David B Menkes1, James C Knight. 1. Psychological Medicine, University of Wales Academic Unit, Wrescam LL13 7YP, UK. d.menkes@bangor.ac.uk
Abstract
OBJECTIVE: To review the production of cardiac arrhythmia by thioridazine, and consider the role of government regulation in light of antipsychotic prescribing trends in New Zealand. METHODS: We conducted a focused literature review on psychotropic-induced cardiotoxicity, including mechanisms and incidence. In addition, we considered trends in antipsychotic prescription in New Zealand and decisions made by regulatory bodies in Australia, North America and the United Kingdom regarding restrictions on the prescription of thioridazine. RESULTS: In general, the cardiotoxicity of antipsychotics, including thioridazine, relates to the ability of these drugs to antagonize voltage-sensitive potassium channels, and thereby prolong the QT interval. This action can lead to malignant arrhythmias in a very small proportion (< < 1%) of patients; the risk may be increased by other drugs or factors which prolong QT or inhibit the metabolism of thioridazine. A review of prescription doses and volumes in New Zealand indicates that thioridazine is prescribed mainly in low doses by non-specialists, and its use has been waning significantly over the past 2 years. These trends predate recent publicity regarding cardiotoxicity. CONCLUSION: Recommendations regarding thioridazine use are presented. Although new patients should not receive this drug, existing patients benefiting from modest doses should not be denied access unless clear-cut risk factors for cardiotoxicity are evident.
OBJECTIVE: To review the production of cardiac arrhythmia by thioridazine, and consider the role of government regulation in light of antipsychotic prescribing trends in New Zealand. METHODS: We conducted a focused literature review on psychotropic-induced cardiotoxicity, including mechanisms and incidence. In addition, we considered trends in antipsychotic prescription in New Zealand and decisions made by regulatory bodies in Australia, North America and the United Kingdom regarding restrictions on the prescription of thioridazine. RESULTS: In general, the cardiotoxicity of antipsychotics, including thioridazine, relates to the ability of these drugs to antagonize voltage-sensitive potassium channels, and thereby prolong the QT interval. This action can lead to malignant arrhythmias in a very small proportion (< < 1%) of patients; the risk may be increased by other drugs or factors which prolong QT or inhibit the metabolism of thioridazine. A review of prescription doses and volumes in New Zealand indicates that thioridazine is prescribed mainly in low doses by non-specialists, and its use has been waning significantly over the past 2 years. These trends predate recent publicity regarding cardiotoxicity. CONCLUSION: Recommendations regarding thioridazine use are presented. Although new patients should not receive this drug, existing patients benefiting from modest doses should not be denied access unless clear-cut risk factors for cardiotoxicity are evident.
Authors: Lili Aslostovar; Allison L Boyd; Mohammed Almakadi; Tony J Collins; Darryl P Leong; Rommel G Tirona; Richard B Kim; Jim A Julian; Anargyros Xenocostas; Brian Leber; Mark N Levine; Ronan Foley; Mickie Bhatia Journal: Blood Adv Date: 2018-08-14
Authors: Lili Aslostovar; Allison L Boyd; Yannick D Benoit; Justin Di Lu; Juan Luis Garcia Rodriguez; Mio Nakanishi; Deanna P Porras; Jennifer C Reid; Ryan R Mitchell; Brian Leber; Anargyros Xenocostas; Ronan Foley; Mickie Bhatia Journal: Cell Rep Med Date: 2021-02-16