Initiation Of Ventricular Fibrillation Research Articles

Paradoxical nocturnal elevation of sympathetic tone and spontaneous ventricular fibrillation in Brugada syndrome

BackgroundNocturnal dominance of the incidence of spontaneous ventricular tachyarrhythmias has been reported in patients with Brugada syndrome (BrS). The purpose of the present study is to analyze the QT dynamics and autonomic balance as well as their diurnal variations in BrS patients. MethodsOf the 33 consecutive patients with BrS included in the study, 14 had a history of cardiopulmonary arrest due to spontaneous ventricular fibrillation (VF) episodes (VF-BrS) and 19 had asymptomatic BrS (A-BrS). QT dynamics and heart rate variability were analyzed using 24-h Holter electrocardiogram recordings. ResultsOf the total 14 first cardiopulmonary arrest episodes due to spontaneous VF, 11 (79%) occurred in VF-BrS patients during the nighttime or at rest. The QT/RR slope during daytime was significantly steeper than that during nighttime in the A-BrS patients (p=0.031), but not in the VF-BrS patients (p=1.0). There were significant diurnal differences pertaining to the high-frequency (HF) and low-frequency (LF)/HF ratios in the A-BrS patients (p=0.019 and p=0.019, respectively), but not in the VF-BrS patients (p=1.0 and p=1.0, respectively). The VF-BrS patients were characterized by relatively high LF/HF ratios, whereas the A-BrS patients were characterized by relatively low LF/HF ratios throughout the daytime and nighttime. Furthermore, the LF/HF ratios during the nighttime in the VF-BrS patients were significantly higher than those in the A-BrS patients (p=0.021). ConclusionsMost first episodes of spontaneous VF in the VF-BrS patients occurred during the nighttime or at rest. The autonomic imbalance of paradoxical nocturnal elevation of the sympathetic tone along with an underlying persistent sympathetic tone throughout the day may play a key role for spontaneous VF initiation in BrS patients.

The effects of remodeling with heart failure on mode of initiation of ventricular fibrillation and its spatiotemporal organization.

The effect of the heart failure substrate on the initiation of ventricular fibrillation (VF) and its resulting mechanism is not known. The objective of this study was to determine the effects of substrate on VF initiation and its spatiotemporal organization in the heart failure model. Optical action potentials were recorded from LV wedge preparations either from structurally normal hearts (control, n = 11) or from congestive heart failure (CHF; n = 7), at the epicardial surface, endocardial surface which included a papillary muscle, and a transmural cross section. Action potential duration (APD(80)) was determined, and VF was initiated. A fast Fourier transform was calculated, and the dominant frequency (DF) was determined. The CHF group showed increased VF vulnerability (69 vs 26 %, p < 0.03), and every mapped surface showed an APD(80) gradient which included islands of higher APDs on the transmural surface (M cells) which was not observed in controls. VF in the CHF group was characterized by stable, discrete, high-DF areas that correlated to either foci or spiral waves located on the transmural surface at the site of the papillary muscle. Overall, the top 10 % of DFs correlated to an APD of 101 ms while the bottom 10 % of DFs correlated to an APD of 126 ms (p < 0.01). In the CHF model, APD gradients correlated with an increased vulnerability to VF, and the highest stable DFs were located on the transmural surface which was not seen in controls. This indicates that the CHF substrate creates unique APD and DF characteristics.

Optical Mapping of Ventricular Fibrillation Dynamics.

There is very limited information regarding the dynamic patterns of the electrical activity during ventricular fibrillation (VF) in humans. Most of the data used to generate and test hypotheses regarding the mechanisms of VF come from animal models and computer simulations and the quantification of VF patterns is non-trivial. Many of the experimental recordings of the dynamic spatial patterns of VF have been obtained from mammals using "optical mapping" or "video imaging" technology in which "phase maps" are derived from high-resolution transmembrane recordings from the heart surface. The surface manifestation of the unstable reentrant waves sustaining VF can be identified as "phase singularities" and their number and location provide one measure of VF complexity. After providing a brief history of optical mapping of VF, we compare and contrast a quantitative analysis of VF patterns from the heart surface for four different animal models, hence providing physiological insight into the variety of VF dynamics among species. We found that in all four animal models the action potential duration restitution slope was actually negative during VF and that the spatial dispersion of electrophysiological parameters were not different during the first second of VF compared to pacing immediately before VF initiation. Surprisingly, our results suggest that APD restitution and spatial dispersion may not be essential causes of VF dynamics. Analyses of electrophysiological quantities in the four animal models are consistent with the idea that VF is essentially a two-dimensional phenomenon in small rabbit hearts whose size are near the boundary of the "critical mass" required to sustain VF, while VF in large pig hearts is three-dimensional and exhibits the maximal theoretical phase singularity density, and thus will not terminate spontaneously.

