A: Printout of the implantable cardiac defibrillator (ICD) during syncope. Ventricular fibrillation is detected and successfully treated with a shock. B: Incidence of VF/VT episodes detected and treated by the ICD under medical treatment and after ablation. AEGM = atrial electrocardiogram; MAR = marker channel; NSVT = nonsustained ventricular tachycardia; VEGM = right ventricular tip-to-ring electrocardiogram; VF = ventricular fibrillation; VT = ventricular tachycardia.

A: Printout of the implantable cardiac defibrillator (ICD) during syncope. Ventricular fibrillation is detected and successfully treated with a shock. B: Incidence of VF/VT episodes detected and treated by the ICD under medical treatment and after ablation. AEGM = atrial electrocardiogram; MAR = marker channel; NSVT = nonsustained ventricular tachycardia; VEGM = right ventricular tip-to-ring electrocardiogram; VF = ventricular fibrillation; VT = ventricular tachycardia.

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... 1,4-9 They can manifest as both MMVT and PMVT in patients with normal hearts as well as in patients with structural heart diseases or channelopathy. [10][11][12] The PS may trigger or maintain these arrhythmias by automaticity, re-entry, or triggered activity during multiple conditions such as electrolyte imbalance, catecholamine or other drug exposure, and acute/ subacute MI, during which Purkinje fibers (PFs) can survive within the border zone of scar. [13][14][15][16][17][18][19] In general, the MMVT in patients with a previous history of MI is commonly caused by re-entry circuits in the myocardial scar area or its borders. ...
... 31 Suppression of VF can be achieved not only by the elimination of triggering PVCs/PPCs but also by substrate modification of possible re-entry circuits in the PN to address multiple foci or local re-entry. 10,18,28 Ablation of the surrounding PS without elimination of the culprit PP may also be sufficient to prevent VF recurrence. 36 However, catheter ablation of the triggered ventricular premature complex is challenging when the earliest activation site cannot be identified or is located close to the His bundle. ...
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The cardiac Purkinje system is capable of very rapid burst activity suggestive of its potential role in being a driver of polymorphic ventricular tachycardia (VT) (PMVT) or ventricular fibrillation (VF). It plays a pivotal role, however, not only in the triggering of but also the perpetuation of ventricular arrhythmias. A varying degree of Purkinje-myocardial complicity has been blamed in determining not only the sustained or non-sustained nature of PMVT but also the pleomorphism of the non-sustained runs. The initial part of PMVT before cascading to the whole ventricle to establish disorganized VF can give important clues for ablation of PMVT and VF. We present a case of an electrical storm after acute myocardial infarction that was successfully ablated after identifying Purkinje potentials that triggered polymorphic, monomorphic, and pleiomorphic VTs and VF.
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Short-coupled idiopathic ventricular fibrillation (IVF) is a subtype of IVF in which episodes of polymorphic ventricular tachycardia or ventricular fibrillation are initiated by short-coupled premature ventricular contractions (PVCs). Our understanding of the pathophysiology is evolving, with evidence suggesting that these malignant PVCs originate from the Purkinje system. In most cases, the genetic underpinning has not been identified. Whereas the implantation of an implantable cardioverter-defibrillator is uncontroversial, the choice of pharmacological treatment is the subject of discussion. In this review, we summarize the available knowledge on pharmacological therapy in short-coupled IVF and provide our recommendations for management of patients with this syndrome.
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Background: Idiopathic ventricular fibrillation (IVF) is mainly associated with and triggered by short-coupled (R-on-T) ventricular ectopics. However, little is known about the risk of VF associated with long-coupled premature ventricular complexes (LCPVCs). Objective: To examine the prevalence and characteristics of IVF patients presenting with LCPVCs. Methods: Consecutive patients with IVF and PVCs from 5 arrhythmia referral centers were reviewed. We included patients presenting LCPVCs, defined as PVCs falling after the end of the T wave, with a normal QTc interval. We evaluated demographics, medical history, and clinical circumstances associated with PVCs and VF episodes. The origin of PVCs was determined by invasive mapping. Results: Seventy-nine patients with IVF were reviewed. Among them, 12 (15.2%) met the inclusion criteria (8 women, age 36±14 years). Eleven patients had documented LCPVCs initiating repetitive PVCs or sustained VF, whereas one had only documented isolated PVCs. In 10 of 12 patients, PVCs were recorded showing both long and short coupling intervals of 418±46 ms and 304±33 ms, respectively. Mapping showed that PVCs originated from the left Purkinje in 10 patients, from the right Purkinje in 1 patient, and both in 1 patient. Compared to other patients from the initial cohort, IVF with LCPVCs was associated with a left-sided origin of PVCs (92% in long-coupled IVF versus 46% of left Purkinje PVCs in short-coupled IVF, p=0.004). Conclusion: Long-coupled fascicular PVCs, traditionally recognized as benign, can be associated with IVF in a subset of patients. They can induce IVF by themselves or in association with short-coupled PVCs. This article is protected by copyright. All rights reserved.
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Idiopathic ventricular fibrillation is responsible for approximately 10% of cases of aborted cardiac arrest. Recent studies have shown that short-coupled ventricular premature complexes are present at the onset of idiopathic ventricular fibrillation in 6.6 to 17% of patients. The present review provided information on 86 patients with short-coupled malignant ventricular arrhythmias which were reported as case reports or small patient series during the last 70 years. In 75% of the 81 patients published during the last 40 years, extended information and follow-up (from 2.63+4.5 to 10.67+7.8 years, p<0.001, between the original publication to the latest update) could be obtained from the authors. The review shows that short-coupled malignant ventricular arrhythmias occurred almost equally in males and females, at the mean age of 40 years. A tendency for later occurrence of the arrhythmia by 4 years was observed in females. A prior history of syncope was noted in 45.3% of the patients while arrhythmic storm occurred in 42% at presentation. The most common mode of revelation of short-coupled malignant ventricular arrhythmias was syncope (53.5%), followed by aborted cardiac arrest (26.7%) and recurrent arrhythmic event after prior ICD implantation for idiopathic ventricular fibrillation (17.4%). For the first time, short-coupled malignant arrhythmias exhibiting “not-so-short” coupling intervals (>350ms) were found in a significant proportion of patients (17.4%). During long-term follow-up, quinidine yielded a slightly higher success rate in arrhythmia control than ablation. Larger studies are necessary to assess the best strategy for the management of this potentially lethal arrhythmia.
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Ventricular fibrillation (VF) electrical storm is a serious and life-threatening event, and is often triggered by premature ventricular complexes (PVCs). Catheter ablation of these PVC triggers have been described in a variety of clinical situations, including post-myocardial infarction (MI), patients with structurally normal heart, as well as in patients with Brugada Syndrome and Long QT Syndrome. We provide a literature review on this topic, using case examples for illustration.