Amiodarone: A multifaceted antiarrhythmic drug

Singh, Bramah N.

doi:10.1007/s11886-006-0074-2

Cited by 46 publications

(48 citation statements)

References 43 publications

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“…The fact that this drug exhibits the added benefit of reducing the parasite burden and at the same time operates synergistically, enhancing the efficacy of other specific antiparasitic agents, highlights the multiple properties of this compound and places this agent as a first-line drug not only for the symptomatic treatment of arrhythmias but as an anti-T. cruzi drug. Nevertheless, its long-term use in some patients may be limited due to its potential side effects, such as pulmonary fibrosis, thyroid dysfunction and skin pigmentation; thus, patients must be carefully monitored [23] .…”

Section: Discussionmentioning

confidence: 99%

Amiodarone and Itraconazole: A Rational Therapeutic Approach for the Treatment of Chronic Chagas’ Disease

Paniz‐Mondolfi¹,

Perez-alvarez²,

Lanza

et al. 2009

Chemotherapy

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In the Americas, approximately 20 million people suffer from the chronic phases of Chagas’ disease, of which chagasic cardiomyopathy is the most important clinical feature. The elimination of Trypanosoma cruzi is a pivotal step in arresting the evolution of the disease. Unfortunately, currently available chemotherapy is mostly ineffective due to its limited efficacy and toxic side effects. The following case highlights the efficacy of new diagnostic and follow-up methods in the evaluation of novel trypanocidal compounds such as amiodarone and itraconazole.

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Section: Discussionmentioning

confidence: 99%

Amiodarone and Itraconazole: A Rational Therapeutic Approach for the Treatment of Chronic Chagas’ Disease

Paniz‐Mondolfi¹,

Perez-alvarez²,

Lanza

et al. 2009

Chemotherapy

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“…It has also been demonstrated that amiodarone inhibits the activity of carnitine palmitoyltransferase-1, an enzyme involved in the metabolism of fatty acids, a potentially harmful energy substrate in situations of ischemia [114]. Amiodarone was shown to prevent induction of the MPTP on heart mitochondria, while being toxic to mitochondria from other tissues [115].…”

Section: Hemodynamic Drugsmentioning

confidence: 99%

Mitochondrial Involvement in Cardiac Apoptosis During Ischemia and Reperfusion: Can We Close the Box?

et al. 2009

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Myocardial ischemia is the main cause of death in the Western societies. Therapeutic strategies aimed to protect the ischemic myocardium have been extensively studied. Reperfusion is the definitive treatment for acute coronary syndromes, especially acute myocardial infarction; however, reperfusion has the potential to exacerbate tissue injury, a process termed reperfusion injury. Ischemia/reperfusion (I/R) injury may lead to cardiac arrhythmias and contractile dysfunction that involve apoptosis and necrosis in the heart. The present review describes the mitochondrial role on cardiomyocyte death and some potential pharmacological strategies aimed at preventing the opening of the box, i.e., mitochondrial dysfunction and membrane permeabilization that result into cell death. Data in the literature suggest that mitochondrial disruption during I/R can be avoided, although uncertainties still exist, including the fact that the optimal windows of treatment are still fairly unknown. Despite this, the protection of cardiac mitochondrial function should be critical for the patient survival, and new strategies to avoid mitochondrial alterations should be designed to avoid cardiomyocyte loss.

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“…Amiodarone is a class III antiarrhythmic drug. It inhibits repolarizing K + currents and so prolongs the cardiac AP; it weakly inhibits depolarizing currents, such as those mediated by the Na + and Ca 2+ channels [32][33][34] . Therefore, it was worth comparing the electrophysiological effects of these two drugs.…”

Section: Discussionmentioning

confidence: 99%

Electrophysiological mechanisms of sophocarpine as a potential antiarrhythmic agent

Yang

Wang

et al. 2011

Acta Pharmacol Sin

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Aim: To examine the electrophysiological effects of sophocarpine on action potentials (AP) and ionic currents of cardiac myocytes and to compare some of these effects with those of amiodarone. Methods: Langendorff perfusion set-up was used in isolated guinea pig heart, and responses to sophocarpine were monitored using electrocardiograph. Conventional microelectrode, voltage clamp technique and perforated patch were employed to record fast response AP (fAP), slow response AP (sAP) and ionic currents in guinea pig papillary muscle or rabbit sinus node cells. Results: Tachyarrhythmia produced by isoprenaline (15 μmol/L) could be reversed by sophocarpine (300 μmol/L). Sophocarpine (10 μmol/L) decreased the amplitude by 4.0%, maximal depolarization velocity (V max ) of the fAP by 24.4%, and Na + current (I Na ) by 18.0%, while it prolonged the effective refractory period (ERP) by 21.1%. The same concentration of sophocarpine could also decrease the amplitude and V max of the sAP, by 26.8% and 25.7%, respectively, and attenuated the Ca 2+ current (I CaL ) and the K + tail current substantially. Comparison of sophocarpine with amiodarone demonstrated that both prolonged the duration and the ERP of fAP and sAP, both decreased the amplitude and V max of the fAP and sAP, and both slowed the automatic heart rate. Conclusion: Sophocarpine could reverse isoprenaline-induced arrhythmia and inhibit I Na , I CaL , and I Kr currents. The electrophysiological effects of sophocarpine are similar to those of amiodarone, which might be regarded as a prospective antiarrhythmic agent.

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Amiodarone: A multifaceted antiarrhythmic drug

Cited by 46 publications

References 43 publications

Amiodarone and Itraconazole: A Rational Therapeutic Approach for the Treatment of Chronic Chagas’ Disease

Amiodarone and Itraconazole: A Rational Therapeutic Approach for the Treatment of Chronic Chagas’ Disease

Mitochondrial Involvement in Cardiac Apoptosis During Ischemia and Reperfusion: Can We Close the Box?

Electrophysiological mechanisms of sophocarpine as a potential antiarrhythmic agent

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