Increased QT dispersion in epileptic children

Akalın, Figen; Tirtir, A; Yüksel, Yılmaz

doi:10.1111/j.1651-2227.2003.tb00624.x

Cited by 46 publications

(35 citation statements)

References 25 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…18,19,34 Furthermore, chronic epilepsy patients display altered autonomic function with a presumably increased sympathetic tone and enhanced QT dispersion (spatial heterogeneity of cardiac repolarization), which are both independent predictors of cardiac mortality. 4,7,35,36 The latter finding is of particular interest, as enhanced QT dispersion facilitates ventricular tachyarrhythmia with short QT interval. 37 Thus, one plausible explanation for SUDEP would be peri-ictal occurrence of pathologic cardiac repolarization resulting in sudden onset of ventricular tachyarrhythmia.…”

Section: Methodsmentioning

confidence: 99%

Enhanced QT shortening and persistent tachycardia after generalized seizures

Surges¹,

Scott²,

Walker³

2010

Neurology

134

109

View full text Add to dashboard Cite

Objective: Generalized tonic-clonic seizures (GTCS) are a major risk factor for sudden unexpected death in epilepsy (SUDEP). We investigated whether ictal/postictal cardiac features were dependent on seizure type within individual patients.Methods: ECG data from patients with medically refractory temporal lobe epilepsy (TLE) undergoing presurgical investigation who had both complex partial seizures and secondarily GTCS during video-EEG telemetry were retrospectively reviewed. Peri-ictal heart rate (HR), corrected QT interval (QTc), HR variability, and cardiac rhythm were assessed.Results: Twenty-five patients were included in this study. Secondarily GTCS led to higher ictal HR, persistent postictal tachycardia, and decreased postictal HR variability. Moreover, abnormal shortening of QTc occurred in 17 patients mainly during the early postictal phase and significantly more often in secondarily GTCS. Abnormal QTc prolongation occurred in 3 patients with no significant association with GTCS. Benign cardiac arrhythmias occurred in 14 patients and were independent of seizure type. Conclusions:Our data suggest a substantial disturbance of autonomic function following secondarily generalized tonic-clonic seizures (GTCS) in patients with medically refractory temporal lobe epilepsy. The observed alterations could potentially facilitate sudden cardiac death and might contribute to the association of sudden unexpected death in epilepsy with GTCS. Neurology ® 2010;74:421-426 GLOSSARY CI ϭ confidence interval; CPS ϭ complex partial seizure; GTCS ϭ generalized tonic-clonic seizures; HR ϭ heart rate; HRV ϭ HR variability; QTc ϭ corrected QT interval; SUDEP ϭ sudden unexpected death in epilepsy; TLE ϭ temporal lobe epilepsy.Sudden unexpected death in epilepsy (SUDEP) is the most frequent epilepsy-related cause of death and is particularly prevalent in patients with chronic epilepsy.1 In younger people with epilepsy (age 20 -40 years), the risk for sudden death is increased about 24-fold compared to the general population.2 Peri-ictal cardiorespiratory alterations are likely to be involved in the pathophysiology of SUDEP and include tachyarrhythmias and bradyarrhythmias as well as central or obstructive hypoventilation and neurogenic pulmonary edema.1 Since generalized tonic-clonic seizures (GTCS) are a major risk factor for SUDEP, 3,4 then determining the specific cardiac characteristics of GTCS may give us a considerable insight into the mechanisms underlying SUDEP. Abnormalities in cardiac repolarization, persistent elevations of heart rate (HR) after exercise, and a decreased HR variability (HRV) are established predictors for cardiac mortality and sudden cardiac death in other medical conditions or in healthy populations. [5][6][7] Previous studies have suggested a greater impact of GTCS on cardiac excitability than nongeneralized seizures with higher ictal heart rates in chronic epilepsy and SUDEP patients 4,[8][9][10][11] and possibly more cardiac arrhythmias following GTCS. 8,10 These studies, however, are confou...

show abstract

Section: Methodsmentioning

confidence: 99%

Enhanced QT shortening and persistent tachycardia after generalized seizures

Surges¹,

Scott²,

Walker³

2010

Neurology

134

109

View full text Add to dashboard Cite

show abstract

“…Missense mutations in Na V 1.1 and Na V 1.2 that increase I NaL amplitude [19][20][21] in hereditary epilepsy seem to confirm this hypothesis. However, epilepsy patients display prolonged QT interval and enhanced expression of Na V 1.1 even in absence of mutations in neuronal Na V s. 22,23 These observations raise the possibility that, as in the brain, epilepsy enhances expression of TTX-sensitive Na V s in cardiac cells thereby modifying their excitability and increasing I NaL . In the heart, we showed that an increase in I NaL is associated with long-QT syndrome 10,11,24 and sudden death.…”

mentioning

confidence: 95%

Prolongation of Action Potential Duration and QT Interval During Epilepsy Linked to Increased Contribution of Neuronal Sodium Channels to Cardiac Late Na ⁺ Current