Is hands-on defibrillation safe when using insulating gloves? A clinical trial

Introduction: Surface electrocardiographic (ECG) changes in ventricular fibrillation (VF) waveform characteristics at its onset in patients experiencing cardiac arrest have not been quantified. The amplitude spectral area (AMSA)methodwas developed to analyze surface ECG VF amplitude and frequency characteristics and contains information related to VF rotor stability and myocardial viability. We aimed to characterize changes in AMSA at the onset of VF to gain insight into myocardial dynamics in patients with a wearable cardioverter defibrillator (WCD). Methods: Out of 30 patients randomly identified from a manufacturer-maintained registry, 25 patients (14 Male, 11 Female, Age=62±14 yr) were included. Remaining patients experienced either sustained monomorphic ventricular tachycardia or hadmotion artifact, precludingAMSAanalysis. Using theWCDECG, AMSA was calculated as the summed product of frequency and square root of power at that frequency from 2 to 48Hz with a continuous sliding 2.1 s Tukey window. The median time to shock for the WCD is 45 s. AMSA was calculated every 0.5 s and averaged every 1 s for up to 45 s after VF initiation. Results are presented as mean± standard error. Results: At onset of VF, AMSA was 33.6±3.3mVHz which decreased progressively to 23.4±2.2mVHz (p<0.01) after 45 sec of untreated VF (Fig. 1).

Dynamic alterations of connexin43, matrix metalloproteinase-2 and tissue inhibitor of matrix metalloproteinase-2 during ventricular fibrillation in canine

The aim of this study is to investigate the dynamic alterations of cardiac connexin 43 (Cx43), matrix metalloproteinase-2 (MMP-2) and tissue inhibitor of metalloproteinase-2 (TIMP-2) in the setting of different ventricular fibrillation (VF) duration. In this study, thirty-two dogs were randomly divided into sham control group, 8-min VF group, 12-min VF group, and 30-min VF group. Cx43 and phosphorylated Cx43 (p-Cx43) in tissues were detected by western blot and immunofluorescence analysis. MMP-2 and TIMP-2 were detected by western blot and immunohistochemistry analysis. The results showed that Cx43 levels in three VF groups were significantly decreased compared with sham control group. p-Cx43 levels in 12-min and 30-min VF groups were significantly reduced compared with sham control group. The ratio of p-Cx43/Cx43 was also decreased in VF groups. Compared with sham controls, no significant difference was observed between the sham control group and 8-min VF group in MMP-2 level, but MMP-2 level increased in 12-min and 30-min VF groups. The ratios of MMP-2/TIMP-2 were higher in VF groups, and were correlated with the duration of VF. A remarkable correlation was observed between the ratio of p-Cx43/Cx43 and MMP-2/TIMP-2 (r = -0.93, P < 0.01). In conclusion, the alteration of Cx43 and/or p-Cx43 levels and the imbalance of MMP-2 and TIMP-2 may contribute to the initiation and/or persistence of VF. Maneuvers managed to modulate Cx43 level or normalize the balance of MMP-2/TIMP-2 are promising to ameliorate prognosis of VF.

