Lacosamide-Induced Recurrent Ventricular Tachycardia in the Acute Care Setting

Abstract

Lacosamide is a new-generation antiepileptic drug (AED) most commonly used adjunctively in the setting of partial-onset seizures refractory to traditional therapy. We describe the first case report, to our knowledge, of a patient who developed recurrent, sustained ventricular tachycardia with multiple administrations of lacosamide in an acute setting. A 70-year-old woman with a history significant for valvular heart disease was admitted to the inpatient cardiology service for worsening heart failure. On hospital day 7, she received a bioprosthetic aortic valve. Prior to surgery and immediately after, the patient's electrocardiogram (ECG) was normal. After developing multiple generalized tonic-clonic seizures refractory to levetiracetam, fosphenytoin, and valproic acid, the decision was made to initiate lacosamide. Two hours following the second lacosamide dose, the patient developed a wide complex QRS that transitioned into sustained ventricular tachycardia requiring electrical cardioversion. Sustained ventricular tachycardia occurred again, just hours after the third dose of lacosamide was given. Following cessation of lacosamide, the patient's QRS interval normalized and has since had no documented episodes of ventricular tachycardia. Clinicians should be aware of the potential for life-threatening rhythmic disturbances in patients initiated on lacosamide and the need for vigilant ECG, electrolyte, and drug-drug monitoring.

Use of Disproportionality Analysis to Identify Previously Unknown Drug-Associated Causes of Cardiac Arrhythmias Using the Food and Drug Administration Adverse Event Reporting System (FAERS) Database

“…Medications causing QTc-prolongation are used in both inpatient and outpatient settings and have been thoroughly studied. 1,[5][6][7] While drug-induced QTc-prolongation is recognized due to the potential for Torsades de Pointes (TdP), 7 literature for many other drug-induced arrhythmias is limited to case reports [8][9][10][11][12] outside of drug-induced arrhythmia reviews with atrial fibrillation 13 and bradyarrhythmias. [14][15][16] A newly published review of drug-induced arrhythmias did add further to the literature by including a section on atrioventricular nodal reentrant tachycardia.…”

Lacosamide induced Brugada I morphology in the setting of septicemia

“…Lacosamide displays 10% to 20% inhibition of the SCN5A cardiac sodium channel at the upper limit of the therapeutic range, which increases in a dose dependent manner; mutations of SCN5A have been associated with Brugada syndrome and sudden death [2,6] . Previous reports have suggested a role for therapeutic lacosamide induction of ventricular tachycardia during co-administration with other sodium channel blockers [2,4] . A recent report demonstrated lacosamide-induced QRS prolongation and seizure after a likely massive overdose in a 48-year-old woman [5] .…”

“…Lacosamide is an antiepileptic agent with a novel mechanism of sodium channel inhibition compared with other antiepileptic or antiarrhythmic medications [2,3] . In prior reports, lacosamide has potentially contributed to cardiac sodium channel blockade in combination with other medications, though its role as a sole agent is limited to massive overdose [2,4,5] . Here, we present a case of Brugada I ECG morphology that was unmasked by lacosamide antiepileptic monotherapy in a patient with septicemia.…”

Lacosamide‐induced symptomatic sinus node dysfunction

“…Lacosamide is an AED that exerts anticonvulsant effects by slow inactivation of voltage‐gated sodium channels. Lacosamide‐associated arrhythmias in previous reports included atrial fibrillation/flutter [1], sinus node dysfunction [2], second‐ or third‐degree atrioventricular block [3–5], ventricular tachycardia [6], and cardiac arrest [7, 8]. Although a case of sinus node dysfunction has been reported, it was asymptomatic and was observed under the high dose of 500 mg/day lacosamide (therapeutic range with normal renal function: 200–400 mg/day) [2].…”

“…In some of the reported cases of arrhythmias in patients receiving low lacosamide doses, the possibility of interaction with other sodium channel blockers or drugs that have negative effects on cardiac conduction (such as bisoprolol and cyclobenzaprine) was suggested [4,7]. In addition to high drug doses, impaired renal function, a history of cardiac disease, and advanced age have been listed as risk factors for arrhythmias with lacosamide [4][5][6]. This is the first reported case of a patient with symptomatic sinus node dysfunction with therapeutic doses of lacosamide.…”