Biet

Morin

Lessard‐Beaudoin

et al. 2015

Circ: Arrhythmia and Electrophysiology

View full text Add to dashboard Cite

Background-Arrhythmias associated with QT prolongation on the ECG often lead to sudden unexpected death in epilepsy.The mechanism causing a prolongation of the QT interval during epilepsy remains unknown. Based on observations showing an upregulation of neuronal sodium channels in the brain during epilepsy, we tested the hypothesis that a similar phenomenon occurs in the heart and contributes to QT prolongation by altering cardiac sodium current properties (I Na ). Methods and Results-We used the patch clamp technique to assess the effects of epilepsy on the cardiac action potential and I Na in rat ventricular myocytes. Consistent with QT prolongation, epileptic rats had longer ventricular action potential durations attributable to a sustained component of I Na (I NaL ). The increase in I NaL was because of a larger contribution of neuronal Na channels characterized by their high sensitivity to tetrodotoxin. As in the brain, epilepsy was associated with an enhanced expression of the neuronal isoform Na V 1.1 in cardiomyocyte. Epilepsy was also associated with a lower I Na activation threshold resulting in increased cell excitability. Conclusions-This is the first study correlating increased expression of neuronal sodium channels within the heart to epilepsy-related cardiac arrhythmias. This represents a new paradigm in our understanding of cardiac complications related to epilepsy. (Circ Arrhythm Electrophysiol. 2015;8:912-920.

show abstract

“…In accordance with this, inhibiting INa,L was shown to shorten QT interval [82,83]. Mutations resulting in facilitation of late sodium current are associated with increased QT dispersion too [52,82]. How increased INa,L leads to increased QT dispersion is not completely understood, but transmural heterogeneity of sodium current is probably also involved [72,84].…”

Section: Contribution Of Plateau Sodium Current To Cardiac Electric Amentioning

confidence: 71%

“…Non-cardiac sodium channels in the heart Association of ECG abnormalities to epilepsy [52,53] and myotonic disorders [54,55] raised the possibility that the same mutated sodium channels which are responsible for hereditary diseases of nervous system or skeletal muscles might cause repolarization abnormalities in the heart. Later, several 'non cardiac' isoforms were identified in cardiac tissue by functional tests based on voltage dependency and drug sensitivity in different species [37,[56][57][58].…”

Section: Window Currentsmentioning

confidence: 99%

An Emerging Antiarrhythmic Target: Late Sodium Current

Bányász

Szentandrássy²,

Magyar³

et al. 2014

CPD

View full text Add to dashboard Cite

The cardiac late sodium current (INa,L) has been in the focus of research in the last decade. The first reports on the sustained component of voltage activated sodium current dates back to the early seventies, but early observations interpreted this tiny current as a product of a few channels that fail to inactivate having neither physiologic nor pathologic implications. INa,L has emerged recently as a potentially major arrhythmogenic mechanism in various heart diseases attracting the attention of both clinicians and researchers. Research activity on INa,L has exponentially increased since Ranolazine, an FDA-approved antianginal drug was shown to successfully suppress cardiac arrhythmias by inhibiting INa,L. This review aims to conclude a series of papers concerned with physiology and regulation of cardiac late sodium current. Focusing on some recent development of the field we discuss here critical evidences implicating INa,L as a potential target for treating myocardial dysfunction and cardiac arrhythmias.

show abstract

Increased QT dispersion in epileptic children

Cited by 46 publications

References 25 publications

Enhanced QT shortening and persistent tachycardia after generalized seizures

Enhanced QT shortening and persistent tachycardia after generalized seizures

Prolongation of Action Potential Duration and QT Interval During Epilepsy Linked to Increased Contribution of Neuronal Sodium Channels to Cardiac Late Na ⁺ Current

An Emerging Antiarrhythmic Target: Late Sodium Current

Contact Info

Product

Resources

About

Increased QT dispersion in epileptic children

Cited by 46 publications

References 25 publications

Enhanced QT shortening and persistent tachycardia after generalized seizures

Enhanced QT shortening and persistent tachycardia after generalized seizures

Prolongation of Action Potential Duration and QT Interval During Epilepsy Linked to Increased Contribution of Neuronal Sodium Channels to Cardiac Late Na + Current

An Emerging Antiarrhythmic Target: Late Sodium Current

Contact Info

Product

Resources

About

Prolongation of Action Potential Duration and QT Interval During Epilepsy Linked to Increased Contribution of Neuronal Sodium Channels to Cardiac Late Na ⁺ Current