Abstract
Acquired QT syndrome is mainly caused by the administration of drugs that prolong ventricular repolarization. On the other hand, the risk of drug-induced torsades de pointes is increased by numerous predisposing factors, such as genetic predisposition, female sex, hypokalemia and cardiac dysfunction. This adverse reaction is induced by different chemical compounds used for the treatment of a variety of pathologies, including arrhythmias. As it is known, antiarrhythmic agents and other cardiovascular drugs can prolong the QT interval, causing this adverse reaction. Of the 20 most commonly reported drugs, 10 were cardiovascular agents and these appeared in 348 of the reports (46%). Class Ia antiarrhythmic agents have frequently been linked to inducing arrhythmia, including torsades de pointes. Sotalol and amiodarone, class III antiarrhythmics, are known to prolong the QT interval by blocking IKr. Due to the severity of events caused by the therapeutic use of these drugs, in this work of revision the cardiovascular drugs that present this property and the factors and evidence will be mentioned.
Keywords: QT interval, drug-induced torsades de pointes, antiarrhythmic drugs, amiodarone, sotalol, HERG channel
Current Drug Safety
Title: Cardiovascular Drugs Inducing QT Prolongation: Facts and Evidence
Volume: 5 Issue: 1
Author(s): Carlos A. Taira, Javier A.W. Opezzo, Marcos A. Mayer and Christian Hocht
Affiliation:
Keywords: QT interval, drug-induced torsades de pointes, antiarrhythmic drugs, amiodarone, sotalol, HERG channel
Abstract: Acquired QT syndrome is mainly caused by the administration of drugs that prolong ventricular repolarization. On the other hand, the risk of drug-induced torsades de pointes is increased by numerous predisposing factors, such as genetic predisposition, female sex, hypokalemia and cardiac dysfunction. This adverse reaction is induced by different chemical compounds used for the treatment of a variety of pathologies, including arrhythmias. As it is known, antiarrhythmic agents and other cardiovascular drugs can prolong the QT interval, causing this adverse reaction. Of the 20 most commonly reported drugs, 10 were cardiovascular agents and these appeared in 348 of the reports (46%). Class Ia antiarrhythmic agents have frequently been linked to inducing arrhythmia, including torsades de pointes. Sotalol and amiodarone, class III antiarrhythmics, are known to prolong the QT interval by blocking IKr. Due to the severity of events caused by the therapeutic use of these drugs, in this work of revision the cardiovascular drugs that present this property and the factors and evidence will be mentioned.
Export Options
About this article
Cite this article as:
Taira A. Carlos, Opezzo A.W. Javier, Mayer A. Marcos and Hocht Christian, Cardiovascular Drugs Inducing QT Prolongation: Facts and Evidence, Current Drug Safety 2010; 5 (1) . https://dx.doi.org/10.2174/157488610789869229
DOI https://dx.doi.org/10.2174/157488610789869229 |
Print ISSN 1574-8863 |
Publisher Name Bentham Science Publisher |
Online ISSN 2212-3911 |
- Author Guidelines
- Graphical Abstracts
- Fabricating and Stating False Information
- Research Misconduct
- Post Publication Discussions and Corrections
- Publishing Ethics and Rectitude
- Increase Visibility of Your Article
- Archiving Policies
- Peer Review Workflow
- Order Your Article Before Print
- Promote Your Article
- Manuscript Transfer Facility
- Editorial Policies
- Allegations from Whistleblowers
Related Articles
-
Taurine-Diabetes Interaction: From Involvement to Protection
Current Diabetes Reviews Drug-induced Cardiac Mitochondrial Toxicity and Protection: From Doxorubicin to Carvedilol
Current Pharmaceutical Design Methods for Identifying Cardiovascular Agents: A Review
Recent Patents on Cardiovascular Drug Discovery IL-1 Cytokines in Cardiovascular Disease: Diagnostic, Prognostic and Therapeutic Implications
Cardiovascular & Hematological Agents in Medicinal Chemistry Utility of the Electrocardiogram in Drug Overdose and Poisoning: Theoretical Considerations and Clinical Implications
Current Cardiology Reviews Left Ventricular Non-compaction: From Recognition to Treatment
Current Pharmaceutical Design Coenzyme Q10 in Neurodegenerative Diseases
Current Medicinal Chemistry Are Markers of Cardiac Dysfunction Useful in the Assessment of Cardiovascular Risk in Dialysis Patients?
Current Pharmaceutical Design Characterization of Supraventricular Tachycardia in Infants: Clinical and Instrumental Diagnosis
Current Pharmaceutical Design Chemokine Receptor CCR5 Antagonist Maraviroc: Medicinal Chemistry and Clinical Applications
Current Topics in Medicinal Chemistry The Role of Heat Shock Protein (HSP) in Atherosclerosis: Pathophysiology and Clinical Opportunities
Current Medicinal Chemistry The Mechanism of Carvedilol in Experimental Viral Myocarditis
Current Pharmaceutical Design Current Developments on Synthesis, Redox Reactions and Biochemical Studies of Selenium Antioxidants
Current Chemical Biology TGR5 as a Therapeutic Target for Treating Obesity
Current Topics in Medicinal Chemistry Quinone-Based Drugs: An Important Class of Molecules in Medicinal Chemistry
Medicinal Chemistry Heart Failure Pharmacotherapy: Differences Between Adult and Paediatric Patients
Current Medicinal Chemistry Drugs Targeting the Canonical NF-κB Pathway to Treat Viral and Autoimmune Myocarditis
Current Pharmaceutical Design Atherosclerosis-Related Functions of C-Reactive Protein
Cardiovascular & Hematological Disorders-Drug Targets Sympathetic Activation in Congestive Heart Failure: Evidence, Consequences and Therapeutic Implications
Current Vascular Pharmacology MicroRNAs: A Critical Regulator and a Promising Therapeutic and Diagnostic Molecule for Diabetic Cardiomyopathy
Current Gene Therapy