Abstract
Early repolarization syndrome (ERS) is characterized by early repolarization (ER) and ventricular fibrillation. Heritability of the ER pattern has been shown, and the search for the genetic factors associated with ERS is in progress. Until now, genetic variants in seven genes, namely, KCNJ8, ABCC9, SCN5A, CACNA1C, CACNB2b, CACNA2D1, and KCND2, have been reported as potential causative genes of ERS. These genes encode potassium, sodium, and calcium ion channels on cardiomyocytes and control the action potentials of cardiomyocytes. The gain or loss of ion channel functions with genetic variants in these genes has been shown, and these functional changes have been linked to ERS. However, the pathogenesis of ERS by mutations in these genes is controversial. In addition, a genome-wide association study failed to identify any specific single nucleotide polymorphisms or genes associated with ER. Therefore, further investigation is required to explore the genetic background of ERS.
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