Initiation of Ventricular Fibrillation by a Single Ectopic Beat in Three Dimensional Numerical Models of Ischemic Heart Disease: Abrupt Transition to Chaos

Background: To explore the conditions most dangerous for the emergence of sustained Ventricular Tachycardia or Ventricular Fibrillation (VT/VF) a new computational model of ventricular myocardium including 2592 finite elements in three dimensions was created. Methods: The fully three dimensional model of right and left ventricular muscle was used to simulate the spread of electrical activation and the resulting electrocardiogram. Localized zones of ischemic muscle tissue were characterized by reduced conduction velocity and reduced refractory period, and VT/VF was initiated by single ectopic beats. The simulated body surface Electrocardiogram (ECG) was also computed. Results: In this system clinically realistic VT/VF is readily produced by single stimuli. Reduced conduction velocity and reduced effective refractory period in localized abnormal muscle predispose to VT/VF. Transition to chaos was abrupt. No one specific pattern of re-entry, spiral waves, or vortices could be identified that later decomposed into VT/VF. Instead, there was a wide variety of activation patterns leading to chaos, depending sensitively on initial conditions. Nonetheless, a clear border between stable vs. chaotic behavior was defined by a critical threshold impulse wavelength, the product of conduction velocity and refractory period, γ*, in local ischemic tissue. This threshold, separating stable and chaotic regimes, can be specified precisely as γ*=FV1/3 , where V is the local volume of diseased tissue and 0 γ F γ 1 is a shape factor, near 1 for compact volumes and progressively smaller for flattened volumes. When the impulse wavelength is ≤γ*, VT/VF happens. Typical values for γ* range from 1 to 3 cm. Such behavior is characteristic of classical chaotic systems. Conclusions: The patterns of muscle activation leading to self-sustaining VT/VF observed in three dimensional diseased hearts are much more complex and variable than traditional re-entry in two dimensions. Instead a model of abrupt transition to chaos emerges from the application of first-principles cardiac electrophysiology, realistic ventricular anatomy, and the pathophysiology of ischemic cardiac muscle. This phenomenon may represent a higher order form of mathematical chaos than has been previously studied.

Suppression of ventricular fibrillation by electrical modification of the Purkinje system in hypertrophic cardiomyopathy

A 56-year-old man in hypertrophic cardiomyopathy had an electrical storm caused by ventricular fibrillation (VF). Mapping during the initiation of the VF triggered by a premature ventricular contraction (PVC1), with right bundle branch block (RBBB)-like morphology and superior axis, demonstrated a prominent Purkinje-muscle junction (PMJ) delay at the distal portion of the left posterior fascicle. Delivery of radiofrequency (RF) energy to this area abolished the VF triggered by the PVC1. However, VF emerged by triggering another PVC (PVC2) with RBBB-like morphology and inferior axis. Similarly, the initiation of VF was associated with the PMJ delay at the peripheral left anterior fascicle, where RF delivery completely suppressed the VF. The PMJ delay and subsequent Purkinje-muscle reentry-like activity could be essential for the initiation of the Purkinje-related VF.

Vagal modulation of cardiac ventricular arrhythmia

What is the topic of this review? This article addresses the relationship between vagus nerve activity and malignant ventricular arrhythmias. It focuses on the clinical association of an impaired vagal tone in cardiac disease states with high mortality from sudden cardiac death and the potential underlying mechanisms. What advances does it highlight? The article summarizes the mounting evidence that vagal innervation in the cardiac ventricle plays a key direct role in the prevention of the initiation of ventricular fibrillation. Data are presented on the role that nitric oxide plays in mediating the effects of vagal protection against ventricular fibrillation, supporting the notion that a separate non-muscarinic, nitrergic population of vagal neurons is responsible for this protection. Sudden cardiac death remains a significant unresolved clinical problem, with many of the deaths being due to malignant ventricular arrhythmias. Markers of abnormal autonomic function have been shown to be strong prognostic predictors, highlighting the important relationship between reduced vagal tone and malignant ventricular arrhythmias, such as ventricular fibrillation, in cardiac patients. Exploring the mechanisms underlying the autonomic modulation of ventricular fibrillation, my group has shown that vagus nerve stimulation protects against ventricular fibrillation in the innervated isolated heart preparation. We have provided direct evidence that nitric oxide is released in the ventricle with cervical vagus nerve stimulation and NO mediates the antifibrillatory actions of vagus nerve stimulation in the ventricle. Classical physiology teaches that vagal postganglionic nerves modulate the heart via acetylcholine acting at muscarinic receptors and, dogmatically, that there is little vagal effect in the ventricle, as innervation was believed to be sparse. Mounting evidence from many species now supports the presence of a rich vagal innervation in the ventricle. Data from my group showing that the protective actions of vagus nerve stimulation against ventricular fibrillation and NO release are preserved in the presence of muscarinic block support the notion that a population of nitrergic neurons could be responsible. This potentially exploitable downstream pathway together with the availability of vagus nerve stimulators make it an exciting time to investigate the development of an effective strategy of vagal protection against ventricular fibrillation in the clinical setting.

