Cellular basis for triggered ventricular arrhythmias that occur in
the setting of compensated hypertrophy and heart failure: considerations
for diagnosis and treatment.
Malignant ventricular tachyarrhythmias are common among patients with
hypertrophy and heart failure, and these arrhythmias can initiate
by triggered activity. Abnormal repolarization and disturbed calcium
handling due to remodeling processes are common features of the hypertrophied
and failing heart that conspire to facilitate triggering events.
These changes have a different cellular origin in compensated hypertrophy
as compared with failure, which underscores the complexity of mechanisms
that predispose the remodeled heart to arrhythmias. This hampers
the identification of the vulnerable patient and adequate antiarrhythmic
pharmacotherapy. Beat-to-beat variability of repolarization has been
proposed as an early (noninvasive) electrographic detection method
of triggered activity. An increase of variability heralds an enhanced
risk of arrhythmias, and controlling this repolarization parameter
by pharmacological agents is antiarrhythmic. Different drugs (flunarizine,
ranolazine, K201, calmodulin kinase blockers) that are able to prevent
and/or suppress triggered arrhythmias by specific mechanisms of action
will be discussed.
Department of Medical Physiology, Division Heart and Lung, University
Medical Center Utrecht, University of Utrecht, Utrecht, The Netherlands.
g.antoons@umcutrecht.nl
%0 Journal Article
%1 Anto_2007_8
%A Antoons, Gudrun
%A Oros, Avram
%A Bito, Virginie
%A Sipido, Karin R
%A Vos, Marc A
%D 2007
%J J Electrocardiol
%K Agents, Anti-Arrhythmia Cardiac Cardiomegaly, Cardiovascular; Conduction Fibrillation, Heart Humans; Low, Models, Output, System, Ventricular complications/diagnosis/drug drug effects/physiopathology; therapeutic therapy/physiopathology therapy/physiopathology; use;
%N 6 Suppl
%P S8--14
%R 10.1016/j.jelectrocard.2007.05.022
%T Cellular basis for triggered ventricular arrhythmias that occur in
the setting of compensated hypertrophy and heart failure: considerations
for diagnosis and treatment.
%U http://dx.doi.org/10.1016/j.jelectrocard.2007.05.022
%V 40
%X Malignant ventricular tachyarrhythmias are common among patients with
hypertrophy and heart failure, and these arrhythmias can initiate
by triggered activity. Abnormal repolarization and disturbed calcium
handling due to remodeling processes are common features of the hypertrophied
and failing heart that conspire to facilitate triggering events.
These changes have a different cellular origin in compensated hypertrophy
as compared with failure, which underscores the complexity of mechanisms
that predispose the remodeled heart to arrhythmias. This hampers
the identification of the vulnerable patient and adequate antiarrhythmic
pharmacotherapy. Beat-to-beat variability of repolarization has been
proposed as an early (noninvasive) electrographic detection method
of triggered activity. An increase of variability heralds an enhanced
risk of arrhythmias, and controlling this repolarization parameter
by pharmacological agents is antiarrhythmic. Different drugs (flunarizine,
ranolazine, K201, calmodulin kinase blockers) that are able to prevent
and/or suppress triggered arrhythmias by specific mechanisms of action
will be discussed.
@article{Anto_2007_8,
abstract = {Malignant ventricular tachyarrhythmias are common among patients with
hypertrophy and heart failure, and these arrhythmias can initiate
by triggered activity. Abnormal repolarization and disturbed calcium
handling due to remodeling processes are common features of the hypertrophied
and failing heart that conspire to facilitate triggering events.
These changes have a different cellular origin in compensated hypertrophy
as compared with failure, which underscores the complexity of mechanisms
that predispose the remodeled heart to arrhythmias. This hampers
the identification of the vulnerable patient and adequate antiarrhythmic
pharmacotherapy. Beat-to-beat variability of repolarization has been
proposed as an early (noninvasive) electrographic detection method
of triggered activity. An increase of variability heralds an enhanced
risk of arrhythmias, and controlling this repolarization parameter
by pharmacological agents is antiarrhythmic. Different drugs (flunarizine,
ranolazine, K201, calmodulin kinase blockers) that are able to prevent
and/or suppress triggered arrhythmias by specific mechanisms of action
will be discussed.},
added-at = {2009-06-03T11:20:58.000+0200},
author = {Antoons, Gudrun and Oros, Avram and Bito, Virginie and Sipido, Karin R and Vos, Marc A},
biburl = {https://www.bibsonomy.org/bibtex/22dc44c92f85263881e3510ac9fe18523/hake},
description = {The whole bibliography file I use.},
doi = {10.1016/j.jelectrocard.2007.05.022},
file = {Anto_2007_8.pdf:Anto_2007_8.pdf:PDF},
institution = {Department of Medical Physiology, Division Heart and Lung, University
Medical Center Utrecht, University of Utrecht, Utrecht, The Netherlands.
g.antoons@umcutrecht.nl},
interhash = {56862691c8d0d14a9e87f54fcb9862a6},
intrahash = {2dc44c92f85263881e3510ac9fe18523},
journal = {J Electrocardiol},
keywords = {Agents, Anti-Arrhythmia Cardiac Cardiomegaly, Cardiovascular; Conduction Fibrillation, Heart Humans; Low, Models, Output, System, Ventricular complications/diagnosis/drug drug effects/physiopathology; therapeutic therapy/physiopathology therapy/physiopathology; use;},
number = {6 Suppl},
pages = {S8--14},
pdf = {Anto_2007_8.pdf},
pii = {S0022-0736(07)00640-1},
pmid = {17993335},
timestamp = {2009-06-03T11:21:00.000+0200},
title = {Cellular basis for triggered ventricular arrhythmias that occur in
the setting of compensated hypertrophy and heart failure: considerations
for diagnosis and treatment.},
url = {http://dx.doi.org/10.1016/j.jelectrocard.2007.05.022},
volume = 40,
year = 2007
}