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Sodium Channel Variants in Heart Disease: Expanding Horizons
Author(s) -
TAN HANNO L.
Publication year - 2006
Publication title -
journal of cardiovascular electrophysiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.193
H-Index - 138
eISSN - 1540-8167
pISSN - 1045-3873
DOI - 10.1111/j.1540-8167.2006.00398.x
Subject(s) - medicine , brugada syndrome , cardiology , cardiomyopathy , heart failure , hypertensive heart disease , long qt syndrome , sodium channel , heart disease , electrical conduction system of the heart , cardiac function curve , disease , qt interval , electrocardiography , sodium , chemistry , organic chemistry
Inherited arrhythmia syndromes have advanced our understanding of cardiac sodium (Na) channel function in health and disease. Long QT syndrome (LQT3) is consistently caused by increased net Na current secondary to inactivation defects, which give rise to persistent Na current. Conversely, various gating changes that ultimately result in reduced Na current may elicit Brugada syndrome, conduction disease, atrial standstill, and sinus node disease. Emerging insights now also link these gating defects to enhanced arrhythmia susceptibility in common, acquired, disease. For instance, action potential prolongation in congestive heart failure may be explained by increased persistent Na current. Of note, recent studies have also linked Na current reduction to structural cardiac defects, notably cardiac fibrosis, dilated cardiomyopathy and, possibly, arrhythmogenic right ventricular cardiomyopathy. These structural changes may also be conducive to (reentrant) arrhythmias. Clearly, these observations highlight the cardiac Na channel as an interesting target for novel therapy strategies.