Vernakalant is an antiarrhythmic approved in Europe specifically for rapid conversion of recent-onset atrial fibrillation. Its unique mechanism compared to other antiarrhythmics is:
- A Atria-selective blockade of Kv1.5 (IKur — ultra-rapid delayed rectifier) channel, which is expressed predominantly in atria and absent in ventricles, combined with rate-dependent sodium channel blockade ✓
- B Selective class III action — pure IKr (hERG) blockade extending atrial refractoriness
- C Non-selective potassium channel opener causing atrial hyperpolarization
- D Selective AV nodal sodium channel blockade slowing conduction exclusively through the AV node
Explanation
Vernakalant targets multiple atria-selective ion channels, most importantly Kv1.5 (encoding IKur — the ultra-rapid delayed rectifier current), which is expressed exclusively in atrial myocytes and absent in ventricular myocytes. Blocking IKur prolongs atrial action potential duration and refractoriness selectively without affecting ventricular repolarization (no QT prolongation, no torsades risk). Additionally, vernakalant exhibits use-dependent (rate-dependent) blockade of INa, more effective at the higher atrial rates of AF. This atrial selectivity makes it uniquely free of ventricular proarrhythmic risk compared to class I and III agents.
Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.
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Written and medically reviewed by the StethoPrep medical team.