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Depressant effect of digoxin on atrioventricular conduction in man
Insights
Digoxin slows atrioventricular (A-V) conduction in heart transplant patients, prolonging the Wenckebach cycle length and S
Area of Science:
- Cardiology
- Pharmacology
- Electrophysiology
Background:
- Digoxin is a cardiac glycoside used to treat heart failure and arrhythmias.
- Its effects on atrioventricular (A-V) conduction, particularly in cardiac transplant recipients, require further elucidation.
Purpose of the Study:
- To investigate the impact of chronic digoxin administration on A-V conduction.
- To determine if digoxin's effect on A-V conduction is neurally mediated.
Main Methods:
- Assessed A-V conduction in nine cardiac transplant recipients.
- Measured S'R interval and Wenckebach periodicity during control and digoxin administration periods.
- Evaluated the influence of atropine and propranolol on digoxin's effects.
Main Results:
- Digoxin significantly prolonged the S'R interval at paced rates of 110 bpm and faster.
- The cycle length for Wenckebach block increased by 14% during digoxin administration.
- These effects reversed upon digoxin discontinuation and were not altered by atropine or propranolol.
Conclusions:
- Digoxin exerts a direct, non-neurally mediated depressant effect on A-V conduction in humans.
- Tachycardia is necessary to unmask digoxin's depressant effect on A-V conduction.
Abstract:
We examined the effect of chronically administered digoxin on atrioventricular (A-V) conduction in nine cardiac transplant recipients. We assessed A-V conduction by measuring the duration from the pacing stimulus to the onset of the QRS complex (S'R interval) and by determining the occurrence of Wenckebach periodicity during rapid atrial pacing. We made measurements during a control period and during a period of digoxin administration of up to 37 days. During the digoxin period, the cycle length at which Wenckebach block occurred was prolonged by 14% of the control value and the S'R interval was significantly prolonged at paced rates of 110 beats per minute and faster. After digoxin was discontinued, the Wenckebach periodicity and S'R interval returned to control values. Atropine and propranolol did not alter digoxin's effect on A-V conduction. We conclude that digoxin exerts a direct (or non-neurally mediated) depressant effect upon A-V conduction in man, although the stress of tachycardia is necessary to demonstrate the effect.