Defibrillation success with high frequency electric fields is related to degree and location of conduction block

We recently demonstrated that high frequency alternating current (HFAC) electric fields can reversibly block propagation in the heart by inducing an oscillating, elevated transmembrane potential (Vm) that maintains myocytes in a refractory state for the field duration and can terminate arrhythmias, including ventricular fibrillation (VF). To quantify and characterize conduction block (CB) induced by HFAC fields and to determine whether the degree of CB can be used to predict defibrillation success. Optical mapping was performed in adult guinea pig hearts (n = 14), and simulations were performed in an anatomically accurate rabbit ventricular model. HFAC fields (50-500 Hz) were applied to the ventricles. A novel power spectrum metric of CB-the loss of spectral power in the 1-30 Hz range, termed loss of conduction power (LCP)-was assessed during the HFAC field and compared with defibrillation success and VF vulnerability. LCP increased with field strength and decreased with frequency. Optical mapping experiments conducted on the epicardial surface showed that LCP and the size of CB regions were significantly correlated with VF initiation and termination. In simulations, subsurface myocardial LCP and CB sizes were more closely correlated with VF termination than surface values. Multilinear regression analysis of simulation results revealed that while CB on both the surface and the subsurface myocardium was predictive, subsurface myocardial CB was the better predictor of defibrillation success. HFAC fields induce a field-dependent state of CB, and defibrillation success is related to the degree and location of the CB.

DYNAMIC ALTERATIONS OF CONNEXIN 43, MATRIX METALLOPROTEINASE-2 AND TISSUE INHIBITOR OF MATRIX METALLOPROTEINASE-2 DURING VENTRICULAR FIBRILLATION IN DOGS

ObjectivesWe aimed to investigate the dynamic alterations of cardiac connexin 43 (Cx 43), matrix metalloproteinase-2 (MMP-2) and tissue inhibitor of metalloproteinase-2 (TIMP-2) in the setting of different ventricular fibrillation (VF)...

Intracellular Calcium Dynamics, Shortened Action Potential Duration, and Late‐Phase 3 Early Afterdepolarization in Langendorff‐Perfused Rabbit Ventricles

To elucidate the mechanism of late-phase 3 early after depolarization (EAD) in ventricular arrhythmogenesis, we hypothesized that intracellular calcium (Ca(i) ) overloading and action potential duration (APD) shortening may promote late-phase 3 EAD and triggered activity, leading to development of ventricular fibrillation (VF). In isolated rabbit hearts, we performed microelectrode recording and simultaneous dual optical mapping of transmembrane potential (V(m) ) and Ca(i) transient on left ventricular endocardium. An I(KATP) channel opener, pinacidil, was used to abbreviate APD. Rapid pacing was then performed. Upon abrupt cessation of rapid pacing with cycle lengths of 60-200 milliseconds, there were APD(90) prolongation and the corresponding Ca(i) overloading in the first postpacing beats. The duration of Ca(i) transient recovered to 50% (DCaT(50) ) and 90% (DCaT(90) ) in the first postpacing beats was significantly longer than baseline. Abnormal Ca(i) elevation coupled with shortened APD produced late-phase 3 EAD induced triggered activity and VF. In additional 6 preparations, the heart tissues were treated with BAPTA-AM, a calcium chelator. BAPTA-AM significantly reduced the maximal Ca(i) amplitude (26.4 ± 3.5% of the control; P < 0.001) and the duration of Ca(i) transients in the mapped region, preventing the development of EAD and triggered activity that initiated VF. I (KATP) channel activation along with Ca(i) overloading are associated with the development of late-phase 3 EAD and VF. Because acute myocardial ischemia activates the I(KATP) channel, late-phase 3 EADs may be a mechanism for VF initiation during acute myocardial ischemia.

