Triggers Of Ventricular Fibrillation Research Articles

Use of Stored Implanted Cardiac Defibrillator Electrograms in Catheter Ablation of Ventricular Fibrillation

Ventricular fibrillation (VF) can be abolished by targeting triggering ventricular ectopy, most often originating in the Purkinje network or right ventricular outflow tract (RVOT). This strategy relies upon the induction of premature ventricular complex (PVC) and/or VF. We sought to evaluate a VF ablation strategy that utilizes analysis of stored implantable cardioverter defibrillator (ICD) electrograms. Eleven consecutive patients experiencing frequent VF episodes (≥three episodes in prior month) underwent electrophysiology study and ablation of VF triggers. PVC and VF induction was intentionally avoided or not possible in all of these patients. Pacemapping at likely sites for PVC triggers of VF using an analysis of the morphology and relative timing of the stored far- and near-field ICD electrograms of VF triggers was used to identify potential culprit locations. Radiofrequency energy was applied to these sites for ablation of the identified VF trigger. Areas targeted for ablation included the left posterior fascicle (six), left anterior fascicle (three), RVOT (three) and left ventricular outflow tract (one); two patients had two separate triggers. Ablation was completed successfully without any complications. With a mean follow-up of 288 days (range 45-649), 10 patients are free of VF. Ablation of VF triggers can be performed successfully with good short-term outcomes in patients with and without underlying heart disease. Use of stored ICD electrograms with a focus on likely target areas permit ablation without the need for PVC or VF induction. This can be useful when ectopy is not present for mapping and to avoid potentially dangerous initiation of multiple episodes of VF.

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 …

Catheter ablation of ventricular fibrillation triggers and electrical storm

Ventricular fibrillation (VF) and electrical storm remain challenging conditions to manage despite the availability of various treatment modalities. Insertion of an implantable cardioverter defibrillator (ICD) remains the gold standard method for lowering the risk of sudden cardiac death in patients deemed to be at greatest risk of ventricular arrhythmias. However, ICDs do not alter the underlying substrate responsible for the arrhythmic events and a significant proportion of patients with ICDs may experience VF storm which may be life threatening and difficult to control with medication. Catheter ablation (CA) of the triggers or abnormal electrical substrate responsible for VF storm is an important treatment option in rare cases. In this article, we present an overview of the current theories underlying the mechanisms of VF and discuss how the technique of CA may be used to treat the triggers of VF and electrical storm. We review the literature on outcomes in patients who have undergone CA for VF in a variety of different settings, including those with structural heart disease and structurally normal hearts (e.g. patients with inherited arrhythmogenic diseases and idiopathic VF) and discuss the future directions in this field.

Fibrosis and Stress: A Double-Hit Prerequisite for a Perfect Storm of Ventricular Arrhythmias

Background: Ventricular fibrillation (VF) is promoted by tissue fibrosis, as seen in diseased and aged hearts. In addition to disrupting myocardial structure, fibroblasts also may communicate via gap junctions with neighboring myocytes. We hypothesize that fibroblast-myocyte coupling may facilitate VF triggers such as early afterdepolarizations (EADs) while simultaneously promoting substrate vulnerability to arrhythmias.

Mitochondrial uncouplers trigger ventricular fibrillation in isolated rat hearts

Sudden cardiac death due to ventricular fibrillation (VF) is a major cause of mortality in the US. The purpose of this study was to investigate the role of mitochondrial depolarization on development of VF during myocardial ischemia. Rat hearts (n=8 per group) were perfused with a modified Krebs solution. After 5 minutes, the perfusion solution was switched to one containing drug vehicle (0.01% DMSO v/v), 0.3μM CCCP, 100μM 2,4‐dinitrophenol, 0.2μM cyclosporine A or 100μM 5‐hydroxydecanoate. After a further 10 minutes, the left main coronary artery was occluded. CCCP and 2,4 dinitrophenol triggered VF in 100% of hearts prior to induction of ischemia, whereas no control heart developed VF in this period (p<0.05). In all cases VF was preceded by QT shortening (e.g. from 49±2 ms 1 min before switch to CCCP to 34±3 ms 5 min after switch to CCCP; p<0.05). During ischemia, neither cyclosporine A (88% VF) nor 5‐hydroxydecanoate (100% VF) reduced the incidence of VF compared to control (100% VF; p>0.05). In addition, neither drug affected the time to onset or the total duration of VF. In conclusion, mitochondrial depolarization is a powerful trigger for VF, and may underlie the mechanism by which VF is triggered during ischemia. Activation of the mitochondrial KATP channel or permeability transition pore is unlikely to underlie mitochondrial depolarization or VF during myocardial ischemia. Supported by a WVSOM intramural grant.

