Torsade de pointes complicating atrioventricular block: report of two cases

N, Maor; Weiss, Dov; Lorber, Avraham

doi:10.1016/0167-5273(87)90015-5

Cited by 11 publications

(4 citation statements)

References 4 publications

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“…Marked QT interval prolongation complicated by torsades , as a sequela of acquired CHB, has been convincingly demonstrated in pediatric 10 and adult 11 patients. In each of these patients, who ranged in age from 18 months to 80 years at initial presentation with torsades , there was QT interval normalization and complete suppression of torsades after institution of ventricular pacing at age‐appropriate rates.…”

Section: Clinical Significance Of Bradycardic Electrical Remodelingmentioning

confidence: 94%

“…These clinical and experimental data, while clearly limited, would appear to suggest that established repolarization abnormalities resulting from bradycardic electrical remodeling might not be readily reversible. Nevertheless, the bulk of published clinical experience clearly indicates that physiologic‐rate pacing can at least prevent complications of bradycardic electrical remodeling, possibly by masking or suppressing underlying repolarization abnormalities 7,8,10,11 …”

Section: Reversibility Of Bradycardic Electrical Remodelingmentioning

confidence: 99%

“…Nevertheless, the bulk of published clinical experience clearly indicates that physiologic-rate pacing can at least prevent complications of bradycardic electrical remodeling, possibly by masking or suppressing underlying repolarization abnormalities. 7,8,10,11…”

Section: Reversibility Of Bradycardic Electrical Remodelingmentioning

confidence: 99%

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Bradycardia‐Mediated Ventricular Electrical Remodeling

Gross

2006

Cardiovasc electrophysiol

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Bradycardic states are associated with myocardial electrical remodeling predisposing to potentially lethal ventricular tachydysrhythmias. We used a novel model of complete heart block (CHB) in the rabbit to test the hypothesis that ventricular activation rate is the primary determinant of early bradycardic electrical remodeling. Chronic endocardial right ventricular demand (VVI) pacing was applied at either the near-physiologic rate of 280 beats/min or at the bradycardic rate of 140 beats/min, beginning immediately after transcatheter radiofrequency AV node ablation. A third group of animals underwent sham ablation and served as non-paced, normal sinus rhythm controls. The major finding of this study was that electrical remodeling was established within 8 days of CHB induction in the bradycardic animals, but was not observed in either of the other 2 groups. Bradycardic animals had significant QT interval prolongation and biventricular downregulation of the delayed rectifier K+ currents, IKr and IKs. The Ca2+-independent transient outward K+ current, I(to), and the inwardly rectifying K+ current, I(K1), were unaffected. This paper highlights these findings in the context of a literature-based review of heart rate-dependent remodeling of the mammalian myocardium, summarizing the current state of knowledge and describing future challenges.

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Section: Clinical Significance Of Bradycardic Electrical Remodelingmentioning

confidence: 94%

Section: Reversibility Of Bradycardic Electrical Remodelingmentioning

confidence: 99%

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Bradycardia‐Mediated Ventricular Electrical Remodeling

Gross

2006

Cardiovasc electrophysiol

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“…Sustained bradycardia decreases I Kr and I Ks [ 67,153,154 ] , causing QT interval prolongation and prominent repolarization delays leading to spontaneous TdP. I Kr alterations in the face of simultaneous I Ks down-regulation (reduced repolarization reserve) appear to be particularly important in the resulting long-QT phenotype, which may explain the association of AV block and clinical TdP syndromes [ 155 ] . Calcium handling abnormalities is also implicated in bradycardia remodelling with enhanced intracellular [Ca 2+ ] and activation of the Ca 2+ -calmodulin-CaMKII system [ 156 ] .…”

Section: Vf Substratementioning

confidence: 98%

Comparisons of Substrates Responsible for Atrial Versus Ventricular Fibrillation

Comtois

Burstein

Nattel

2013

Electrical Diseases of the Heart

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The fundamental mechanisms underlying fi brillation have long been debated. The classical notion of multiple circuit reentry has been challenged by recent ideas suggesting that in some cases a single high-frequency rotor or even a rapidly-fi ring focus can underlie fi brillation that can cause wave breakup and fi brillation. There is increasing awareness that arrhythmias do not usually begin in perfectly normal tissue, but require changes in tissue structure or function that constitute the arrhythmic substrate. In this chapter, atrial and ventricular changes (including alterations in ion channel function, intercellular coupling, and fi brosis) playing a role in fi brillation are reviewed. We focus particularly on ischemic substrates, congestive heart failure remodeling, genetic factors, neuroregulatory determinants, and arrhythmic remodeling. Atrial (AF) and ventricular (VF) fi brillation-substrates have many features in common but also a number of important speci fi c differences. Consideration of these mechanistic determinants will lead to improved understanding of the pathophysiology of AF and VF, and ultimately to improve arrhythmia-speci fi c therapeutic approaches.

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Signal‐averaged electrocardiographic late potentials in children with complete heart block

Hayabuchi

Matsuoka

Kubo

et al. 1994

Clinical Cardiology

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Summary:The purpose of this study was to examine signalaveraged electrocardiographic (SA-ECG) late potentials to predict ventricular arrhythrmas during intrinsic cardiac rhythm and during ventricular pacing in children with complete heart block (CHB). Recordings of SA-ECG were obtained from eight patients (aged 3-18 years) with documented CHB. The etiology of CHB was congenital in four cases and acquired in four cases. Six of these patients underwent permanent pacemaker implantation. Comparisons of the SA-ECG were made before and during ventricular pacing. Abnormalities of SA-ECG during intrinsic cardiac rhythm were noted in four patients, all of whom were older than 14 years. Although there was no significant difference in SA-ECG parameters between patients with congenital CHB and acquired CHB, abnormal SA-ECG was noted in one of four patients with congenital CHB and in three of four patients with acquired CHB. Two patients without permanent pacemaker implantation had normal SA-ECG, but four of six patients with permanent pacemaker implantation had abnormal SA-ECG. Three of the four patients had abnormal SA-ECG during ventricular pacing, but the abnormal SA-ECG in one patient had normalized during ventricular pacing. It is important to record SA-ECG before and during ventricular pacing to detect late potentials in patients with CHB. It may be useful to record SA-ECG while changing the pacing site to h d ideal sites for electrode implantation for the potential prevention of ventricular arrhythmias.

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Torsade de pointes complicating atrioventricular block: report of two cases

Cited by 11 publications

References 4 publications

Bradycardia‐Mediated Ventricular Electrical Remodeling

Bradycardia‐Mediated Ventricular Electrical Remodeling

Comparisons of Substrates Responsible for Atrial Versus Ventricular Fibrillation

Signal‐averaged electrocardiographic late potentials in children with complete heart block

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