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Effects of digoxin on acute, atrial fibrillation-induced changes in atrial refractoriness

C Sticherling1, H Oral, J Horrocks

  • 1Division of Cardiology, Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor, MI 48109-0022, USA.

Circulation
|November 15, 2000
PubMed
Abstract

Insights

Digoxin worsens atrial refractoriness after atrial fibrillation (AF) episodes, increasing the risk of recurrent AF. This effect is likely due to digoxin

Area of Science:

  • Cardiovascular Electrophysiology
  • Cardiac Arrhythmias
  • Pharmacology

Background:

  • Atrial fibrillation (AF) shortens the atrial effective refractory period (ERP), increasing susceptibility to further AF episodes.
  • Acute changes in atrial refractoriness may stem from tachycardia-induced intracellular calcium overload.

Purpose of the Study:

  • To investigate if digoxin, a drug that increases intracellular calcium, potentiates the acute effects of AF on atrial refractoriness in humans.

Main Methods:

  • Measured atrial ERP in 38 healthy adults after autonomic blockade, with 19 receiving digoxin treatment.
  • Assessed atrial ERP at basic drive cycle lengths (BDCLs) of 350 and 500 ms before and after a brief AF episode.
  • Compared post-AF ERP changes and incidence of secondary AF episodes between digoxin and control groups.

Main Results:

  • Post-AF atrial ERP was significantly shorter in both groups compared to pre-AF values.
  • The reduction in atrial ERP was significantly greater in the digoxin group than in the control group at both BDCLs.
  • Secondary AF episodes occurred more frequently in the digoxin group (32%) compared to the control group (16%).

Conclusions:

  • Digoxin augments the acute shortening of atrial refractoriness following AF episodes.
  • This augmentation by digoxin predisposes patients to AF reinduction, independent of vagotonic effects.
  • The findings suggest digoxin's effects on intracellular calcium contribute to its pro-arrhythmic potential in AF.

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