Ambulatory sudden cardiac death: Mechanisms of production of fatal arrhythmia on the basis of data from 157 cases

Luna, Antonio; Coumel, Philippe; Leclercq, Jean

doi:10.1016/0002-8703(89)90670-4

Cited by 874 publications

(316 citation statements)

References 24 publications

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“…54,55 More recent studies, however, suggest that the incidence of VF or pulseless VT as the first recorded rhythm in out-of-hospital cardiac arrest has declined to <30 % in the past few decades. [56][57][58] Pulseless electrical activity (electromechanical dissociation) and asystole are proportionally more frequent mechanisms than VT/VF.…”

Section: Pathophysiologymentioning

confidence: 99%

A Clinical Perspective on Sudden Cardiac Death

2016

Arrhythmia &Amp; Electrophysiology Review

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This article presents the epidemiology, aetiology and pathophysiology of sudden cardiac death. The modern management of survivors as well as of family members of victims is discussed, as are the relevant recommendations of guidelines prepared by learned societies. KeywordsOut-of-hospital cardiac arrest, sports-related sudden death, sudden cardiac death, sudden unexplained death syndrome Disclosure: The authors have no conflicts of interest to declare.

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Section: Pathophysiologymentioning

confidence: 99%

A Clinical Perspective on Sudden Cardiac Death

2016

Arrhythmia &Amp; Electrophysiology Review

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“…2 Ventricular tachycardia (VT) or ventricular fibrillation (VF) is the initiating event in the majority of SCD cases. 3 Ejection fraction (EF) remains the only major criterion to stratify patients for risk of SCD and implantable cardioverter-defibrillator (ICD) implantation, but this strategy alone is insensitive and nonspecific. 4 Genetic susceptibility to SCD in the setting of CAD is supported by several epidemiologic studies demonstrating that a family history of SCD is an independent risk factor for SCD and primary VF.…”

Section: Introductionmentioning

confidence: 99%

Common ß-adrenergic receptor polymorphisms are not associated with risk of sudden cardiac death in patients with coronary artery disease

et al. 2008

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“…Ventricular fibrillation (VF) is a terminal cardiac dysrhythmia in humans,1, 2 occurring either as a primary or a secondary event to concomitant cardiac and noncardiac diseases. Currently, there is no cure for VF, with only rudimentary treatment options available; thus, sudden cardiac death from VF remains a major worldwide health problem 3, 4.…”

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confidence: 99%

Elimination of Purkinje Fibers by Electroporation Reduces Ventricular Fibrillation Vulnerability

Livia

Sugrue

Witt

et al. 2018

JAHA

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BackgroundThe Purkinje network appears to play a pivotal role in the triggering as well as maintenance of ventricular fibrillation. Irreversible electroporation (IRE) using direct current has shown promise as a nonthermal ablation modality in the heart, but its ability to target and ablate the Purkinje tissue is undefined. Our aim was to investigate the potential for selective ablation of Purkinje/fascicular fibers using IRE.Methods and ResultsIn an ex vivo Langendorff model of canine heart (n=8), direct current was delivered in a unipolar manner at various dosages from 750 to 2500 V, in 10 pulses with a 90‐μs duration at a frequency of 1 Hz. The window of ventricular fibrillation vulnerability was assessed before and after delivery of electroporation energy using a shock on T‐wave method. IRE consistently eradicated all Purkinje potentials at voltages between 750 and 2500 V (minimum field strength of 250–833 V/cm). The ventricular electrogram amplitude was only minimally reduced by ablation: 0.6±2.3 mV (P=0.03). In 4 hearts after IRE delivery, ventricular fibrillation could not be reinduced. At baseline, the lower limit of vulnerability to ventricular fibrillation was 1.8±0.4 J, and the upper limit of vulnerability was 19.5±3.0 J. The window of vulnerability was 17.8±2.9 J. Delivery of electroporation energy significantly reduced the window of vulnerability to 5.7±2.9 J (P=0.0003), with a postablation lower limit of vulnerability=7.3±2.63 J, and the upper limit of vulnerability=18.8±5.2 J.ConclusionsOur study highlights that Purkinje tissue can be ablated with IRE without any evidence of underlying myocardial damage.

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Ambulatory sudden cardiac death: Mechanisms of production of fatal arrhythmia on the basis of data from 157 cases

Cited by 874 publications

References 24 publications

A Clinical Perspective on Sudden Cardiac Death

A Clinical Perspective on Sudden Cardiac Death

Common ß-adrenergic receptor polymorphisms are not associated with risk of sudden cardiac death in patients with coronary artery disease

Elimination of Purkinje Fibers by Electroporation Reduces Ventricular Fibrillation Vulnerability

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