Vernakalant Versus Flecainide: Atrial Contractility

Overview

Atrial fibrillation (AF) is associated with decreased atrial contractility which is associated with stroke. Decreased contractility becomes apparent after cardioversion of atrial fibrillation, a short period (weeks) during which stroke risk is increased. Improved contractility immediately after cardioversion may prevent arrhythmia progression. In addition, it may reduce the stroke risk. Vernakalant is a new antiarrhythmic drug able to convert atrial fibrillation to sinus rhythm and at the same time increase atrial contractility. The latter has not yet been shown in humans and is subject of the present investigation. Our hypothesis is that in humans the contractility of the atria is higher after administration of vernakalant compared to flecainide. If indeed vernakalant improves atrial contractility after cardioversion further studies into the effect on long-term arrhythmia progression and stroke prevention may follow.

Full Title of Study: “Effects of Vernakalant and Flecainide on Atrial Contractility in Patients With Atrial Fibrillation”

Study Type

  • Study Type: Interventional
  • Study Design
    • Allocation: Randomized
    • Intervention Model: Parallel Assignment
    • Primary Purpose: Diagnostic
    • Masking: Single (Investigator)
  • Study Primary Completion Date: August 2013

Interventions

  • Drug: Vernakalant
    • 10-minute infusion of 3 mg/kg vernakalant, followed by a 15 minute observation period. If the patient is still in atrial fibrillation, an additional 10-minute infusion of 2 mg/kg vernakalant will be given.
  • Drug: Flecainide
    • 10-minute infusion of 2 mg/kg (maximal 150 mg)

Arms, Groups and Cohorts

  • Active Comparator: Flecainide
    • Patients randomized to flecainide will receive a 10-minute infusion of 2 mg/kg (maximal 150 mg) flecainide. If the patient is still in AF 1 hour after the infusion, electrical cardioversion will be performed according to protocol.
  • Active Comparator: Vernakalant
    • Patients randomized to vernakalant will receive a 10-minute infusion of 3 mg/kg vernakalant, followed by a 15 minute observation period. If the patient is still in atrial fibrillation, an additional 10-minute infusion of 2 mg/kg vernakalant will be given. If the patient is still in AF 1 hour after the infusion, electrical cardioversion will be performed according to protocol.

Clinical Trial Outcome Measures

Primary Measures

  • Atrial contractility measured by echocardiography
    • Time Frame: After successful cardioversion to sinus rhythm (this can be during infusion of medication or during the first hour after infusion) an echocardiography will be performed within one hour.
    • Echocardiography will be performed when the patient has sinus rhythm. Transmitral flow will be measured by pulsed Doppler from an apical four chamber view. Peak velocities of the early filling (E) wave and atrial filling (A) will be determined. We will also determine the E/A ratio and the atrial volumes and the total atrial conduction time (PA-TVI).

Secondary Measures

  • Conversion to sinus rhythm
    • Time Frame: Within one hour after drug administration
    • Heart rhythm will be assessed on monitor and confirmed on ECG.
  • Recurrence of AF
    • Time Frame: At one month follow-up
    • Heart rhythm will be assessed by ECG.

Participating in This Clinical Trial

Inclusion Criteria

  • persistent AF or paroxysmal AF – eligible for treatment with vernakalant or flecainide infusion to restore sinus rhythm – receiving adequate anticoagulant therapy (or having an episode of AF lasting < 24 hours) Exclusion Criteria:

  • refusal or inability to give informed consent to participate in this study – atrial flutter – contra-indications for receiving vernakalant or flecainide according to MUMC+ protocol (unstable hemodynamic condition, LVEF < 40%, inadequate potassium levels, acute ischaemia, sinus node dysfunction) – age < 18 years

Gender Eligibility: All

Minimum Age: 18 Years

Maximum Age: N/A

Are Healthy Volunteers Accepted: No

Investigator Details

  • Lead Sponsor
    • Maastricht University Medical Center
  • Provider of Information About this Clinical Study
    • Sponsor
  • Overall Official(s)
    • Harry Crijns, MD, PhD, Principal Investigator, Maastricht University Hospital
  • Overall Contact(s)
    • Ione Limantoro, MD, +31433875119, ione.limantoro@mumc.nl

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