Acute and chronic effects of amiodarone on ventricular refractoriness, intraventricular conduction and ventricular tachycardia induction

• Published in: Journal of the American College of Cardiology 1986-01, Vol.7 (1), p.148-157
• Main Authors: Morady, Fred, DiCarlo, Lorenzo A., Krol, Ryszard B., Baerman, Jeffrey M., de Buitleir, Michael
• Format: Article
• Language: English
• Subjects: Administration, Oral; Aged; Amiodarone - administration & dosage; Amiodarone - analogs & derivatives; Amiodarone - blood; Amiodarone - pharmacology; Antiarythmic agents; Benzofurans - administration & dosage; Biological and medical sciences; Cardiac Pacing, Artificial; Cardiovascular system; Electric Stimulation; Electrophysiology; Female; Heart Conduction System - drug effects; Heart Ventricles - drug effects; Humans; Infusions, Parenteral; Male; Medical sciences; Middle Aged; Pharmacology. Drug treatments; Tachycardia - drug therapy; Tachycardia - etiology; Tachycardia - physiopathology; Time Factors; Triiodothyronine - blood
• ISSN: 0735-1097; 1558-3597
• DOI: 10.1016/S0735-1097(86)80273-X

In eight patients, the right ventricular effective refractory period, rate-dependent changes in intraventricular conduction (as reflected by QRS duration during ventricular paced cycle lengths of 600 to 250 ms) and results of programmed ventricular stimulation were determined in the control state, 5 minutes after the intravenous infusion of 10 mg/kg body weight of amiodarone and after 2 months of treatment with oral amiodarone. The right ventricular effective refractory period was 230 ± 30 ms (mean ± SD) in the control study, 248 ± 27 ms after intravenous amiodarone (p < 0.001) and 296 ± 26 ms after oral amiodarone (p < 0.001). In the control state, QRS duration was constant at all paced cycle lengths. Intravenous amiodarone resulted in a rate-dependent prolongation of QRS duration. This rate-dependent prolongation was markedly accentuated by oral amiodarone in six patients who had an elevated serum level of reverse triiodothyronine (T3) after 2 months of oral treatment, but it was not more pronounced than the effects of intravenous amiodarone in two patients with a normal reverse T3serum level after oral therapy. Both intravenous and oral amiodarone either suppressed or modified the induction of ventricular tachycardia by programmed stimulation in some patients, but in a discordant fashion. The relative effects of intravenous and oral amiodarone on ventricular refractoriness and conduction and on ventricular tachycardia induction did not correlate with serum amiodarone levels. Chronic amiodarone therapy results in a marked prolongation in ventricular refractoriness compared with the relatively small but significant increase that occurs after intravenous amiodarone. Accentuation by oral amiodarone of the rate-dependent slowing of intraventricular conduction caused by intravenous amiodarone may be related to a direct electrophysiologic effect of amiodarone that is potentiated by an amiodarone-induced abnormality in thyroid hormone metabolism. The different effects of intravenous and oral amiodarone on ventricular tachycardia induction may be explained by different relative effects on refractoriness and conduction.