© 1997 by European Society of Cardiology
Copyright © 1997, European Society of Cardiology
Cellular electropharmacology of amiodarone
Departments of Circulation and Humoral Regulation, Research Institute of Environmental Medicine, Nagoya University, Furo-cho, Chikusa-ku, Nagoya 464-01, Japan
* Corresponding author. Tel. +81 (52) 789-5007; fax: +81 (52) 789-5003.
Received 6 January 1997; accepted 21 April 1997
KEYWORDS Amiodarone; Desethylamiodarone; Action potential; Ion channels; Ion channel expression; Thyroid hormone
| The first 150 words of the full text of this article appear below. |
| 1 Introduction |
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Antiarrhythmic strategies have changed dramatically during the last decade. The Cardiac Arrhythmia Suppression Trial (CAST) reported the harmful effects of flecainide, encainide and moricizine in patients with ventricular premature beats who had had myocardial infarction [162, 163]. Compared with placebo, these three drugs were associated with increased mortality from cardiac death. Numerous meta-analytic studies also provided evidence that drugs that act fundamentally by blocking cardiac sodium channels (Class I agents in Vaughan Williams' classification [171]) may, in general, have the potential to increase mortality in patients with significant structural heart disease even though they may suppress cardiac arrhythmias [2, 31, 49, 99, 161, 187]. The use of Class I drugs in subsets of patients at risk for sudden death is therefore declining. Along with this trend, the therapeutic role of drugs that have antiarrhythmic actions mainly through a prolongation of action potential duration (APD) and refractoriness (Class
| 2 Acute effects of amiodarone |
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2.1 Action potentials
2.2 Ionic currents
| 3 Chronic effects of amiodarone |
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3.1 Action potentials
3.2 Ionic currents
3.3 Desethylamiodarone
| 4 Amiodarone and thyroid hormones |
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4.1 Hypothyroid-like actions of amiodarone
4.2 Modulation of thyroid hormone action
4.3 T3 antagonism
| 5 Summary and conclusions |
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