Oscillation in Cycle Length Induces Transient Discordant and Steady-State Concordant Alternans in the Heart

Alternans is a beat-to-beat alternation of the cardiac action potential duration (APD) or intracellular calcium (Cai) transient. In cardiac tissue, alternans can be spatially concordant or discordant, of which the latter has been shown to increase dispersion of repolarization and promote a substrate for initiation of ventricular fibrillation. Alternans has been studied almost exclusively under constant cycle length pacing conditions. However, heart rate varies greatly on a beat-by-beat basis in normal and pathological conditions. The purpose of this study was to determine if applying a repetitive but non-constant pacing pattern, specifically cycle length oscillation (CLO), promotes or suppresses a proarrhythmic substrate. We performed computational simulations and optical mapping experiments to investigate the potential consequences of CLO. In a single cell computational model, CLO induced APD and Cai alternans, which became “phase-matched” with the applied oscillation. As a consequence of the phase-matching, in one-dimensional cable simulations, neonatal rat ventricular myocyte monolayers, and isolated adult guinea pig hearts CLO could transiently induce spatial and electromechanical discordant alternans followed by a steady-state of concordance. Our results demonstrated that under certain conditions, CLO can initiate ventricular fibrillation in the isolated hearts. On the other hand, CLO can also exert an antiarrhythmic effect by converting an existing state of discordant alternans to concordant alternans.

Electronic Control Devices

The use of deadly force by law enforcement personnel is a hot-button issue in contemporary society. Their responsibility is to handle life-threatening situations while, as much as possible, avoiding fatalities or serious injuries of suspects, bystanders, or themselves. In these settings, the use of lethal weapons must be weighed against reactions to circumstances that do not pose an imminent threat of a fatal outcome. Moreover, use of intense physical restraint instead of lethal weapons in less ominous situations is not without risk either, in that fatal events due to asphyxia have occurred as an unintended consequence of this nonlethal control strategy. In addition, the decision whether deployment of a lethal weapon, as opposed to physical restraint, is the proper action in a specific confrontation often must be made quickly, leaving little time for assessing options. Article see p 2417 The development of electronic control devices (ECDs), or stun guns, emerged as an alternative strategy, allegedly effective for controlling a threatening confrontation without resorting to needless serious injuries or fatalities. In principle, the ECD is more forgiving of errors of judgment than a firearm. The ECD is designed to deliver a painful and physically disabling electric shock, temporarily incapacitating a threatening individual. Although a significant number of deaths in association with, or following the use of, ECDs have been cited in a lay publication,1 peer-reviewed literature on the topic has been limited to several case reports, largely in the form of letters to the editors of journals.2 However, associations or correlations, in the absence of extremely strong population-based hazard ratios,3 are inadequate to support a scientific conclusion of causation, without additional information supporting the likelihood of a direct causal relation in an individual case. Data limited to a few case reports make it difficult to provide informed statements …

Spontaneous Ventricular Fibrillation in Right Ventricular Failure Secondary to Chronic Pulmonary Hypertension

Right ventricular failure (RVF) in pulmonary hypertension (PH) is associated with increased incidence of sudden death by a poorly explored mechanism. We test the hypothesis that PH promotes spontaneous ventricular fibrillation (VF) during a critical post-PH onset period characterized by a sudden increase in mortality. Rats received either a single subcutaneous dose of monocrotaline (MCT, 60 mg/kg) to induce PH-associated RVF (PH, n=24) or saline (control, n=17). Activation pattern of the RV-epicardial surface was mapped using voltage-sensitive dye in isolated Langendorff-perfused hearts along with single glass-microelectrode and ECG-recordings. MCT-injected rats developed severe PH by day 21 and progressed to RVF by approximately day 30. Rats manifested increased mortality, and ≈30% rats died suddenly and precipitously during 23-32 days after MCT. This fatal period was associated with the initiation of spontaneous VF by a focal mechanism in the RV, which was subsequently maintained by both focal and incomplete reentrant wave fronts. Microelectrode recordings from the RV-epicardium at the onset of focal activity showed early afterdepolarization-mediated triggered activity that led to VF. The onset of the RV cellular triggered beats preceded left ventricular depolarizations by 23±8 ms. The RV but not the left ventricular cardiomyocytes isolated during this fatal period manifested significant action potential duration prolongation, dispersion, and an increased susceptibility to depolarization-induced repetitive activity. No spontaneous VF was observed in any of the control hearts. RVF was associated with significantly reduced RV ejection fraction (P<0.001), RV hypertrophy (P<0.001), and RV fibrosis (P<0.01). The hemodynamic function of the LV and its structure were preserved. PH-induced RVF is associated with a distinct phase of increased mortality characterized by spontaneous VF arising from the RV by an early afterdepolarization-mediated triggered activity.

