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- W4298444432 abstract "Cardiac channelopathies are genetically determined diseases that may cause sudden arrhythmic death in young subjects with a structurally normal heart. Abnormal cellular electrophysiology related to dysfunctional ion channels is the underlying substrate. Some types of idiopathic epilepsy are also caused by ion channel dysfunction in the neuronal cell membrane. is shared pathophysiologic mechanism lets us hypothesize about an arrhythmic cause for some cases of sudden death in epilepsy. In this chapter, cardiac19.1 Introduction 285 19.1.1 Sudden Cardiac Death in Subjects with a Structurally Normal Heart 286 19.1.2 Ion Channels and Channelopathies 286 19.1.3 e Cardiac Action Potential 287 19.1.4 Inherited Primary Arrhythmia Syndromes 28719.2 Long QT Syndrome 289 19.2.1 Clinical Manifestations 289 19.2.2 Genetic Background and Pathophysiology 290 19.2.3 Risk Stratication and Management 29119.3 Brugada Syndrome 291 19.3.1 Clinical Manifestations 292 19.3.2 Genetic Background and Pathophysiology 293 19.3.3 Risk Stratication and Management 29419.4 Catecholaminergic Polymorphic Ventricular Tachycardia 295 19.4.1 Clinical Manifestations 295 19.4.2 Genetic Background and Pathophysiology 295 19.4.3 Management 29619.5 Short QT Syndrome 296 19.5.1 Clinical Manifestations 296 19.5.2 Genetic Background and Pathophysiology 297 19.5.3 Management 29719.6 Considerations about Cardiac Channelopathies, Epilepsy, and SUDEP 297 19.6.1 Brugada ECG and Epilepsy 298 19.6.2 LQT and Epilepsy 298 19.6.3 e Hypothesis of a Common Channelopathy 299 19.6.4 SUDEP and Channelopathies 299References 299channelopathies related to sudden death are reviewed and data supporting a potential relationship with epilepsy are exposed in the last section." @default.
- W4298444432 created "2022-10-02" @default.
- W4298444432 creator A5025421407 @default.
- W4298444432 date "2010-11-08" @default.
- W4298444432 modified "2023-09-29" @default.
- W4298444432 title "Animal Model for Sudden Cardiac Death" @default.
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- W4298444432 doi "https://doi.org/10.1201/b10317-28" @default.
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