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Aminophylline induced atrial fibrillation
1Cardiology Division, Cabrini Medical Center, New York Medical College, New York 10003.
Pacing and Clinical Electrophysiology : PACE
|October 1, 1993
Summary
Intravenous aminophylline can induce atrial fibrillation (AF) with rapid ventricular response, even in patients without prior heart issues. AF resolved after aminophylline withdrawal, with diltiazem proving more effective than digoxin for rate control.
Area of Science:
- Cardiology
- Pulmonology
- Pharmacology
Background:
- Atrial fibrillation (AF) is a common arrhythmia.
- Aminophylline is used to treat pulmonary diseases.
- Theophylline toxicity is a known risk factor for cardiac arrhythmias.
Purpose of the Study:
- To investigate the induction of atrial fibrillation by intravenous aminophylline in patients with pulmonary disease.
- To evaluate the efficacy of diltiazem versus digoxin in controlling the ventricular rate during aminophylline-induced AF.
- To understand the potential mechanisms of aminophylline-induced AF.
Main Methods:
- Case series of three patients with symptomatic pulmonary disease treated with intravenous aminophylline.
- Monitoring of serum theophylline concentrations.
- Assessment of cardiac rhythm and ventricular rate control using intravenous diltiazem and digoxin.
- Observation of AF resolution after aminophylline cessation.
Main Results:
- Three patients developed atrial fibrillation with rapid ventricular response during intravenous aminophylline therapy.
- Serum theophylline levels were therapeutic in two patients and toxic in one.
- AF resolved spontaneously 9-14 hours after aminophylline discontinuation.
- Intravenous diltiazem was more effective than digoxin in controlling the ventricular rate prior to sinus rhythm conversion.
Conclusions:
- Intravenous aminophylline can precipitate atrial fibrillation, irrespective of theophylline toxicity.
- Aminophylline-induced AF is reversible upon drug withdrawal.
- Diltiazem demonstrates superior efficacy over digoxin for ventricular rate control in this context.
- Potential mechanisms involve shortened atrial refractory periods and dispersed excitability recovery, promoting reentrant circuits.