Premature Ventricular Complexes as a Trigger for Ventricular Fibrillation

The mechanisms that trigger ventricular fibrillation (VF) are poorly understood. The aim of this study was to analyze the initiation of VF in electrograms stored in implantable cardioverter-defibrillators (ICDs). We analyzed ICD electrograms from patients who had suffered at least one episode of VF. Of 250 patients with ICDs, 13 (10 male and 3 female, age 49+/-22 years) had at least one episode of VF. The diagnoses were Brugada syndrome (n=4), ischemic heart disease (n=3), dilated cardiomyopathy (n=2), hypertrophic cardiomyopathy (n=1), short-coupled variant of torsades de pointes (n=1), endocardial fibroelastosis (n=1) and idiopathic VF (n=1). In 7 patients, VF was the reason for ICD implantation. Overall, 31 episodes of VF were recorded, including three episodes of arrhythmic storm. In the 7 patients who had more than one episode of VF (within minutes or up to 3 years apart), all episodes started with premature ventricular complexes (PVCs) that had the same morphology and similar coupling intervals. A short-long-short cycle was observed in 2 patients. In 21 episodes, PVCs that did not trigger VF were observed during sinus rhythm. There was no significant difference between them and PVCs that did trigger VF in terms of morphology, coupling interval (409+/-121 ms vs. 411+/-123 ms) or the preceding sinus rhythm RR interval (801+/-233 ms vs. 793+/-230 ms). Spontaneous VF in the form of an arrhythmic storm or an isolated episode were triggered by PVCs. On occasions, PVCs preceded VF without triggering it.

Commotio Cordis—Sudden Cardiac Death with Chest Wall Impact

Commotio cordis (CC), sudden death as a result of a blunt, often innocent-appearing chest wall blow, is being reported with increasing frequency. The clinical spectrum is diverse; however, a substantial number of cases occur in youth athletics. In events that occur during sport, victims are struck by projectiles regarded as standard implements of the game. Sudden death is instantaneous and victims are most often found in ventricular fibrillation (VF). Overall survival is poor; however, successful resuscitation can be achieved with early defibrillation. Autopsy is notable for the absence of any significant cardiac or thoracic injury. Development of an experimental model has allowed for substantial insights into the underlying mechanisms of sudden death. In anesthetized juvenile swine, induction of VF is instantaneous following chest wall blows occurring during a vulnerable window before the T wave peak. Crucial variables including the velocity of impact, impact location, and hardness of the impact object have been identified. Rapid left ventricular (LV) pressure rise following chest impact likely results in activation of ion channels via mechano-electric coupling. The generation of inward current via mechano-sensitive ion channels likely results in augmentation of repolarization and nonuniform myocardial activation, and is the cause of premature ventricular depolarizations that are triggers of VF in CC. While softer-than-standard safety baseballs reduce the risk of CC, commercially available chest protectors are ineffective in preventing CC. The development of more effective chest protectors and more widespread use of automated external defibrillators at youth sporting events are needed.

Role of Purkinje conducting system in triggering of idiopathic ventricular fibrillation

Ventricular fibrillation is the main mechanism of sudden cardiac death, but the source of its spontaneous initiation has not been mapped. 16 patients were investigated by electrography and radiofrequency ablation after resuscitation from recurrent idiopathic ventricular fibrillation. Triggers of ventricular fibrillation originated from various locations within the Purkinje system in 12 patients and from the ordinary myocardial muscle in four. The accuracy of mapping was confirmed by acute elimination of triggers by radiofrequency delivery, and there was no recurrence of ventricular fibrillation in 14 patients. Long-term follow-up is necessary to establish that ablation is curative and avoids use of a defibrillator.

Intracellular calcium and ventricular fibrillation. Studies in the aequorin-loaded isovolumic ferret heart.

To elucidate the role of changes in [Ca2+]i in the induction of ventricular fibrillation (VF), Ca2+i signals, epicardial electrical potentials, and isovolumic left ventricular pressure were simultaneously recorded in isolated intact ferret hearts loaded with aequorin, a bioluminescent protein. When the preparations were perfused with 3 microM acetylstrophanthidin and 8 mM Ca2+, or with a low Na+ solution (18 mM Na+, 100 mM Li+), spontaneous transitions to the VF state were consistently observed within a short period of time. The initiation of spontaneous VF was preceded by development of a Ca2+i overload state, coincidental with the ascending phase of diastolic Ca2+i oscillations, and was followed by further elevation in Ca2+i levels, which were associated with augmented Ca2+i oscillations of a saw-toothed pattern. Pretreatment with 10 microM ryanodine, which blocked Ca2+i oscillations in the preparation, did not eliminate inducibility of VF by means of AC electrical stimulations; however, VF no longer occurred spontaneously, and the threshold for VF induction increased markedly. In the absence of a state of Ca2+i overload, spontaneous defibrillation occurred within a minute after the initiation of VF. We conclude that 1) VF can be induced in the absence of Ca2+i oscillations; however, 2) Ca2+i oscillations play a crucial role as a trigger for VF and therefore are an important determinant of the vulnerability to VF; and 3) the augmented Ca2+i oscillations after the transition to VF state may support the maintenance of this type of arrhythmia.