Postpacing abnormal repolarization in catecholaminergic polymorphic ventricular tachycardia associated with a mutation in the cardiac ryanodine receptor gene

Catecholaminergic polymorphic ventricular tachycardia (CPVT) is an arrhythmogenic disease for which electrophysiological studies (EPS) have shown to be of limited value. This study presents a CPVT family in which marked postpacing repolarization abnormalities during EPS were the only consistent phenotypic manifestation of ryanodine receptor (RyR2) mutation carriers. The study was prompted by the observation of transient marked QT prolongation preceding initiation of ventricular fibrillation during atrial fibrillation in a boy with a family history of sudden cardiac death (SCD). Family members underwent exercise and pharmacologic electrocardiographic testing with epinephrine, adenosine, and flecainide. Noninvasive clinical test results were normal in 10 patients evaluated, except for both epinephrine- and exercise-induced ventricular arrhythmias in 1. EPS included bursts of ventricular pacing and programmed ventricular extrastimulation reproducing short-long sequences. Genetic screening involved direct sequencing of genes involved in long QT syndrome as well as RyR2. Six patients demonstrated a marked increase in QT interval only in the first beat after cessation of ventricular pacing and/or extrastimulation. All 6 patients were found to have a heterozygous missense mutation (M4109R) in RyR2. Two of them, presenting with aborted SCD, also had a second missense mutation (I406T- RyR2). Four family members without RyR2 mutations did not display prominent postpacing QT changes. M4109R- RyR2 is associated with a high incidence of SCD. The contribution of I406T to the clinical phenotype is unclear. In contrast to exercise testing, marked postpacing repolarization changes in a single beat accurately predicted carriers of M4109R- RyR2 in this family.

Successful Catheter Ablation of Focal Ventricular Fibrillation in a Patient with Nonischemic Dilated Cardiomyopathy

A 64-year-old man with nonischemic dilated cardiomyopathy and a biventricular defibrillator presented with recurrent ventricular fibrillation (VF) and defibrillator shocks. Evaluation of the intracardiac electrograms from his defibrillator demonstrated the consistent initiation of VF by unifocal premature ventricular complexes (PVCs). Noncontact mapping demonstrated the origin of the PVC to be near the left ventricular outflow tract toward the mitral valve ring. Several applications of radiofrequency at this position led to complete cessation of PVCs and prevented further VF. He has not had any further ventricular arrhythmias or defibrillator discharges during follow-up.

Deciphering the electrogram in ventricular fibrillation to extract physiological information

d w m e a u T m The term ventricular fibrillation (VF) is a challenging one: defining it and describing it, let alone understanding it, has been a daunting task for physiologists and clinicians. In its most basic conceptualization, VF is purely a pattern in the electrogram, rather than a pathophysiological event. Definitions in nursing, physiology, and medicine textbooks are vague and purely descriptive: “. . .grossly irregular undulations of varying amplitudes, contours, and rates. . . .” Such definitions contain little insight, but have been clinically useful because they are effective in communications and interactions among clinicians, similar to the idea that “you will know it when you see it.” Although most health professionals at all levels would have little problem recognizing VF based on these vague but intuitive definitions, few could actually give a cogent description or meaningful account of the mechanisms of the underlying physiological phenomenon. To health professionals involved in sudden death resuscitation, it is obvious that not all VFs are the same, and that during the course of resuscitation efforts in individual patients, there are changes in the electrocardiographic waveform that roughly correlate with the progress of such efforts. For example, most clinicians would understand terms such as agonal fibrillation when referring to the slow fibrillatory undulations that precede asystole in failing resuscitations, particularly in comparison with the fine fibrillation patterns present at VF initiation. The terms agonal and fine are vague and gross, but effective when used in individual examples (Figure 1). Most readers will agree that VF changes during the example shown, and would correctly identify fine VF as the initial VF, and agonal VF as the final VF. Again, the pervasive paradigm of “you’ll know it when you see it,” effective in communicating but deceptive in understanding. Physiologists have attempted to correlate electrocardiographic patterns in VF with specific activation patterns and thereby mechanisms of VF, but such correlations require

