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Clinical use of antidepressant therapy and associated cardiovascular risk

Authors Waring WS

Received 21 June 2012

Accepted for publication 26 July 2012

Published 17 August 2012 Volume 2012:4 Pages 93—101

DOI https://doi.org/10.2147/DHPS.S28804

Checked for plagiarism Yes

Review by Single-blind

Peer reviewer comments 3


W Stephen Waring

Acute Medical Unit, York Teaching Hospital NHS Foundation Trust, York, UK

Abstract: 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.

Keywords: arrhythmia, electrocardiography, QT prolongation, selective serotonin reuptake inhibitors, torsades de pointes, tricyclic antidepressants

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