Lacosamide Intoxication-induced Wide QRS Tachycardia Successfully Treated with Veno-arterial Extracorporeal Membrane Oxygenation

Takai, Chihiro; Misumi, Kayo; Kaito, Daiki; Nishida, Hiroaki; Yoshii, Masami; Yamada, So; Kobayashi, Takaomi; Koinuma, Toshitaka; Kadoya, Takashi; Kimura, T.; Hagiwara, Yoshihiro; Ogura, Takayuki

doi:10.2169/internalmedicine.0145-22

Cited by 5 publications

(3 citation statements)

References 24 publications

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“…Lacosamide is characterized by its stronger and faster binding to the slow-inactivated state compared to the fast-inactivated state, which may contribute to infrahisian conduction delay and QRS prolongation (1). In patients with SCN5A mutations, the use of lacosamide may cause the augmentation of slow inactivation of cardiac sodium channels, potentially leading to re-entrant arrhythmias and early afterdepolarizations in ventricular cardiac tissue (1,21), which greatly increases the risk of refractory ventricular tachyarrhythmias and sudden cardiac arrest. In vitro, lacosamide has been shown to exert a concentration-dependent inhibitory effect on the peak amplitude of sodium currents in human embryonic kidney (HEK293T) cells expressing SCN5A (22).…”

Section: Discussionmentioning

confidence: 99%

Case Report: Lacosamide unmasking SCN5A-associated Brugada syndrome in a young female with epilepsy

Shen,

Wu,

Lin

et al. 2024

Front. Cardiovasc. Med.

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BackgroundLacosamide is frequently used as a mono- or adjunctive therapy for the treatment of adults with epilepsy. Although lacosamide is known to act on both neuronal and cardiac sodium channels, potentially leading to cardiac arrhythmias, including Brugada syndrome (BrS), its adverse effects in individuals with genetic susceptibility are less understood.CaseWe report a 33-year-old female with underlying epilepsy who presented to the emergency department with a four-day history of seizure clusters, and was initially treated with lacosamide therapy. During the intravenous lacosamide infusion, the patient developed sudden cardiac arrest caused by ventricular arrhythmias necessitating resuscitation. Of note, the patient had a family history of sudden cardiac death. Workup including routine laboratory results, 12-lead electrocardiogram (ECG), echocardiogram, and coronary angiogram was non-specific. However, a characteristic type 1 Brugada ECG pattern was identified by ajmaline provocation testing; thus, confirming the diagnosis of BrS. Subsequently, the genotypic diagnosis was confirmed by Sanger sequencing, which revealed a heterozygous mutation (c.2893C>T, p.Arg965Cys) in the SCN5A gene. Eventually, the patient underwent implantable cardioverter-defibrillator implantation and was discharged with full neurological recovery.ConclusionThis case highlights a rare but lethal adverse event associated with lacosamide treatment in patients with genetic susceptibility. Further research is warranted to investigate the interactions between lacosamide and SCN5A variants.

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Section: Discussionmentioning

confidence: 99%

Case Report: Lacosamide unmasking SCN5A-associated Brugada syndrome in a young female with epilepsy

Shen,

Wu,

Lin

et al. 2024

Front. Cardiovasc. Med.

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“…3 By restoring haemodynamics and tissue perfusion in patients with circulatory collapse, VA-ECMO can bridge patients with drug-refractory ES complicated by cardiogenic shock to definitive treatment, as well as enables optimization of antiarrhythmic drugs and catecholamine weaning, all of which may contribute to ending ES. 1,[4][5][6][7] VA-ECMO has been successfully used for drug-refractory ES with reversible triggers such as acute coronary syndromes, 8 decompensated heart failure, 9 drug toxicity, 10 electrolyte disturbances, 11 thyrotoxicosis, 12 and concomitant acute illness with fever. 9 However, reversible causes of ES are identified in only 10% of patients.…”

Section: Introductionmentioning

confidence: 99%

“…VA‐ECMO has been successfully used for drug‐refractory ES with reversible triggers such as acute coronary syndromes, 8 decompensated heart failure, 9 drug toxicity, 10 electrolyte disturbances, 11 thyrotoxicosis, 12 and concomitant acute illness with fever. 9 However, reversible causes of ES are identified in only 10% of patients.…”

Section: Introductionmentioning

confidence: 99%

ECMO for drug‐refractory electrical storm without a reversible trigger: a retrospective multicentric observational study

Durães‐Campos,

Costa,

Ferreira

et al. 2024

ESC Heart Failure

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AimsDrug‐refractory electrical storm (ES) is a life‐threatening medical emergency. We describe the use of venoarterial extracorporeal membrane oxygenation (VA‐ECMO) in drug‐refractory ES without a reversible trigger, for which specific guideline recommendations are still lacking.Methods and resultsRetrospective observational study in four Iberian centres on the indications, treatment, complications, and outcome of drug‐refractory ES not associated with acute coronary syndromes, decompensated heart failure, drug toxicity, electrolyte disturbances, endocrine emergencies, concomitant acute illness with fever, or poor compliance with anti‐arrhythmic drugs, requiring VA‐ECMO for circulatory support. Thirty‐four (6%) out of 552 patients with VA‐ECMO for cardiogenic shock were included [71% men; 57 (44–62) years], 65% underwent cardiopulmonary resuscitation before VA‐ECMO implantation, and 26% during cannulation. Left ventricular unloading during VA‐ECMO was used in 8 (24%) patients: 3 (9%) with intraaortic balloon pump, 3 (9%) with LV vent, and 2 (6%) with Impella. Thirty (88%) had structural heart disease and 8 (24%) had an implantable cardioverter‐defibrillator. The drug‐refractory ES was mostly due to monomorphic ventricular tachycardia (VT) and ventricular fibrillation (VF) (59%), isolated monomorphic VT (26%), polymorphic VT (9%), or VF (6%). Thirty‐one (91%) required deep sedation, 44% overdrive pacing, 36% catheter ablation, and 26% acute autonomic modulation. The main complications were nosocomial infection (47%), bleeding (24%), and limb ischaemia (21%). Eighteen (53%) were weaned from VA‐ECMO, and 29% had heart transplantation. Twenty‐seven (79%) survived to hospital discharge (48 (33–82) days). Non‐survivors were older [62 (58–67) vs. 54 (43–58); P < 0.01] and had a higher first rhythm disorder‐to‐ECMO interval [0 (0–2) vs. 2 (1‐11) days; P = 0.02]. Seven (20%) had rehospitalization during follow‐up [29 (12–48) months], with ES recurrence in 6%.ConclusionsVA‐ECMO bridged drug‐refractory ES without a reversible trigger with a high success rate. This required prolonged hospital stays and coordination between the ECMO centre, the electrophysiology laboratory, and the heart transplant programme.

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Reversibilität einer kritischen intraventrikulären Leitungsverzögerung unter Flecainid und Lacosamid durch Natriumbicarbonat

Gallinger,

Osei-Davies,

Hennersdorf

2024

Innere Medizin

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Lacosamide Intoxication-induced Wide QRS Tachycardia Successfully Treated with Veno-arterial Extracorporeal Membrane Oxygenation

Cited by 5 publications

References 24 publications

Case Report: Lacosamide unmasking SCN5A-associated Brugada syndrome in a young female with epilepsy

Case Report: Lacosamide unmasking SCN5A-associated Brugada syndrome in a young female with epilepsy

ECMO for drug‐refractory electrical storm without a reversible trigger: a retrospective multicentric observational study

Reversibilität einer kritischen intraventrikulären Leitungsverzögerung unter Flecainid und Lacosamid durch Natriumbicarbonat

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