Torsade de Pointes during Combined Treatment with Risperidone and Citalopram

Blaschke, Daniel N.; Parwani, Abdul Shokor; Huemer, Martin; Rolf, Sascha; Boldt, Leif‐Hendrik; Dietz, Robert M.; Haverkamp, Wilhelm

doi:10.1055/s-2007-992147

Cited by 22 publications

(15 citation statements)

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“…Of the male subjects, 18 had a QT interval of > 450 ms and 1 had a QT interval of > 480 ms. Of the female subjects, 47 had a QT interval of > 450 ms and 6 had a QT interval of > 480 ms. Our data confi rmed female gender as a risk for QT interval prolongation [ 4 ] . Despite one report which indicates a risk of life-threatening arrhythmia through use of multiple QT prolongation potentiating drugs [ 11 ] , no signifi cant diff erence in QTc interval between monotherapy and polymedication was found [analysis of variance, F(1, 501) = 1.11, p = 0.22] in our research.…”

Section: Discussioncontrasting

confidence: 99%

Pharmacotherapeutic Determinants for QTc Interval Prolongation in Japanese Patients with Mood Disorder

et al. 2012

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An increased incidence of sudden death has been observed among patients treated with antidepressants. A prolonged QTc interval is a known prognostic factor for fatal arrhythmia, and several studies have shown that the use of antidepressants can cause a prolonged QTc interval. However, few studies, especially in Japan, have compared the effects of multiple drugs on QTc interval or examined dose relationships in a clinical setting.We compared the effects of antidepressants on QT interval, corrected to QTc by Bazett's formula, in 729 Japanese patients who were diagnosed with mood disorder.Using stepwise multiple linear regression analysis, we found that the use of tricyclic antidepressants (P<0.01) and concomitant use of antipsychotics (P<0.05), as well as advanced age and being female (known factors for prolonged QTc interval; both P<0.01), significantly prolonged the QTc interval. Analysis of individual antidepressants also revealed that the use of clomipramine (P<0.01) and amitriptyline (P<0.05) significantly prolonged the QTc interval.Our results reveal that tricyclic antidepressants, especially clomipramine and amitriptyline, confer a risk of prolonged QTc interval in a dose-dependent manner. The selective serotonin reuptake inhibitors investigated (fluvoxamine, paroxetine, sertraline) were not indicated as risk factors for QTc prolongation.

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Section: Discussioncontrasting

confidence: 99%

Pharmacotherapeutic Determinants for QTc Interval Prolongation in Japanese Patients with Mood Disorder

et al. 2012

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“…88 Like other antipsychotic agents, application of risperidone can also induce alterations in myocardial repolar ization. [91][92][93][94] A meta-analysis suggested a significantly elevated incidence of cardiac events compared with placebo. 95 A marked prolongation of cardiac repolar ization at supratherapeutic doses was observed in a dog model.…”

Section: Antipsychotic and Antidepressant Drugsmentioning

confidence: 99%

Drug-induced proarrhythmia: risk factors and electrophysiological mechanisms

2015

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Drug-induced ventricular tachyarrhythmias can be caused by cardiovascular drugs, noncardiovascular drugs, and even nonprescription agents. They can result in arrhythmic emergencies and sudden cardiac death. If a new arrhythmia or aggravation of an existing arrhythmia develops during therapy with a drug at a concentration usually considered not to be toxic, the situation can be defined as proarrhythmia. Various cardiovascular and noncardiovascular drugs can increase the occurrence of polymorphic ventricular tachycardia of the 'torsade de pointes' type. Antiarrhythmic drugs, antimicrobial agents, and antipsychotic and antidepressant drugs are the most important groups. Age, female sex, and structural heart disease are important risk factors for the occurrence of torsade de pointes. Genetic predisposition and individual pharmacodynamic and pharmacokinetic sensitivity also have important roles in the generation of arrhythmias. An increase in spatial or temporal dispersion of repolarization and a triangular action-potential configuration have been identified as crucial predictors of proarrhythmia in experimental models. These studies emphasized that sole consideration of the QT interval is not sufficient to assess the proarrhythmic risk. In this Review, we focus on important triggers of proarrhythmia and the underlying electrophysiological mechanisms that can enhance or prevent the development of torsade de pointes.

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“…In other reports, cardiac effects have been found to occur when a selective serotonin reuptake inhibitor has been administered in combination with other drugs that are independently capable of prolonging QTc 68,69. Elsewhere, the association between selective serotonin reuptake inhibitor administration and the occurrence of QTc prolongation may be explained by the coexistence of other factors, including hypokalemia and hypomagnesemia 70,71.…”

Section: Differential Risk Between Antidepressant Classesmentioning

confidence: 96%

Clinical use of antidepressant therapy and associated cardiovascular risk

Waring¹

2012

DHPS

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A number of different psychotropic agents have been associated with an increased risk of cardiovascular disease, and these relationships have been difficult to interpret due to the presence of confounding factors. Recently, there has been renewed interest in the potential for certain antidepressants to cause QT prolongation, which is a predisposing factor for arrhythmia. However, the optimum means of determining QT remains contentious due to discrepancies between methods that may be readily applied in a clinical setting versus more detailed techniques during regulatory assessment. A number of different pharmacological mechanisms might explain the occurrence of adverse cardiac effects, and these differ according to the type of antidepressant agent. Emerging data indicate that citalopram exhibits a dose-effect relationship for QT prolongation. Whereas cardiotoxicity is readily apparent in the context of intentional antidepressant overdose, the occurrence of cardiac effects as a result of therapeutic administration is less certain. Pre-existing cardiac disease and other factors that independently predispose to arrhythmia are important considerations. Therefore, clinical judgment is needed to evaluate the overall risk or benefit of a particular antidepressant in any patient. Close monitoring should be considered for those at greatest risk of QT prolongation and arrhythmia.

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Torsade de Pointes during Combined Treatment with Risperidone and Citalopram

Cited by 22 publications

References 1 publication

Pharmacotherapeutic Determinants for QTc Interval Prolongation in Japanese Patients with Mood Disorder

Pharmacotherapeutic Determinants for QTc Interval Prolongation in Japanese Patients with Mood Disorder

Drug-induced proarrhythmia: risk factors and electrophysiological mechanisms

Clinical use of antidepressant therapy and associated cardiovascular risk

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