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Free Radical Reactions in the Pathomechanism of Amiodarone Liver Toxicity

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Free Radicals and the Liver

Abstract

Amiodarone (AMI) is one of our most potent antiarrhythmic drugs, with special chemical, pharmacokinetic, and electrophysiological properties. It is effective in arrhythmias originating from every part of the myocardium, applicable in grave, perilous rhythm disturbances (e.g., refractory ventricular tachycardia, atrial fibrillation with a high ventricular rate associated with anterograde Kent bundle conduction, and refractory supraventricular tachycardia). AMI treatment is the only therapeutic approach capable of preventing or at least significantly reducing the incidence of sudden death in hypertrophic obstructive cardiomyopathy in low doses. In survivors of sudden arrhythmic death — the group which is considered to be the most rigorous test of an antiarrhythmic agent — AMI treatment was effective in the significant reduction of mortality in contrast to the failure of conventional antiarrhythmic drugs. A further great advantage of AMI compared to other antiarrhythmic agents is that it has only insignificant proarrhythmic activity, and can be safely administered to patients with decreased left ventricular function [27, 28, 11].

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© 1992 Springer-Verlag Berlin Heidelberg

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Vereckei, A., Fehér, E., Blázovics, A., György, J., Toncser, H., Fehér, J. (1992). Free Radical Reactions in the Pathomechanism of Amiodarone Liver Toxicity. In: Csomós, G., Fehér, J. (eds) Free Radicals and the Liver. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-76874-3_10

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  • DOI: https://doi.org/10.1007/978-3-642-76874-3_10

  • Publisher Name: Springer, Berlin, Heidelberg

  • Print ISBN: 978-3-642-76876-7

  • Online ISBN: 978-3-642-76874-3

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