Key result
Intravenous lacosamide loading in critically ill epilepsy patients resulted in a mild, clinically insignificant increase in PR interval and no life-threatening cardiac adverse effects.
Why the study?
Sodium channel blocking antiseizure medications can have unwanted cardiac effects, and there are limited data regarding the cardiac safety and proarrhythmic potential of rapid intravenous lacosamide administration.
Does intravenous lacosamide cause clinically significant cardiac adverse effects in patients with acute seizures or status epilepticus?
Observational (n=38)
No
Does intravenous lacosamide cause clinically significant cardiac adverse effects in patients with acute seizures or status epilepticus?
Absolute Event Rate: 152% vs 146%
p-value: p=0.025
Intravenous lacosamide infused over 30 minutes in critically ill epilepsy patients causes mild, clinically insignificant increases in PR interval and decreases in blood pressure, suggesting an acceptable cardiovascular safety profile.
Supports short-term cardiac safety of IV lacosamide in acute epilepsy; hypothesis-generating and requires randomized confirmation.
Objective: Voltage-gated sodium channels (VGSCs) play an important role in neuronal excitability and epilepsies. In addition to the brain, VGSCs are also abundant enriched in cardiac tissues and are responsible for normal cardiac rhythm. Theoretically, sodium channel blocking antiseizure medications (SCB-ASMs) may have unwanted cardiac side effects. Lacosamide (LCM) is increasingly used in patients with status epilepticus (SE) due to the availability of intravenous formula. The concerns about the proarrhythmic effect are even higher due to the need for rapid administration of LCM. There were limited data on the cardiac safety of intravenous LCM. Hereby, we performed a study to observe the effect of intravenous loading of LCM in patients with seizures in our Neurological Intensive Care Unit (NICU). Methods: We retrospectively reviewed the patients using parenteral LCM for seizures in NICU. A routine infusion time of 30 min was performed. The electrocardiogram (ECG) and blood pressure were recorded before and after LCM injection. Results: We retrospectively reviewed the clinical data of 38 patients using LCM for treating seizures. Two patients had cardiac side effects after LCM loading, one (3.0%) with new-onset first-degree AV block and the other (3.0%) with atrial premature complex. For the quantitative changes of ECG parameter analysis, there was no change in QRS complex, corrected QT intervals, and heart rate except that the PR interval was mildly increased. A mild decrease in the diastolic blood pressure and mean arterial pressure were also observed. None of the above-mentioned parameter alterations required clinical intervention. Conclusion: We evaluated the cardiac safety concern in real-world epilepsy patients requiring intravenous LCM. Near half of this cohort responded to LCM therapy and there was no life-threatening cardiac adverse effect. Intravenous LCM does have some effects on the ECG parameters and blood pressure but without clinical relevance. Despite the theoretical concern of cardiac adverse effects of LCM, the benefit of seizure control outweighed the risk in patients with status epilepticus or seizure clusters, such as hyperthermia, pulmonary edema, cardiac arrhythmias, or cardiovascular collapse.
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Lu et al. (2022) conducted an observational in Acute seizures, seizure clusters, and status epilepticus (n=38). Intravenous Lacosamide vs. Baseline (pre-lacosamide) was evaluated on PR interval (ms) (p=0.025). Intravenous lacosamide loading in critically ill epilepsy patients resulted in a mild, clinically insignificant increase in PR interval and no life-threatening cardiac adverse effects.
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