QTc dispersion on the baseline ECG predicts arrhythmias during electroconvulsive therapy.

Rasmussen, Keith G.; Hooten, W. Mike; Dodd, M. Leann; Ryan, Debra A.

doi:10.2143/ac.62.4.2022277

Cited by 27 publications

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“…This is also in line with the finding that QTd was increased in children with epilepsy regardless of AED treatment (Akalin et al., 2003). Pathologic QTd was also shown to predict cardiac arrhythmias during electroconvulsive therapy (Rasmussen et al., 2007), but we did not observe a significant association between arrhythmias and pathologic QTd (mixed logistic regression model, p = 0.571).…”

Section: Discussioncontrasting

confidence: 76%

Pathologic cardiac repolarization in pharmacoresistant epilepsy and its potential role in sudden unexpected death in epilepsy: A case–control study

et al. 2010

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SUMMARYPurpose: To determine whether abnormal cardiac repolarization and other electrocardiography (ECG) predictors for cardiac mortality occur in epilepsy patients and whether they are associated with an increased risk for sudden unexpected death in epilepsy (SUDEP). Methods: In a matched-pair case-control study, recordings of adult patients with pharmacoresistant focal epilepsies who died from SUDEP and who had previously had presurgical video-EEG (electroencephalography) telemetry were reviewed. Living controls were matched for age, gender, and date of admission for video-EEG telemetry. Periictal heart rate (HR), corrected QT interval (QTc), postictal HR recovery, HR variability, and cardiac rhythm were assessed. QT dispersion was analyzed with 12-lead ECG. Results: A total of 38 patients (19 per group) had 91 recorded seizures. QTc was prolonged above pathologic upper limits in 9 of 89 seizures and 5 of 38 patients. Nine of 34 patients displayed pathologic QT dispersion. Presence of neither pathologic cardiac repolarization nor other ECG features were specifically associated with SUDEP. SUDEP patients were, however, more likely to lack pathologic cerebral magnetic resonance imaging (MRI) findings, less likely to experience antiepileptic drug reduction during telemetry, and had more secondarily generalized tonic-clonic seizures (SGTCS) per year. Discussion: Our study did not reveal a clear-cut

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Section: Discussioncontrasting

confidence: 76%

Pathologic cardiac repolarization in pharmacoresistant epilepsy and its potential role in sudden unexpected death in epilepsy: A case–control study

et al. 2010

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“…In apparently healthy populations, QTd >50 ms (or >60 ms) is considered abnormal, indicating an increased risk for tachyarrhythmia (Zaidi et al, 1997;Macfarlane et al, 1998). Pathologic QTd also seems to predict arrhythmias (mainly premature atrial and ventricular contractions) with electroconvulsive therapy (Rasmussen et al, 2007). Therefore, seizure activity in the presence of pathologic QTd could favor the onset of cardiac arrhythmia.…”

Section: Qt Dispersionmentioning

confidence: 99%

Too long or too short? New insights into abnormal cardiac repolarization in people with chronic epilepsy and its potential role in sudden unexpected death

Taggart²,

et al. 2010

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SUMMARYSudden unexpected death in epilepsy (SUDEP) is probably caused by periictal cardiorespiratory alterations such as central apnea, bradyarrhythmia, and neurogenic pulmonary edema. These alterations may occur in people with epilepsy and vary in duration and severity. Seizurerelated ventricular tachyarrhythmias have also been hypothesized to be involved in SUDEP, but compelling evidence of these, or of predisposition to these, is lacking. Ventricular tachyarrhythmias are facilitated by pathologic cardiac repolarization. Electrocardiography (ECG) indicators of pathologic cardiac repolarization, such as prolongation or shortening of QT intervals as well as increased QT dispersion, are established risk factors for life-threatening tachyarrhythmia and sudden cardiac death (SDC). Abnormalities in cardiac repolarization have recently been described in people with epilepsy. Importantly, periictal ventricular tachycardia and fibrillation have also been reported in the absence of any underlying cardiac disease. Therefore, pathologic cardiac repolarization could promote SCD in people with epilepsy and could be one plausible cause for SUDEP.Herein, we review abnormal cardiac repolarization in people with epilepsy, describe the putative contribution of antiepileptic drugs, and discuss the potential role of pathologic cardiac repolarization in SUDEP. Based on these, measures to reduce the risk of or prevent SUDEP may include antiarrhythmic medication and implantation of cardiac combined pacemaker-defibrillator devices.

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“…Tricyclic antidepressants are known to induce prolongation of the QT interval. Rasmussen et al 24 reported that QTcD as measured on the baseline ECG positively correlated with number of arrhythmias during ECT. 22,23 The baseline values of the QTD and QTcD in 90% of patients were also higher than the upper normal limits of 50 milliseconds.…”

Section: Discussionmentioning

confidence: 99%

Assessment of QT Interval and QT Dispersion During Electroconvulsive Therapy Using Computerized Measurements

Tezuka

Egawa²,

Fukagawa³

et al. 2010

The Journal of ECT

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QTc dispersion on the baseline ECG predicts arrhythmias during electroconvulsive therapy.

Abstract: We conclude that QTc dispersion appears to be a valid predictor of arrhythmias.

Cited by 27 publications

References 0 publications

Pathologic cardiac repolarization in pharmacoresistant epilepsy and its potential role in sudden unexpected death in epilepsy: A case–control study

Pathologic cardiac repolarization in pharmacoresistant epilepsy and its potential role in sudden unexpected death in epilepsy: A case–control study

Too long or too short? New insights into abnormal cardiac repolarization in people with chronic epilepsy and its potential role in sudden unexpected death

Assessment of QT Interval and QT Dispersion During Electroconvulsive Therapy Using Computerized Measurements

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