The ion channel basis of pharmacological effects of amiodarone on myocardial electrophysiological properties, a comprehensive review
Amiodarone is a benzofuran-based class III antiarrhythmic agent frequently used for the treatment of atrial and ventricular arrhythmias. The primary target of class III antiarrhythmic drugs is the cardiac human ether-a-go-go-related gene (hERG) encoded channel, KCNH2, commonly known as HERG, that co...
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| Published in | Biomedicine & pharmacotherapy Vol. 174; p. 116513 |
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| Main Authors | , , , , , , , , |
| Format | Journal Article |
| Language | English |
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01.05.2024
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| Abstract | Amiodarone is a benzofuran-based class III antiarrhythmic agent frequently used for the treatment of atrial and ventricular arrhythmias. The primary target of class III antiarrhythmic drugs is the cardiac human ether-a-go-go-related gene (hERG) encoded channel, KCNH2, commonly known as HERG, that conducts the rapidly activating delayed rectifier potassium current (IKr). Like other class III antiarrhythmic drugs, amiodarone exerts its physiologic effects mainly through IKr blockade, delaying the repolarization phase of the action potential and extending the effective refractory period. However, while many class III antiarrhythmics, including sotalol and dofetilide, can cause long QT syndrome (LQTS) that can progress to torsade de pointes, amiodarone displays less risk of inducing this fatal arrhythmia. This review article discusses the arrhythmogenesis in LQTS from the aspects of the development of early afterdepolarizations (EADs) associated with Ca2+ current, transmural dispersion of repolarization (TDR), as well as reverse use dependence associated with class III antiarrhythmic drugs to highlight electropharmacological effects of amiodarone on the myocardium. |
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| AbstractList | Amiodarone is a benzofuran-based class III antiarrhythmic agent frequently used for the treatment of atrial and ventricular arrhythmias. The primary target of class III antiarrhythmic drugs is the cardiac human ether-a-go-go-related gene (hERG) encoded channel, KCNH2, commonly known as HERG, that conducts the rapidly activating delayed rectifier potassium current (I
). Like other class III antiarrhythmic drugs, amiodarone exerts its physiologic effects mainly through I
blockade, delaying the repolarization phase of the action potential and extending the effective refractory period. However, while many class III antiarrhythmics, including sotalol and dofetilide, can cause long QT syndrome (LQTS) that can progress to torsade de pointes, amiodarone displays less risk of inducing this fatal arrhythmia. This review article discusses the arrhythmogenesis in LQTS from the aspects of the development of early afterdepolarizations (EADs) associated with Ca
current, transmural dispersion of repolarization (TDR), as well as reverse use dependence associated with class III antiarrhythmic drugs to highlight electropharmacological effects of amiodarone on the myocardium. Amiodarone is a benzofuran-based class III antiarrhythmic agent frequently used for the treatment of atrial and ventricular arrhythmias. The primary target of class III antiarrhythmic drugs is the cardiac human ether-a-go-go-related gene (hERG) encoded channel, KCNH2, commonly known as HERG, that conducts the rapidly activating delayed rectifier potassium current (IKr). Like other class III antiarrhythmic drugs, amiodarone exerts its physiologic effects mainly through IKr blockade, delaying the repolarization phase of the action potential and extending the effective refractory period. However, while many class III antiarrhythmics, including sotalol and dofetilide, can cause long QT syndrome (LQTS) that can progress to torsade de pointes, amiodarone displays less risk of inducing this fatal arrhythmia. This review article discusses the arrhythmogenesis in LQTS from the aspects of the development of early afterdepolarizations (EADs) associated with Ca2+ current, transmural dispersion of repolarization (TDR), as well as reverse use dependence associated with class III antiarrhythmic drugs to highlight electropharmacological effects of amiodarone on the myocardium. Amiodarone is a benzofuran-based