Effects of thioridazine (Mellaril) on ventricular electrophysiologic properties

Yoon, Myung S.; Han, Jaok; Dersham, George H.; Jones, Susan

doi:10.1016/0002-9149(79)90147-4

Cited by 25 publications

(7 citation statements)

References 8 publications

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“…227 Numerous cases of electrocardiographic changes and ventricular arrhythmias with thioridazine have been reported. [228][229][230][231][232][233][234][235][236][237][238][239] This adverse reaction has been reported with both standard dosing as well as in overdose situations. A recent epidemiologic study 121 found that in patients taking psychotropic therapy, those receiving thioridazine were at higher risk for QTc interval lengthening compared with other phenothiazines (only droperidol put patients at higher risk).…”

Section: Definite Associationmentioning

confidence: 99%

“…Thioridazine has quinidine-like effects, slowing fast sodium entry and cardiac conduction and prolonging ventricular repolarization. 229,239 One group 240 demonstrated thioridazine' s blockade of I Kr . In 1996, other investigators 241 showed that thioridazine' s effects on the QT interval increased with increasing dosages and that the parent drug is primarily responsible.…”

Section: Definite Associationmentioning

confidence: 99%

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Clinical Relevance and Management of Drug‐Related QT Interval Prolongation

2003

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Much attention recently has focused on drugs that prolong the QT interval, potentially leading to fatal cardiac dysrhythmias (e.g., torsade de pointes). We provide a detailed review of the published evidence that supports or does not support an association between drugs and their risk of QT prolongation. The mechanism of drug-induced QT prolongation is reviewed briefly, followed by an extensive evaluation of drugs associated with QT prolongation, torsade de pointes, or both. Drugs associated with QT prolongation are identified as having definite, probable, or proposed associations. The role of the clinician in the prevention and management of QT prolongation, drug-drug interactions that may occur with agents known to affect the QT interval, and the impact of this adverse effect on the regulatory process are addressed.

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Section: Definite Associationmentioning

confidence: 99%

Section: Definite Associationmentioning

confidence: 99%

Clinical Relevance and Management of Drug‐Related QT Interval Prolongation

2003

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“…QT prolongation was observed with several agents used in the treatment of CNS disturbances. Most reports are given for thioridazine [51,61,108,212,246,247]. These data indicate a dose-related QT prolongation, sometimes associated with T-wave inversion [212] and frequently associated with torsades de pointes.…”

Section: Characteristics Of Proarrhythmia After Drug-lnduced Qt Prolomentioning

confidence: 99%

QT-Interval prolonging drugs: Mechanisms and clinical relevance of their arrhythmogenic hazards

Zehender

Hohnloser

Just

1991

Cardiovasc Drug Ther

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The antiarrhythmic principle of drug-induced QT-interval prolongation is well known. However, with the widespread use of the presently known and new Class III antiarrhythmic agents under investigation, and the growing number of agents not primarily designed as antiarrhythmic drugs that potentially cause QT prolongation, we have also become aware of the proarrhythmic hazards associated with many of these agents. The proarrhythmic risk differs markedly from one agent to another and interferes with many individual clinical variables (e.g., hypokalemia, sinus bradycardia). This paper summarizes the present data on the proarrhythmic risk of drug-induced QT prolongation, including the value and problems of the rate-corrected QT interval, the mechanisms involved in the genesis of proarrhythmia, and the clinical cofactors that facilitate the occurrence of proarrhythmic events. In addition, an extensive database provides information on the known proarrhythmic risk of all currently used QT-prolonging agents.

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“…This agent has quinidine-like electrophysiologic effects, slowing fast sodium entry and his-Purkinje cardiac conduction and prolonging ventricular repolarization. 19,20 This may be a potent proarrhythmic combination; in overdose thioridazine appears to be more cardiotoxic,21 and in normal doses ECG abnormalities appear more commonly than with other antipsychotic drugs. 4 In Finland, thioridazine was involved in more than half of the sudden deaths of patients taking psychiatric drugs.…”

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confidence: 99%