New antiarrhythmic targets to control intracellular calcium handling

Sudden cardiac death due to ventricular arrhythmias is a major problem. Drug therapies to prevent SCD do not provide satisfying results, leading to the demand for new antiarrhythmic strategies. New targets include Ca(2+)/Calmodulin-dependent protein kinase II (CaMKII), the Na/Ca exchanger (NCX), the...

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Detalles Bibliográficos
Autores principales: Driessen, H. E., Bourgonje, V. J. A., van Veen, T. A. B., Vos, M. A.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Bohn Stafleu van Loghum 2014
Materias:
Review Article
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4016334/
https://www.ncbi.nlm.nih.gov/pubmed/24733689
http://dx.doi.org/10.1007/s12471-014-0549-5
Descripción
Sumario:Sudden cardiac death due to ventricular arrhythmias is a major problem. Drug therapies to prevent SCD do not provide satisfying results, leading to the demand for new antiarrhythmic strategies. New targets include Ca(2+)/Calmodulin-dependent protein kinase II (CaMKII), the Na/Ca exchanger (NCX), the Ryanodine receptor (RyR, and its associated protein FKBP12.6 (Calstabin)) and the late component of the sodium current (I (Na-Late)), all related to intracellular calcium (Ca(2+)) handling. In this review, drugs interfering with these targets (SEA-0400, K201, KN-93, W7, ranolazine, sophocarpine, and GS-967) are evaluated and their future as clinical compounds is considered. These new targets prove to be interesting; however more insight into long-term drug effects is necessary before clinical applicability becomes reality.

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