How does Lacosamide (Vimpat) cause PR interval prolongation?

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DS

Dainyal Siddiqui, MD

Internal Medicine

MJ

Manuel Jimenez, MD

Cardiology

FP

Franz Pierre-Louis, MD

Infectious Disease

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Last updated: March 28, 2025 • View editorial policy

From the Guidelines

Lacosamide causes PR interval prolongation by affecting cardiac conduction, particularly through its action on voltage-gated sodium channels, leading to delayed conduction time between the atria and ventricles. This mechanism is associated with small dose-related increases in the PR interval, as noted in clinical trials 1. The effect of lacosamide on sodium channels in cardiac tissue results in slowing the movement of electrical impulses through the atrioventricular (AV) node, which manifests as PR interval prolongation on electrocardiogram (ECG).

Key Points to Consider

  • The drug's effect on cardiac conduction is dose-dependent, with higher doses more likely to cause significant PR prolongation.
  • Patients with pre-existing cardiac conduction abnormalities, those taking other medications that affect cardiac conduction, or individuals with severe cardiac disease are at higher risk for this effect.
  • ECG monitoring is recommended before and during treatment with lacosamide, particularly when using higher doses or in patients with known cardiac risk factors.

Clinical Implications

  • Clinicians should be aware of the potential for lacosamide to cause PR interval prolongation and monitor patients accordingly.
  • The benefits of using lacosamide for its approved indications, such as adjunctive treatment of partial-onset seizures, should be weighed against the potential risks, including cardiac effects 1.
  • Further studies are needed to fully understand the mechanisms and clinical implications of lacosamide-induced PR interval prolongation.

From the Research

Mechanism of PR Interval Prolongation

  • Lacosamide enhances slow inactivation of voltage-gated sodium channels, which can lead to dose-dependent PR interval prolongation 2, 3.
  • The enhancement of slow inactivation of voltage-gated sodium channels by lacosamide can affect cardiac sodium channels and lead to cardiovascular consequences, including PR interval prolongation 3.

Effects on Cardiac Sodium Channels

  • Lacosamide reduces human cardiac sodium currents in a concentration-, voltage-, and state-dependent manner 3.
  • The reduction in cardiac sodium currents can lead to a delay in cardiac conduction, resulting in PR interval prolongation 3.

Clinical Evidence

  • Studies have reported dose-dependent PR and QRS prolongation and ECG abnormalities, including loss of P waves, atrioventricular and intraventricular blocks, and junctional premature contractions, in patients receiving lacosamide 3, 4.
  • A systematic review of the literature found that ventricular tachycardia, new-onset atrial fibrillation, complete heart block, and Mobitz type 1 atrioventricular block were among the most reported lacosamide-related arrhythmias 5.

Risk Factors

  • Baseline bradycardia and early repolarization changes may increase the risk of lacosamide-induced PR interval prolongation and atrioventricular block 2.
  • Medical comorbidities and older age may also portend a greater risk of PR prolongation 2, 4.

References

3
Research

Cardiac safety of lacosamide: the non-clinical perspective.

Acta neurologica Scandinavica, 2015

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This information is intended for healthcare professionals. Any medical decision-making should rely on clinical judgment and independently verified information. The content provided herein does not replace professional discretion and should be considered supplementary to established clinical guidelines. Healthcare providers should verify all information against primary literature and current practice standards before application in patient care. Dr.Oracle assumes no liability for clinical decisions based on this content.

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