Prolongation of QT Interval Induced by Electroconvulsive Therapy is Attenuated by Landiolol

Matsura, Masayo; Fujiwara, Yoshihiro; Ito, Hiroshi; Kandatsu, Nobuhisa; Kato, Naoko; Harada, Jun; Komatsu, Toru

doi:10.1097/yct.0b013e3181a95d8c

Cited by 10 publications

(6 citation statements)

References 17 publications

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“…With respect to the QTc interval, it has been pointed out that mECT can provoke prolongation of QTc intervals [17,18]. In our patient, the QTc interval spread to 0.46 s following the convulsions.…”

Section: Discussionmentioning

confidence: 92%

“…However, it is clear that, under the condition of uncontrolled hemodynamics, considerable sympathotonic increases in BP and HR following the electric stimuli augmented the cardiac oxygen demand, myocardial contractility, and serum catecholamine level, resulting in relative myocardial ischemia [20]. Therefore, the use of calcium channel and/or beta blockers before applying electric stimuli should be considered in order to attenuate hemodynamic hyperactivity [8,15,17]. We used nicardipine, a calcium channel blocker, against persisting hypertension even after the restoration of normal sinus rhythm.…”

Section: Discussionmentioning

confidence: 99%

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A case of nonsustained ventricular tachycardia immediately following modified electroconvulsive therapy in a depressive patient

et al. 2011

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Modified electroconvulsive therapy (mECT) with the use of hypnotics and muscle relaxants is an optional and prevailing treatment for depression in patients who have failed on antidepressant regimens. We describe a patient who developed ventricular tachycardia (VT) immediately after mECT. A 64-year-old man with no remarkable past history underwent a course of mECT for drug-resistant depression. Anesthesia was induced with intravenous thiopental (150 mg) followed by rocuronium (50 mg). Three minutes after the administration of rocuronium, the brain was electrically stimulated using a pulse wave. The first mECT session was performed uneventfully. However, the second session 2 days later elicited acute hypertension (182/134 mmHg) and tachycardia (130 bpm), resulting in the appearance of single and couplets of premature ventricular contractions on the electrocardiogram followed by VT lasting about 10 s. The chest was immediately compressed several times, then normal sinus rhythm was spontaneously restored without administering antiarrhythmic agents. The patient recovered from anesthesia without complications. Postoperatively, close examination was unable to definitively determine the cause of VT, resulting in the cancellation of subsequent mECT sessions. It is important to bear in mind that mECT can induce life-threatening arrhythmias such as VT.

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Section: Discussionmentioning

confidence: 92%

Section: Discussionmentioning

confidence: 99%

A case of nonsustained ventricular tachycardia immediately following modified electroconvulsive therapy in a depressive patient

et al. 2011

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“…Pretreatment with d-tubocurarine, 76 or selective b-1 blockers (practolol, 77 metoprolol, 77 landiolol, 112 possibly esmolol), 79 99 attenuates the QT and QTc lengthening induced by succinylcholine. A similar effect was also demonstrated for alfentanil 25-75 mg kg 21 , 98 -100 but not for smaller doses (10 mg kg 21 ), 100 suggesting a dose-related effectiveness.…”

Section: Neuromuscular Blocking and Reversal Agentsmentioning

confidence: 99%

Impact of anaesthetic drugs and adjuvants on ECG markers of torsadogenicity

Staikou

Stamelos

Stavroulakis

2014

British Journal of Anaesthesia

103

119

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Drug-induced prolongation of cardiac repolarization may trigger malignant ventricular arrhythmias, such as torsade de pointes. The duration of QT interval, QT corrected for heart rate (QTc), JT interval, QT dispersion (QTd), QT variability index, and transmular dispersion of repolarization (TDR) are ECG markers of torsadogenicity. All volatiles, especially isoflurane and desflurane, have been found to prolong QTc and QTcd, while sevoflurane has probably no effects on TDR. Among i.v. anaesthetics, propofol seems superior due to its minimal effects on QTc and TDR; moreover, a decrease in QTc and QTcd has been demonstrated in many studies. Regarding opioids, fentanyl, alfentanil, and remifentanil produce no effects on QTc, while sufentanil, at high doses, may induce QT prolongation. Succinylcholine, but not the non-depolarizing neuromuscular blockers, produces QTc prolongation which can be attenuated by opioids and β-blockers. Reversal of neuromuscular block with anticholinesterase-anticholinergic combinations has been associated with significant QTc prolongation, while such an effect has not been demonstrated for sugammadex, even at high doses. Local anaesthetics have probably no intrinsic action on duration of repolarization; nevertheless, an extensive subarachnoid sympathetic block may increase the duration of QTc. On the contrary, thoracic epidural anaesthesia has been associated with a decrease in both QTc and TDR. Among adjuvants, midazolam seems to have no effect on QTc and TDR, while commonly used antiemetics, such as droperidol, domperidone, and most 5-HT3 antagonists, produce significant QT prolongation. The effects of anaesthetic drugs and techniques on electrocardiographic torsadogenic markers should be considered in the perioperative management of patients with preexisting repolarization abnormalities.

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“…Landiolol, an ultrashort acting β-1 blocker, is 9 times more potent in β-1 blocking activity and 8 times more cardioselective than esmolol. 3,5,8 Previous studies 5,8 have demonstrated the efficacy of landiolol for the stabilization of systemic hemodynamics; however, the appropriate dose for the stabilization of all parameters, systemic blood pressure, cardiac output, and cerebral blood flow velocity has yet to be reported. Our study findings suggest that 0.25 mg/kg of landiolol may be an adequate dose for preventing an increase in systemic hemodynamics, including cardiac output, despite having no effect on prevention of the increase in middle cerebral artery (MCA) flow velocity.…”

Section: Discussionmentioning

confidence: 97%

Optimal Dose of Landiolol for Preventing Abrupt Changes in Both Cardiac Output and Middle Cerebral Artery Flow Velocity After Electroconvulsive Therapy

Kikuchi

Saito²

2014

The Journal of ECT

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The purpose of this study was to examine the dose-dependent effects of landiolol on systemic hemodynamics, cardiac output, and cerebral artery blood flow. Eight patients undergoing electroconvulsive therapy (ECT) received 1 of the 3 drugs/doses (saline, 0.125 mg/kg of landiolol, 0.25 mg/kg of landiolol), in turn, for 3 ECT sessions, immediately after the administration of succinylcholine. In the case of 0.25 mg/kg of landiolol, heart rate, mean arterial pressure, and cardiac output remained unchanged throughout the study period.We believe that 0.25 mg/kg of landiolol may be suitable for preventing the increase in systemic hemodynamics, including cardiac output after ECT.

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Prolongation of QT Interval Induced by Electroconvulsive Therapy is Attenuated by Landiolol

Abstract: The prolongation of QT interval caused by SUX and ECT was partially attenuated by landiolol.

Cited by 10 publications

References 17 publications

A case of nonsustained ventricular tachycardia immediately following modified electroconvulsive therapy in a depressive patient

A case of nonsustained ventricular tachycardia immediately following modified electroconvulsive therapy in a depressive patient

Impact of anaesthetic drugs and adjuvants on ECG markers of torsadogenicity

Optimal Dose of Landiolol for Preventing Abrupt Changes in Both Cardiac Output and Middle Cerebral Artery Flow Velocity After Electroconvulsive Therapy

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