Since its initial cloning in 1992, SCN5A (Nav1.5) has become known as “the” cardiac sodium channel.1 SCN5A encodes a tetrodotoxin (TTX)-resistant channel that is responsible for the inward sodium current (INa), which initiates the cardiac action potential. Its RNA and protein expression dominate the sodium channel landscape in the ventricle, atrium, and specialized conduction system. Mice heter...

It was thought previously that cardiac muscle gap junctions provide low-resistance connections between cells and permit the local-circuit current to flow. Some evidences show that myocardial cells may not require low-resistance connections for successful propagation of the action potential (AP). It seems that some other types of mechanisms must be involved in AP propagation. In this article, we...

Familial cardiac conduction disorder of a progressive nature has been reported in adult and paediatric patients. An underlying cardiomyopathy was found in most of these patients, either of hypertrophic, restrictive or dilated variety. Systemic diseases like juvenile rheumatoid arthritis and other collagen disorders and familial dysautonomia infrequently have associated conduction abnormalities....

The incidence of ischemic heart disease (IHD) is increasing worldwide. number patients with IHD or without interventions coming for non-cardiac surgical procedures are increasing. These have an increased risk myocardial ischemia, infarction (MI), conduction disturbances, morbidity, and mortality during the peri-operative period.

The SCN5A-encoded voltage-gated cardiac sodium channel -subunit (hNaV1.5) is one of the critical ion channels necessary to orchestrate both the cardiac action potential and excitation-contraction coupling of the ventricular myocyte.1 Rare mutations in SCN5A have been implicated in a cadre of the cardiac channelopathies, including congenital long-QT syndrome (LQTS), Brugada syndrome (BrS), progr...

BACKGROUND Transient receptor potential melastatin member 4 (TRPM4) is a nonselective cation channel. TRPM4 mutations have been linked to cardiac conduction disease and Brugada syndrome. The mechanisms underlying TRPM4-dependent conduction slowing are not fully understood. The aim of this study was to characterize TRPM4 genetic variants found in patients with congenital or childhood atrioventri...

Normal heart function is critically dependent on the timing and coordination provided by a complex network of specialized cells: the cardiac conduction system. We have employed functional assays in zebrafish to explore early steps in the patterning of the conduction system that previously have been inaccessible. We demonstrate that a ring of atrioventricular conduction tissue develops at 40 hou...

on the electrophysiological properties of normal Purkinje fibers and those surviving acute myocardial infarction (abstr). FedProc33:476 Schmitt FO, Erlanger J (1928-1929) Directional differences in the conduction of the impulse through heart muscle and their possible relation to extrasystolic and fibrillary contractions. Am J Physiol 87: 326-347 Singh BN, Vaughan-Williams EM (1971) Effect of al...