QT dispersion in these patients was increased in the afternoon compared to the morning. It is concluded that QT dispersion has a clear diurnal variation in patients with chronic heart failure. These findings have potentially significant implications for therapy and prevention of sudden cardiac death in patients with chronic heart failure.

Runaway Pacemakers in Ventricular Fibrillation

Arunaway pacemaker is a malfunctioning pacemaker that paces the heart at rapid rates. A report from Australia 30 years ago1 described a patient with runaway pacemaker that paced the ventricles at 280 bpm. The patient survived only because one of the coauthors alertly cut the pacemaker wires to disconnect the high-frequency focal source from the myocardium. In this issue of Circulation , Thomas et al2 report that they occasionally detected sustained high-frequency sources during ventricular fibrillation (VF) in sheep with myocardial infarction (MI). Specifically, in 3 of 12 hearts, they detected periodic high-frequency activations at 1.3% of the intramural electrodes sampled. The authors propose that these findings support the hypothesis3 that a relatively stable periodic source (“mother rotor”), with fibrillatory conduction block occurring in the remainder of the ventricle, may be the mechanism of VF in this model. This mother rotor mechanism of fibrillation contrasts with the multiple wavelet mechanism, in which all rotors are unstable and wavebreak is the engine driving fibrillation. Both mechanisms of fibrillation have been documented in various settings,4 but controversy exists over which is the most common in and clinically relevant to diseased human hearts. This issue has therapeutic implications because it has been suggested that ablation of the mother rotor may be a strategy to abolish VF. At the same time, ablation of the mother rotor may just allow the next-fastest daughter rotor to take its place because fibrillatory wavebreaks act as niduses for new rotors. In any case, however, to even test this intriguing therapeutic strategy, it is first necessary to identify the location of the mother rotor, which has been elusive to date, especially in large animals.5 The findings of the present study, in a large-animal diseased heart model, are therefore significant. They also raise important questions. …

Delay in right ventricular activation contributes to Brugada syndrome-electrophysiological and pathological study-

Pathogenesis of Brugada syndrome (BS) has been reported to be phase 2 reentry based on the shortening of action potential at the epicardial site of right ventricular (RV) outflow tract (RVOT). However, several reports showed that BS had high incidence of ventricular late potential (LP) and high induction rate of ventricular fibrillation (VF) by programmed ventricular stimulation (PVS). The aim of this study was to investigate the role of slow conduction at the RVOT for the initiation of VF by PVS in BS and underlying pathological findings.

The role of action potential duration restitution in vulnerability to reentry in a mathematical model of canine ventricle

The mechanism of initiation of ventricular fibrillation (VF) in normal and diseased heart is poorly understood. It has been shown that VF starts with a simple reentry, or ventricular tachycardia (VT), which then degenerates into the multiple meandering wavelets that characterize VF. Although a steeply-sloped action potential duration restitution (APDR) curve promotes the transition of VT to VF, its role in the initiation of reentry is less clear. We performed a comprehensive study using a detailed anatomic model of the canine heart to investigate the role of APDR in initiating reentry by a single extrastimulus (S2). In normal heart, S2 beats failed to initiate reentry with either steep or flat APDR. However, when diseased heart was simulated by adding an ischemic region (modeled by lowered excitability due to increased extracellular potassium), reentry was more easily induced by an S2 when APDR slope was steep (left figure). Flattening APDR reduced the “vulnerability window,” defined as the set of S2 intervals for which reentry was induced (right figure, black bars), from 60msec to 30msec. (White bars indicate that a propagated beat was initiated by S2 without reentry, gray bars indicate that the S2 beat failed to propagate). Flattening APDR may therefore be a promising therapy for preventing both initiation of reentry and the subsequent transition from VT to VF.

The duration of ventricular fibrillation required to produce pulseless electrical activity

The duration of untreated (no cardiopulmonary resuscitation) ventricular fibrillation (VF) needed to produce postdefibrillation pulseless electrical activity (PEA) was determined in 9 anesthetized swine ranging in weight from 20 to 30 kg. VF was induced electrically by a right ventricular catheter electrode, while arterial pressure and the electrocardiogram were recorded. VF was confirmed by the presence of VF waves in the electrocardiogram and a loss of pulsatile arterial pressure. VF was allowed to persist for 15-second increments (eg, 15, 30, 45, etc), after which defibrillation was achieved with transchest electrodes and the presence or absence of PEA was noted. If PEA was present, rhythmic chest compressions were applied to rescue the animal. Just after initiation of VF and just before defibrillation, VF wave frequency was measured. PEA was encountered in 100% of the trials after 180 seconds of VF. The threshold duration for PEA was 60 seconds. VF wave frequency decreased with the passage of time. At VF initiation, VF wave frequency ( f 0) ranged from 6 to 15 per second, with a mean of 10.1 ± 2.1 per second. At 180 seconds ( f 180), the mean frequency was 4.0 ± 0 per second. It was only possible to eliminate PEA and restore pumping in 1 animal when untreated VF lasted more than 180 seconds. There was no clear transition in the frequency of the VF waves with the passage of time that could predict the possibility of postdefibrillation PEA. Moreover, because of the different initial VF wave frequencies and the different rates of decrease with time, a measurement of VF wave frequency is unlikely to be informative on how long VF had been present. A consistent finding in this swine study of prolonged untreated VF was a rise in blood K + which increased from a normal prefibrillation value of about 4 mEq/L to 8 to 12 mEq/L at 180 seconds. The longer the duration of VF, the higher the K +.

A Catheter Ablation Approach to Treat VF Storms in Select Patients

Premature ventricular contractions (PVCs) in the Purkinje system have been implicated in the initiation of ventricular fibrillation (VF) in patients

Mode of initiation and ablation of ventricular fibrillation storms in patients with ischemic cardiomyopathy

ObjectivesWe report on the initiation of ventricular fibrillation (VF) storm in patients with ischemic cardiomyopathy (ICM) and the results of targeted ablation to treat VF storm. BackgroundMonomorphic premature ventricular contractions (PVCs) have been shown to initiate VF in patients without structural heart disease. MethodsA total of 29 patients with ICM and documented VF initiation were identified. In 21 patients, VF storm was controlled with antiarrhythmic drugs and/or treatment of heart failure. Eight patients with VF (mean 52 ± 25 episodes) refractory to medical management required ablation. All patients underwent three-dimensional electroanatomical mapping using CARTO (Biosense-Webster Inc., Diamond Bar, California), and PVCs were mapped when present. Scarred areas were identified using voltage mapping. ResultsMonomorphic PVCs initiated VF in all 29 identified patients. Five of eight patients requiring ablation had frequent PVCs that allowed PVC mapping. The earliest activation site was consistently located in the scar border zone. The PVCs were always preceded by a Purkinje-like potential (PLP). Ablation was successfully performed at these sites. In three patients, infrequent PVCs prevented mapping, but PLPs were recorded around the scar border. Ablation targeting these potentials along the scar border was successfully performed. During follow-up (10 ± 6 months), one patient had a single VF episode and another developed sustained, monomorphic ventricular tachycardia. There was no recurrence of VF storm. ConclusionsVentricular fibrillation in ICM is triggered by monomorphic PVCs originating from the scar border zone with preceding PLPs; targeting these PVCs may prevent VF recurrence. In the absence of PVCs, both substrate mapping and ablation appear to be equally effective.