Flecainide-induced arrhythmia in canine ventricular epicardium. Phase 2 reentry? | Zendy

Subramaniam Krishnan | Zendy; Charles Antzelevitch | Zendy

AI Assistant Blog Pricing

Home ZAIA Blog

Open Access

Flecainide-induced arrhythmia in canine ventricular epicardium. Phase 2 reentry?

Author(s) -

Subramaniam Krishnan,

Charles Antzelevitch

Publication year - 1993

Publication title -

circulation

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 7.795

H-Index - 607

eISSN - 1524-4539

pISSN - 0009-7322

DOI - 10.1161/01.cir.87.2.562

Subject(s) - flecainide , endocardium , reentry , repolarization , refractory period , medicine , cardiology , sodium channel , sodium channel blocker , ventricle , cardiac transient outward potassium current , electrophysiology , anesthesia , sodium , chemistry , patch clamp , atrial fibrillation , organic chemistry

We recently reported that sodium channel block can produce opposite effects on action potential duration (APD) and refractoriness in epicardial versus endocardial tissues of the canine ventricle. In addition, strong sodium channel current inhibition was found to cause loss of the action potential dome in epicardium but not endocardium, thus inducing a marked dispersion of repolarization and refractoriness between epicardium and endocardium as well as among neighboring epicardial sites. The marked heterogeneity that evolves under these conditions provides a substrate for the development of arrhythmias. Flecainide was found to induce extrasystolic activity more readily than other sodium blockers. The present study contrasts the electrophysiological actions of flecainide in canine ventricular epicardium and endocardium and examines the characteristics of flecainide-induced arrhythmias in epicardial sheets of canine ventricle.

The content you want is available to Zendy users.

Already have an account? Click here to sign in.

Having issues? You can contact us here

Accelerating Research