class III antiarrhythmic agent frequently used for the treatment of atrial and ventricular arrhythmias. The primary target of class III antiarrhythmic drugs is the cardiac human ether-a-go-go-related gene (hERG) encoded channel, KCNH2, commonly known as HERG, that conducts the rapidly activating delayed rectifier potassium current (IKr). Like other class III antiarrhythmic drugs, amiodarone exerts its physiologic effects mainly through IKr blockade, delaying the repolarization phase of the action potential and extending the effective refractory period. However, while many class III antiarrhythmics, including sotalol and dofetilide, can cause long QT syndrome (LQTS) that can progress to torsade de pointes, amiodarone displays less risk of inducing this fatal arrhythmia. This review article discusses the arrhythmogenesis in LQTS from the aspects of the development of early afterdepolarizations (EADs) associated with Ca2+ current, transmural dispersion of repolarization (TDR), as well as reverse use dependence associated with class III antiarrhythmic drugs to highlight electropharmacological effects of amiodarone on the myocardium.Amiodarone is a benzofuran-based class III antiarrhythmic agent frequently used for the treatment of atrial and ventricular arrhythmias. The primary target of class III antiarrhythmic drugs is the cardiac human ether-a-go-go-related gene (hERG) encoded channel, KCNH2, commonly known as HERG, that conducts the rapidly activating delayed rectifier potassium current (IKr). Like other class III antiarrhythmic drugs, amiodarone exerts its physiologic effects mainly through IKr blockade, delaying the repolarization phase of the action potential and extending the effective refractory period. However, while many class III antiarrhythmics, including sotalol and dofetilide, can cause long QT syndrome (LQTS) that can progress to torsade de pointes, amiodarone displays less risk of inducing this fatal arrhythmia. This review article discusses the arrhythmogenesis in LQTS from the aspects of the development of early afterdepolarizations (EADs) associated with Ca2+ current, transmural dispersion of repolarization (TDR), as well as reverse use dependence associated with class III antiarrhythmic drugs to highlight electropharmacological effects of amiodarone on the myocardium. |
| ArticleNumber | 116513 |
| Author | Gelman, Illia Tomei, Nicole Sharma, Neelakshi Lee, Peter Mckeeman, Olivia Baranchuk, Adrian Campagna, Noah Zhang, Shetuan El-Diasty, Mohammad |
| Author_xml | – sequence: 1 givenname: Illia orcidid: 0009-0007-8109-9143 surname: Gelman fullname: Gelman, Illia organization: Department of Biomedical and Molecular Sciences, Queens’s University, Kingston, ON, Canada – sequence: 2 givenname: Neelakshi surname: Sharma fullname: Sharma, Neelakshi organization: Department of Biomedical and Molecular Sciences, Queens’s University, Kingston, ON, Canada – sequence: 3 givenname: Olivia surname: Mckeeman fullname: Mckeeman, Olivia organization: Department of Biomedical and Molecular Sciences, Queens’s University, Kingston, ON, Canada – sequence: 4 givenname: Peter surname: Lee fullname: Lee, Peter organization: Division of Cardiology, Department of Medicine, Queen's University, Kingston, ON, Canada – sequence: 5 givenname: Noah surname: Campagna fullname: Campagna, Noah organization: Department of Biomedical and Molecular Sciences, Queens’s University, Kingston, ON, Canada – sequence: 6 givenname: Nicole surname: Tomei fullname: Tomei, Nicole organization: Department of Biomedical and Molecular Sciences, Queens’s University, Kingston, ON, Canada – sequence: 7 givenname: Adrian surname: Baranchuk fullname: Baranchuk, Adrian organization: Division of Cardiology, Department of Medicine, Queen's University, Kingston, ON, Canada – sequence: 8 givenname: Shetuan surname: Zhang fullname: Zhang, Shetuan email: shetuan.zhang@queensu.ca organization: Department of Biomedical and Molecular Sciences, Queens’s University, Kingston, ON, Canada – sequence: 9 givenname: Mohammad surname: El-Diasty fullname: El-Diasty, Mohammad email: 20med4@queensu.ca organization: Department of Biomedical and Molecular Sciences, Queens’s University, Kingston, ON, Canada |
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| Keywords | Anti-arrhythmic drugs Ion channels Amiodarone Electropharmacology Cardiac electrophysiology |
| Language | English |
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