QTc interval prolongation and antipsychotic drug treatments: focus on sertindole
(2005) In International Journal of Neuropsychopharmacology 8(4). p.615-629- Abstract
- Since the 1960s, physicians have been aware of electrocardiographic (ECG) abnormalities and cases of sudden death associated with the use of antipsychotic drugs in patients with schizophrenia. Explanations for Such deaths have traditionally focused on drug-induced prolongation of the QT interval leading to the development of life-threatening ventricular arrhythmias such as torsade de pointes (TdP). It is now apparent that most conventional and atypical antipsychotics can cause dose-related prolongation of the corrected QT interval (QTc), although there are important differences in the potency of individual agents. This review discusses potential mechanisms underlying QTc prolongation and arrhythinogenesis and examines the evidence for a... (More)
- Since the 1960s, physicians have been aware of electrocardiographic (ECG) abnormalities and cases of sudden death associated with the use of antipsychotic drugs in patients with schizophrenia. Explanations for Such deaths have traditionally focused on drug-induced prolongation of the QT interval leading to the development of life-threatening ventricular arrhythmias such as torsade de pointes (TdP). It is now apparent that most conventional and atypical antipsychotics can cause dose-related prolongation of the corrected QT interval (QTc), although there are important differences in the potency of individual agents. This review discusses potential mechanisms underlying QTc prolongation and arrhythinogenesis and examines the evidence for a relationship between antipsychotic drugs and prolongation of the QTc interval. New electrophysiological and epidemiological data are presented which suggest there may not be a clear-cut cause-effect relationship between QTc prolongation and the development of ventricular tachyarrhythmias for all atypical antipsychotics. For at least one of these agents (sertindole), counterbalancing mechanisms may act to reduce the risk of proarrhythmic activity arising as a result of QTc prolongation. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/212184
- author
- Lindstrom, E ; Farde, L ; Eberhard, Jonas LU and Haverkamp, W
- organization
- publishing date
- 2005
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- sertindole, antipsychotic agents, QT interval, torsade de pointes
- in
- International Journal of Neuropsychopharmacology
- volume
- 8
- issue
- 4
- pages
- 615 - 629
- publisher
- Cambridge University Press
- external identifiers
-
- pmid:15963244
- wos:000233476700016
- scopus:25844479293
- pmid:15963244
- ISSN
- 1469-5111
- DOI
- 10.1017/S1461145705005250
- language
- English
- LU publication?
- yes
- id
- 1d3b308f-f684-4abb-bca1-babd41dcf7bd (old id 212184)
- date added to LUP
- 2016-04-01 12:09:39
- date last changed
- 2024-01-08 10:33:52
@article{1d3b308f-f684-4abb-bca1-babd41dcf7bd,
abstract = {{Since the 1960s, physicians have been aware of electrocardiographic (ECG) abnormalities and cases of sudden death associated with the use of antipsychotic drugs in patients with schizophrenia. Explanations for Such deaths have traditionally focused on drug-induced prolongation of the QT interval leading to the development of life-threatening ventricular arrhythmias such as torsade de pointes (TdP). It is now apparent that most conventional and atypical antipsychotics can cause dose-related prolongation of the corrected QT interval (QTc), although there are important differences in the potency of individual agents. This review discusses potential mechanisms underlying QTc prolongation and arrhythinogenesis and examines the evidence for a relationship between antipsychotic drugs and prolongation of the QTc interval. New electrophysiological and epidemiological data are presented which suggest there may not be a clear-cut cause-effect relationship between QTc prolongation and the development of ventricular tachyarrhythmias for all atypical antipsychotics. For at least one of these agents (sertindole), counterbalancing mechanisms may act to reduce the risk of proarrhythmic activity arising as a result of QTc prolongation.}},
author = {{Lindstrom, E and Farde, L and Eberhard, Jonas and Haverkamp, W}},
issn = {{1469-5111}},
keywords = {{sertindole; antipsychotic agents; QT interval; torsade de pointes}},
language = {{eng}},
number = {{4}},
pages = {{615--629}},
publisher = {{Cambridge University Press}},
series = {{International Journal of Neuropsychopharmacology}},
title = {{QTc interval prolongation and antipsychotic drug treatments: focus on sertindole}},
url = {{http://dx.doi.org/10.1017/S1461145705005250}},
doi = {{10.1017/S1461145705005250}},
volume = {{8}},
year = {{2005}},
}