Effects of phenobarbital and levetiracetam on PR and QTc intervals in patients with post-stroke seizure (original) (raw)
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Epilepsia, 2010
Purpose: 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 patho-logic 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 ECG predictor for SUDEP. Pathologic cardiac repolarization is not uncommon in adult patients with pharmacoresistant focal epilepsy and could favor occurrence of fatal tachyarrhythmia as one plausible cause for SUDEP. SGTCS are a risk factor for SUDEP, have, as compared to complexpartial seizures, a greater, unfavorable impact on heart activity, and may thereby additionally compromise cardiac function.
Sudden cardiac death is associated both with epilepsy and with use of antiepileptic medications
Heart (British Cardiac Society), 2015
Epilepsy is associated with increased risk for sudden cardiac death (SCD). We aimed to establish, in a community based study, whether this association is mediated by epilepsy per se, use of antiepileptic medications (AEMs), or both. We studied SCD cases and age/sex matched controls in a case-control study in a large scale general practitioners' research database (n=478 661 patients). SCD risk for symptomatic epilepsy (seizure <2 years before SCD), stable epilepsy (no seizure <2 years before SCD), and use of AEMs (any indication) was determined. We identified 926 SCD cases and 9832 controls. Fourteen cases had epilepsy. Epilepsy was associated with an increased SCD risk (cases 1.5%, controls 0.5%; adjusted OR 2.8, 95% CI 1.4 to 5.3). SCD risk was increased for symptomatic epilepsy (cases 0.9%, controls 0.1%; adjusted OR 5.8, 95% CI 2.1 to 15.6), but not with stable epilepsy (cases 0.6%, controls 0.4%; adjusted OR 1.6, 95% CI 0.7 to 4.1). AEM use was found in 23 cases and wa...
The potential for QT prolongation by antiepileptic drugs in children
Pediatric Neurology, 2004
Cardiac arrhythmia may be one of the major causes of sudden unexpected death in children with epilepsy. We assessed drug-induced QT prolongation to establish whether the use of antiepileptic drugs contributes to sudden unexpected death. A total of 178 children with epilepsy (93 males and 85 females, with ages ranging from 1 month to 18.9 years; mean age 7.0 ؎ 4.1 years) were involved in the study. The QT intervals were manually measured and corrected using Fridericia's formula (QTFc ؍ QT/RR 1/3). The mean corrected QT interval (QTc) of 152 children on antiepileptic drugs during the study period was 0.40 ؎ 0.03 s, and for 26 age-matched, antiepileptic drug-free control patients it was 0.40 ؎ 0.03 s. The mean QTc of the children with monotherapy was 0.40 ؎ 0.03 s for the valproate group (n ؍ 42), 0.39 ؎ 0.02 s for the carbamazepine/oxcarbazepine group (n ؍ 34), and 0.40 ؎ 0.02 s for the topiramate group (n ؍ 26), respectively. There was no statistically significant difference among the groups as assessed by analysis of variance. In addition, there was no significant difference between the monotherapy group (n ؍ 109; 0.40 ؎ 0.02 s) and the polytherapy group (n ؍ 43; 0.39 ؎ 0.03 s). Major antiepileptic drugs may not precipitate prolongation of the QT interval into sudden unexpected death in children with epilepsy, however further studies are required.
Levetiracetam in newly diagnosed late-onset post-stroke seizures: A prospective observational study
Epilepsy Research, 2008
Levetiracetam (LEV) monotherapy was investigated in 35 patients (pts) (16M/19F, 71.9 ± 7.3 years of age) with late-onset post-stroke seizures (i.e. seizures occurring at least 2 weeks after an ischemic stroke) in a prospective open-label study. Overall, 27 pts (77.1%) achieved a condition of seizure freedom (defined as 1 year without seizures): 19 (54.3%) at a daily LEV dose of 1000 mg, 7 (20.0%) at 1500 mg, 1 (2.8%) at 2000 mg. Four pts (11.4%) discontinued the drug because of intolerable side effects (drowsiness associated to gait disturbance in 1 pt, and aggressive behaviour in the remaining 3 pts); 3 pts were unresponsive at a dose of 3000 mg, and 1 pt was lost at follow-up. These observations suggest that LEV exhibits safety and efficacy profiles which make it an optimal candidate as a first-choice drug against post-stroke seizures.
