Abstract
The early repolarization pattern (ERP) or J wave in the ECG is commonly observed but associated with an increased risk of sudden cardiac death in some cases, so-called early repolarization syndrome (ERS). ERP is often overlapped with the Brugada syndrome. Although a lot of clinical and basic studies about the ERS and Brugada syndrome have been reported in the past two decades, the mechanisms of the ERP by which the risk of arrhythmias increased are still controversial. There are mainly two hypotheses for the ionic and cellular basis underlying the ERP: repolarization and depolarization abnormalities. The former is based on the transient outward potassium current (Ito)-mediated action potential notch in the epicardium but not endocardium, giving rise to transmural heterogeneity of ventricular repolarization, whereas the latter is based on the clinical electrophysiology such as late potentials and fractionated delayed potential in the epicardium. The repolarization and depolarization abnormalities are impossible to be completely separated in the same heart, and both contribute to the manifestation of the J wave/ERP and arrhythmogenicity.
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Aiba, T. (2018). Ionic and Cellular Basis Underlying ERS. In: Shimizu, W. (eds) Early Repolarization Syndrome. Springer, Singapore. https://doi.org/10.1007/978-981-10-3379-7_4
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DOI: https://doi.org/10.1007/978-981-10-3379-7_4
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