Higher Sodium Channel Excitability in Cardiac Purkinje Fibers

Laurent, 2012, Multifocal ectopic Purkinje-related premature contractions: a new SCN5A-related cardiac channelopathy, J Am Coll Cardiol, 60, 144, 10.1016/j.jacc.2012.02.052 Nair, 2012, Escape capture bigeminy: phenotypic marker of cardiac sodium channel voltage sensor mutation R222Q, Heart Rhythm, 9, 1681, 10.1016/j.hrthm.2012.06.029 Beckermann, 2014, Novel SCN5A mutation in amiodarone-responsive multifocal ventricular ectopy-associated cardiomyopathy, Heart Rhythm, 11, 1446, 10.1016/j.hrthm.2014.04.042 Calloe, 2022, The G213D variant in Nav1.5 alters sodium current and causes an arrhythmogenic phenotype resulting in a multifocal ectopic Purkinje-related premature contraction phenotype in human-induced pluripotent stem cell-derived cardiomyocytes, Europace, 24, 2015, 10.1093/europace/euac090 Doisne, 2020, A novel gain-of-function mutation in SCN5A responsible for multifocal ectopic Purkinje-related premature contractions, Human Mutation, 41, 850, 10.1002/humu.23981 Chen, 2016, Distinctive property and pharmacology of voltage-gated sodium current in rat atrial vs ventricular myocytes, Heart Rhythm, 13, 762, 10.1016/j.hrthm.2015.11.022 Li, 2017, Larger rate dependence of late sodium current in cardiac Purkinje cells: a potential link to arrhythmogenesis, Heart Rhythm, 14, 422, 10.1016/j.hrthm.2016.11.036 Dumaine, 2007, Comparison of K+ currents in cardiac Purkinje cells isolated from rabbit and dog, J Mol Cell Cardiol, 42, 378, 10.1016/j.yjmcc.2006.10.019 Mann, 2012, R222Q SCN5A mutation is associated with reversible ventricular ectopy and dilated cardiomyopathy, J Am Coll Cardiol, 60, 1566, 10.1016/j.jacc.2012.05.050 Haïssaguerre, 2020, Idiopathic ventricular fibrillation: role of Purkinje system and microstructural myocardial abnormalities, J Am Coll Cardiol EP, 6, 591 Rosso, 2021, Polymorphic ventricular tachycardia, ischaemic ventricular fibrillation, and torsade de pointes: importance of the QT and the coupling interval in the differential diagnosis, Eur Heart J, 42, 3965, 10.1093/eurheartj/ehab138 Vaidyanathan, 2013, The ionic bases of the action potential in isolated mouse cardiac Purkinje cell, Heart Rhythm, 10, 80, 10.1016/j.hrthm.2012.10.002 Hu, 2009, A mutation in the beta 3 subunit of the cardiac sodium channel associated with Brugada ECG phenotype, Circ Cardiovasc Genet, 2, 270, 10.1161/CIRCGENETICS.108.829192 Angsutararux, 2021, Molecular pathology of sodium channel beta-subunit variants, Front Pharmacol, 12, 10.3389/fphar.2021.761275 Watanabe, 2008, Sodium channel β1 subunit mutations associated with Brugada syndrome and cardiac conduction disease in humans, J Clin Invest, 118, 2260 Valdivia, 2010, Loss-of-function mutation of the SCN3B-encoded sodium channel {beta}3 subunit associated with a case of idiopathic ventricular fibrillation, Cardiovasc Res, 86, 392, 10.1093/cvr/cvp417 Zakrzewska-Koperska, 2020, A combination of quinidine/mexiletine reduces arrhythmia in dilated cardiomyopathy in two patients with R814W SCN5A mutation, ESC Heart Fail, 7, 4326, 10.1002/ehf2.12993 Nguyen, 2008, Divergent biophysical defects caused by mutant sodium channels in dilated cardiomyopathy with arrhythmia, Circ Res, 102, 364, 10.1161/CIRCRESAHA.107.164673 Daniel, 2019, SCN5A variant R222Q generated abnormal changes in cardiac sodium current and action potentials in murine myocytes and Purkinje cells, Heart Rhythm, 16, 1676, 10.1016/j.hrthm.2019.05.017 Moreau, 2015, Gating pore currents are defects in common with two Nav1.5 mutations in patients with mixed arrhythmias and dilated cardiomyopathy, J Gen Physiol, 145, 93, 10.1085/jgp.201411304 Burashnikov, 2007, Atrium-selective sodium channel block as a strategy for suppression of atrial fibrillation: differences in sodium channel inactivation between atria and ventricles and the role of ranolazine, Circulation, 116, 1449, 10.1161/CIRCULATIONAHA.107.704890