Amiodarone: Electropharmacologic Properties

QT-Interval prolonging drugs: Mechanisms and clinical relevance of their arrhythmogenic hazards

“…A similar protective effect was discussed in hypothyroidism-induced QT prolongation [15,62]. Electrophysiologic changes after long-term amiodarone therapy are very similar to those during hypothyroidism, which argues for a similar cellular mode of action [208]. This mechanism implicates a homogeneous effect of amiodarone on cellular repolarization and reduces the probability of focal reexcitation.…”

“…In recent years, increasing interest has focused on this problem after a variety of cardiac and noncardiac drugs have shown the antiarrhythmic, as well as the proarrhythmic, consequences of drug-induced QT interval prolongation [23,206,208,209]. This interest was stimulated 1.…”

Block of cardiac sodium channels by amiodarone studied by using of action potential in single ventricular myocytes

“…Amiodarone is one of the most effective drugs currently available for the treatment of both supraventricular and ventricular tachyarrhythmias (Mason, 1987;Singh, 1989). This drug has long been classified as a Class-ITT antiarrhythmic drug, because it prolongs action potential duration and refractory period of cardiac muscle (Singh & Vaughan Williams, 1970;Vaughan Williams, 1984).…”

Pharmacokinetic and pharmacodynamic effects of UK‐68,798, a new potential class III antiarrhythmic drug.

“…The doses (1.5 -6.0 jig kg-') are in contrast to the doses of sotalol and amiodarone required to achieve comparable acute effects on QTc, which are in the range 1.5-5.0 mg kg-' (Cobbe, 1989;Singh, 1989).…”

“…Unfortunately, an assessment of the therapeutic potential of Class III activity has been limited hitherto by the absence of selective agents without ancillary properties. Thus, of the currently available agents, amiodarone has additional Class I, II and IV actions (Singh, 1989), sotalol is also a non-selective P-adrenoceptor antagonist (Cobbe, 1989) and bretylium causes catecholamine release followed by prejunctional sympathetic blockade (Gokhale et al, 1963).…”