Epilepsia, 2010
Sudden 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.
Seizure, 1997
Sudden unexpected death (SUD) has been associated with low or undetectable concentrations of antiepileptic drugs in patients with epilepsy suggesting that a sudden fall in plasma levels of these drugs might be a critical factor for the occurrence of SUD. We studied the changes in arrhythmia profile and heart-rate variability, during abrupt withdrawal of carbamazepine and phenytoin treatment in 10 patients with side effects on these drugs. Continuous ECG recording and daily measurements of drug plasma concentrations were performed from the last day of steady-state treatment and the following 4 days. Three patients had a IO-fold increase in ventricular premature beats. In addition, there was a significant reduction in heart-rate variability, assessed over 24 hours, in both the time (SDNN index, P = 0.03) and frequency domains from days 1-5. In the frequency domain analysis there was a significant reduction in total power (P = 0.01). very-low-frequency power (P = 0.004) and in low-frequency (LF) power (P = 0.01). Similar reductions in heart-r&e variability and increases in ventricular automaticity have been associated with increased mortality in other patient groups. Two factors that might contribute to the increased rate of SUD in patients with epilepsy have thus been identified.
The effects of antiepileptic drugs on vascular risk factors: A narrative review
Seizure, 2014
Epilepsy is associated with increased cardiovascular disease (CVD) morbidity and mortality. The exact causes of this link are not clearly defined. The role of antiepileptic drugs (AEDs) in influencing CVD risk in patients with epilepsy remains controversial. A link between epilepsy, AEDs and cardiac arrhythmias has been proposed and may be responsible for sudden unexpected death in epilepsy (SUDEP). Methods: We searched MEDLINE up to December 1, 2013 for relevant publications using combinations of keywords. We also examined the reference list of articles identified by this search and selected those we judged relevant. These were included in this narrative review. Results: AEDs may exert both beneficial and adverse cardiovascular effects. This narrative review considers the influence of AEDs on some predictors of vascular risk [i.e. weight, insulin resistance, metabolic syndrome, lipids, lipoprotein (a), C-reactive protein, homocysteine, vitamins, coagulation factors, uric acid, carotid intima media thickness, markers of oxidative status and matrix metalloproteinase-9]. Certain AEDs can also have pro-arrhythmic properties. Conclusions: AEDs may exert different effects on various established and emerging predictors of vascular risk. Furthermore, pharmacokinetic interactions between AEDs and drugs used to reduce vascular risk (e.g. statins) need to be better documented. Whether this knowledge, in terms of individualizing antiepileptic and CVD prevention treatment, will prove to be relevant in clinical practice remains to be established.
Corrected QT interval and QT dispersion in temporal lobe epilepsy
The Egyptian Journal of Neurology, Psychiatry and Neurosurgery
Background Cardiac arrhythmias are expected among patients with epilepsy due to the effect of anti-epileptic drugs. Temporal lobe epilepsy also causes autonomic seizures that may affect heart rhythm. Prolongation of the corrected QT interval and QT dispersion is a risk factor for cardiac arrhythmia. Objectives We aimed to assess corrected QT interval and QT dispersion in patients with epilepsy and if there is a difference between patients with temporal epilepsy versus non-temporal epilepsy. Methods This study was conducted on 100 patients (50 patients with temporal epilepsy and 50 patients with non-temporal epilepsy) and 50 age- and sex-matched healthy controls. They underwent a prolonged (6 to 24 h) 22 channel computerized electroencephalogram monitor with a 10–20 system. QT dispersion, QT interval, and corrected QT interval (using Bazett’s formula) were calculated. Results This study showed significantly higher QT dispersion and corrected QT interval in patients with epilepsy when...