Purkinje-related Arrhythmias

The Purkinje system has been found to be responsible for the mechanism of some ventricular tachyarrhythmias. These ventricular tachyarrhythmias can be called Purkinjerelated arrhythmias, and are manifested as monomorphic ventricular tachycardia (VT) and polymorphic VT, including ventricular fibrillation (VF). In monomorphic VTs, 4 distinct tachycardias have been found to be related to the Purkinje system: (1) verapamil-sensitive left fascicular VT, (2) Purkinje fiber-mediated VT post infarction, (3) bundle branch reentry (BBR) and interfascicular reentry VTs, and (4) focal Purkinje VT. In polymorphic VT and VF, the Purkinje system may also play an important role. The Purkinje network plays a pivotal role in both the initiation and perpetuation of VF. A triggering ventricular premature beat could arise from either the right or left Purkinje system, and the catheter ablation of the trigger results in a very high cure rate for VF. In patients with an electrical storm, catheter ablation of the triggering VPBs from the Purkinje system should be used as an electrical bailout therapy.

Catheter Ablation of Ventricular Fibrillation: State of the Art

Catheter ablation of the triggering ventricular premature beats (VPBs) is feasible for idiopathic and ischemic ventricular fibrillation (VF) and can be used for a bailout therapy of VF storm. Also, it can reduce the number of the shock from an implantable defibrillator, one of the poor prognostic factors. In VF or polymorphic ventricular tachycardia (VT) from right ventricular outflow tract (RVOT), suppression of VF was achieved by catheter ablation at RVOT or pulmonary artery. In the short-coupled variant of torsade de pointes and ischemic VF, VF was suppressed by catheter ablation of the Purkinje network. Focal firing from Purkinje fiber and reentry at the Purkinje network may play an important role in the initiation and perpetuation of VF. The same approach with good short-term results has been reported in a small number of patients with other heart diseases (i.e., amyloidosis, chronic myocarditis, nonischemic cardiomyopathy, Brugada syndrome, Long-QT syndrome, and catecholaminergic polymorphic VT).

Real-time electrogram analysis for monitoring coronary blood flow during human ventricular fibrillation: Implications for CPR

Effective chest compressions during prolonged ventricular fibrillation (VF) have been shown to increase the chances of successful defibrillation to a rhythm associated with a sustainable cardiac output. There is currently no effective method of recording the degree of antegrade coronary artery flow during chest compression in VF. This study sought to quantify the relationship between the antegrade coronary flow and the characteristics of human VF using near real-time wavelet-based electrocardiographic markers. VF experiments were conducted in 8 isolated human hearts. The Langendorff perfusion enabled different flow rates (perfusion) during VF, which allowed for the simulation of chest compression with different efficacies. After the initiation of VF, the hearts were maintained in ischemia (no flow) for 3 minutes, followed by a 2-minute reperfusion and defibrillation. The experiments were repeated at flows of 0%, 30%, and 100% of baseline perfusion, and volume-conducted surface electrograms were recorded and analyzed using continuous wavelet transform in 5-second frames. Near real-time wavelet features were derived that demonstrated significant differences in the multicomponent nature of VF signals and predicted perfusion rate characteristics for different flow rates (i.e., 0%, 30%, and 100%; P < .0006). A pattern classifier was trained using the feature values from 5 hearts, and the flow rates for 3 additional hearts were predicted with an accuracy of 90%. VF electrogram characteristics as measured by wavelet analysis relate to antegrade coronary flow rate during VF. These findings suggest that chest compression efficacy of physiological importance could be monitored using near real-time wavelet analysis.