Amiodarone: Pharmacology and Antiarrhythmic and Adverse Effects

Naccarelli, Gerald V.; Rinkenberger, Robert L.; Dougherty, Anne H.; Giebel, Ruth A.

doi:10.1002/j.1875-9114.1985.tb03434.x

Cited by 59 publications

(25 citation statements)

References 105 publications

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“…In contrast, no triggered phenomenon occurred in the immature age group. If early afterdepolarizations and triggered activity are the underlying mechanism for drug-induced torsade de pointes, we may anticipate that d-sotalol treatment of children may be less likely to produce new onset arrhythmias (27,28). This result may seem paradoxical at first.…”

Section: Methodsmentioning

confidence: 99%

Developmental Cellular Electrophysiologic Effects of d-Sotalol on Canine Cardiac Purkinje Fibers

Moak

1991

Pediatr Res

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ABSTRACT. d-Sotalol may be a clinically useful class I11 antiarrhythmic agent for controlling ventricular arrhythmias in children. Because age-related differences in repolarization currents may contribute to developmental differences in response to antiarrhythmic agents that primarily affect repolarization, the electrophysiologic effects of dsotalol were compared in Purkinje fibers from neonatal and adult dogs. Significant age-related changes characterized the antiarrhythmic profile of d-sotalol. d-Sotalol M) significantly prolonged the action potential duration of adult Purkinje fibers (310 f 8 to 380 f 7 ms, p < 0.01) and neonatal fibers (247 f 5 to 342 f 9 ms, p < 0.01).However, the lengthening of action potential duration was significantly greater in the immature age group. d-Sotalol had no significant effect on maximum diastolic potential, action potential amplitude, or phase zero upstroke velocity in normally polarized fibers. In contrast, different electrophysiologic effects were observed in K+-depolarized Purkinje fibers. Superfusion of adult K+-depolarized fibers with d-sotalol suppressed excitability in five (38%) of 13 fibers and significantly decreased action potential amplitude (88 f 2 to 83 f 1 mV, p < 0.05) and phase zero upstroke velocity (180 f 14 to 105 f 3 V/s, p < 0.01) in the other eight fibers. The membrane depressant effects observed in the younger age group were significantly less [no suppression of excitability and a smaller decrease in phase zero upstroke velocity (121 f 22 to 101 f 23 V/s, p < 0.05). The magnitude of action potential duration prolongation by d-sotalol in K+-depolarized fibers was less than in normally polarized fibers. These results suggest that at the clinical level the mechanism of d-sotalol's antiarrhythmic action will depend not only on the developmental maturity, but also on the resting membrane potential of the tissue treated. (Pediatr Res 29: 104-109, 1991)Abbreviations APA, action potential amplitude APDw, action potential duration to 50% repolarization APD,,, action potential duration to full repolarization MDP, maximum diastolic potential V, . , , phase zero upstroke velocity Arrhythmia control by lengthening of cardiac repolarization has emerged as an effective antiarrhythmic mechanism (1). A

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Section: Methodsmentioning

confidence: 99%

Developmental Cellular Electrophysiologic Effects of d-Sotalol on Canine Cardiac Purkinje Fibers

Moak

1991

Pediatr Res

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“…frequent adverse cardiovascular effect is symptomatic bradycardia which is dose-dependent; pacemaker implantation may be necessary (Naccarelli et al 1985). This effect is more common in the elderly, particularly when combination therapy with digoxin or i3-blockers is used and when amiodarone is administered for control of tachycardia in the bradycardia-tachycardia syndrome.…”

Section: Cardiac Adverse Effectsmentioning

confidence: 96%

Risk-Benefit Assessment of Amiodarone in the Treatment of Cardiac Arrhythmias

Counihan

McKenna

1990

Drug Safety

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Cardiac arrhythmias are a cause of significant morbidity and mortality in patients with cardiac disease, and thus represent a major management problem. The recognition that antiarrhythmic drugs have the potential to aggravate as well as to attenuate arrhythmias has prompted clinicians to reconsider treatment strategies and weight the benefits of treatment against the risks. In this context, amiodarone has emerged as an effective antiarrhythmic agent and when used at the lowest effective dose has an acceptable side effect profile. This review focuses on the current clinical usage of amiodarone in a broad variety of cardiac arrhythmias, and addresses the risk-benefits arising from its use. It further discusses the current position of amiodarone in the management of sudden cardiac death.

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“…They appear to be dose dependent and occur more commonly when the dose exceeds 600mg/day [88,89]. At low doses, there is no significant difference when compared to placebo [89].…”

Section: Gastrointestinalmentioning

confidence: 99%

Amiodarone - A ‘Broad Spectrum’ Antiarrhythmic Drug

Punnam

Goyal

Kotaru

et al. 2010

CHDDT

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Amiodarone, an iodinated benzofuran derivative, introduced in 1960's as an anti-anginal agent, emerged as a potent anti-arrhythmic agent by 1970's and is currently one of the most commonly prescribed drugs in US for ventricular and atrial arrhythmias. Although amiodarone is considered a class III anti-arrhythmic agent, it also has class I, II, IV actions, making it a unique and effective anti-arrhythmic agent. Because of its minimal negative inotropic activity and very low rate of pro-arrhythmia, it is considered safe in treating arrhythmias in patients with Coronary Artery Disease and Left ventricular systolic dysfunction. Despite these advantages, long term oral therapy with amiodarone is limited by side effect profile involving various organs like thyroid, lung, heart, liver, skin etc. Though the side effects can be decreased significantly by keeping the maintenance dose at 200 to 300 mg/day, patients on amiodarone should be followed closely. Amiodarone interacts with medications such as Warfarin, Digoxin, Macrolides, Floroquinolones etc., which share Cytochrome P450 metabolic pathway. Hence reducing their doses prior to starting amiodarone is recommended. Amiodarone, a category D drug, is contraindicated in pregnant and breast feeding women. This review discusses the pharmacokinetics of amiodarone, its evolving clinical indications, management of toxicity and drug interactions.

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Amiodarone: Pharmacology and Antiarrhythmic and Adverse Effects

Cited by 59 publications

References 105 publications

Developmental Cellular Electrophysiologic Effects of d-Sotalol on Canine Cardiac Purkinje Fibers

Developmental Cellular Electrophysiologic Effects of d-Sotalol on Canine Cardiac Purkinje Fibers

Risk-Benefit Assessment of Amiodarone in the Treatment of Cardiac Arrhythmias

Amiodarone - A ‘Broad Spectrum’ Antiarrhythmic Drug

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Amiodarone: Pharmacology and Antiarrhythmic and Adverse Effects

Cited by 59 publications

References 105 publications

Developmental Cellular Electrophysiologic Effects of d-Sotalol on Canine Cardiac Purkinje Fibers

Developmental Cellular Electrophysiologic Effects of d-Sotalol on Canine Cardiac Purkinje Fibers

Risk-Benefit Assessment of Amiodarone in the Treatment of Cardiac Arrhythmias

Amiodarone - A &#x2018;Broad Spectrum&#x2019; Antiarrhythmic Drug

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Amiodarone - A ‘Broad Spectrum’ Antiarrhythmic Drug