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.
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