ArticleCurrent cardiology reviews2009
Iatrogenic QT Abnormalities and Fatal Arrhythmias: Mechanisms and Clinical Significance.
Article in Current cardiology reviews, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
22 citing papers in PubMed, 56 citations in OpenAlex.
- Single therapeutic and supratherapeutic doses of sacubitril/valsartan (LCZ696) do not affect cardiac repolarization.European journal of clinical pharmacology · 2016Trial
- Review
- Is Arsenic Exposure a Risk Factor for Metabolic Syndrome? A Review of the Potential Mechanisms.Frontiers in endocrinology · 2022Review
- Antiviral and anti-inflammatory drugs to combat COVID-19: Effects on cardiac ion channels and risk of ventricular arrhythmias.BioImpacts : BI · 2022Review
- Genetic and Molecular Aspects of Drug-Induced QT Interval Prolongation.International journal of molecular sciences · 2021Review
- Cushing Syndrome in a Pediatric Patient With a KCNJ5 Variant and Successful Treatment With Low-dose Ketoconazole.The Journal of clinical endocrinology and metabolism · 2021Article
- Effects of Anisodine Hydrobromide on the Cardiovascular and Respiratory Functions in Conscious Dogs.Drug design, development and therapy · 2020Article
- A literature-based algorithm for the assessment, management, and monitoring of drug-induced QTc prolongation in the psychiatric population.Neuropsychiatric disease and treatment · 2019Review
- Article
- Drug-induced Inhibition and Trafficking Disruption of ion Channels: Pathogenesis of QT Abnormalities and Drug-induced Fatal Arrhythmias.Current cardiology reviews · 2016Review
- In silico screening of the impact of hERG channel kinetic abnormalities on channel block and susceptibility to acquired long QT syndrome.Journal of molecular and cellular cardiology · 2015Article
- [Long QT syndrome. History, genetics, clinical symptoms, causes and therapy].Der Anaesthesist · 2015Review
- Management of gastrointestinal involvement in scleroderma.Current treatment options in rheumatology · 2015Article
- Mechanisms underlying probucol-induced hERG-channel deficiency.Drug design, development and therapy · 2015Article
- In silico screening of the impact of hERG channel kinetic abnormalities on channel block and susceptibility to acquired long QT syndrome.Journal of molecular and cellular cardiology · 2014Article
- Voriconazole associated torsades de pointes in two adult patients with haematological malignancies.Medical mycology case reports · 2014Article
- Intravenous palonosetron increases the incidence of QTc prolongation during sevoflurane general anesthesia for laparotomy.Korean journal of anesthesiology · 2013Article
- Drug induced QT prolongation: the measurement and assessment of the QT interval in clinical practice.British journal of clinical pharmacology · 2013Review
- Pregnancy outcome after gestational exposure to erythromycin - a population-based register study from Norway.British journal of clinical pharmacology · 2012Article
- Chemotherapy-induced nausea and vomiting: pathophysiology and therapeutic principles.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2012Review
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Severe and occasionally fatal arrhythmias, commonly presenting as Torsade de Pointes [TdP] have been reported with Class III-antiarrhythmics, but also with non-antiarrhythmic drugs. Most cases result from an action on K(+) channels encoded by the HERG gene responsible for the IKr repolarizing current, leading to a long QT and repolarization abnormalities. The hydrophobic central cavity of the HERG-K+ channels, allows a large number of structurally unrelated drugs to bind and cause direct channel inhibition. Some examples are dofetilide, quinidine, sotalol, erythromycin, grepafloxacin, cisapride, dolasetron, thioridazine, haloperidol, droperidol and pimozide. Other drugs achieve channel inhibition indirectly by impairing channel traffic from the endoplasmic reticulum to the cell membrane, decreasing channel membrane density (pentamidine, geldalamicin, arsenic trioxide, digoxin, and probucol). Whereas, ketoconazole, fluoxetine and norfluoxetine induce both direct channel inhibition and impaired channel trafficking. Congenital long QT syndrome, subclinical ion-channel mutations, subjects and relatives of subjects with previous history of drug-induced long QT or TdP, dual drug effects on cardiac repolarization [long QT plus increased QT dispersion], increased transmural dispersion of repolarization and T wave abnormalities, use of high doses, metabolism inhibitors and/or combinations of QT prolonging drugs, hypokalemia, structural cardiac disease, sympathomimetics, bradycardia, women and older age, have been shown to increase the risk for developing drug-induced TdP. Because most of these reactions are preventable, careful evaluation of risk factors and increased knowledge of drugs use associated with repolarization abnormalities is strongly recommended. Future genetic testing and development of practical and simple provocation tests are in route to prevent iatrogenic TdP.
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