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Review
. 2008 Mar;7(2):181-94.
doi: 10.1517/14740338.7.2.181.

Sudden cardiac death secondary to antidepressant and antipsychotic drugs

Serge Sicouri  1 , Charles Antzelevitch
Affiliations
Review

Sudden cardiac death secondary to antidepressant and antipsychotic drugs

Serge Sicouri et al. Expert Opin Drug Saf. 2008 Mar.

Abstract

A number of antipsychotic and antidepressant drugs are known to increase the risk of ventricular arrhythmias and sudden cardiac death. Based largely on a concern over QT prolongation and the development of life-threatening arrhythmias, a number of antipsychotic drugs have been temporarily or permanently withdrawn from the market or their use restricted. Some antidepressants and antipsychotics have been linked to QT prolongation and the development of Torsade de pointes arrhythmias, whereas others have been associated with a Brugada syndrome phenotype and the development of polymorphic ventricular arrhythmias. This review examines the mechanisms and predisposing factors underlying the development of cardiac arrhythmias, and sudden cardiac death, associated with antidepressant and antipsychotic drugs in clinical use.

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Figures

Figure 1
Figure 1. A. Self limiting TdP episode. B. TdP leading to ventricular fibrillation
TdP is preceded by a short-long-short sequence. Modified from [111] with permission. TdP: Torsade de pointes.
Figure 2
Figure 2. Brugada syndrome phenotype induced by an overdose of desipramine and clonazepam in a 44-year-old man previously medicated with desipramine, clonazepam and trazodone
A. ECG shows sinus bradycardia, first-degree AV block (228 ms), prolonged QRS interval (132 ms), and downsloping ST elevation (Type 1) in leads V1 – V2, ST elevation in lead V3, upsloping ST depression in leads II, III, and aVF. B. Baseline ECG from 1 year ago is normal. Modified from [42], with permission. ECG: Electrocardiogram.
Figure 3
Figure 3. Proposed mechanisms of arrhythmias in the long QT syndrome
APD: Action potential duration; DAD: Delayed after-depolarization; EAD: Early after-depolarization.
Figure 4
Figure 4. Proposed mechanism for the Brugada syndrome
A shift in the balance of currents serves to amplify existing heterogeneities by causing loss of the action potential dome at some epicardial but not endocardial sites. A vulnerable window develops as a result of the dispersion of repolarization and refractoriness within epicardium as well as across the wall. Epicardial dispersion leads to the development of Phase II re-entry, which provides the extrasystole that captures the vulnerable window and initiates VT/VF via a circus movement re-entry mechanism. Modified from [122], with permission. APD: Action potential duration.
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