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Cardiovascular Drugs and Therapy

, Volume 1, Issue 6, pp 599–603 | Cite as

Clinical electrophysiologic effects of flecainide acetate

  • Davendra Mehta
  • A. John Camm
  • David E. Ward
Focus On Arrhythmias

Summary

Flecainide acetate depresses the rate of depolarization of action potential (Vmax), the so-called “membrane stablizing action.” In the intact heart it has a unique profile of substantial effect on conduction with modest effect on refractoriness. After intravenous administration, clinical electrophysiologic studies show that conduction through atrial myocardium, atrioventricular (AV) node, His-Purkinje system, and ventricular myocardium is depressed, the most prominent effect being on the His-Purkinje system. Refractorines of the normal atrial and AV nodal myocardium is not prolonged while that of the ventricular muscle is slightly increased. Atrial fibrillation (60% to 70%), atrial tachycardia (90% to 100%), and nodal and AV tachycardia (80% to 90%) are generally terminated, while flutter is usually slowed, but in a small proportion of patients (10% to 20%) might be terminated by the intravenous use of flecainide acetate. This drug has also been shown to be effective in terminating stable ventricular tachycardia (70%). However, it appears to be slightly less effective in suppressing inducibility of ventricular arrhythmias. Administered orally, flecainide is very effective in decreasing ventricular ectopic activity (80% to 95%) and nonsustained ventricular tachycardia. Thus, flecainide has a wide range of antiarrhythmic properties, making it a useful agent in the management of a variety of supraventricular and ventricular arrhythmias. In a small proportion of patients, however, its use can lead to apparent arrhythmogenic effects, the most dangerous being exacerbation of ventricular tachycardia.

Key words

Flecainide acetate paroxysmal tachycardia electrophysiology monophasic action potential 

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Copyright information

© Kluwer Academic Publishers 1988

Authors and Affiliations

  • Davendra Mehta
    • 1
  • A. John Camm
    • 1
  • David E. Ward
    • 1
  1. 1.Department of Cardiological SciencesSt. George's Hospital Medical SchoolLondonEngland

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