Inhibition of RyR2 hyperactivity with dantrolene not only prevents VT/VF and SCD but also heart failure by mitigating calcium dysfunction in pressure-overloaded hearts.

The transcription factor Meis1 is a dedicated maintenance factor for sympathetic neurons and controls the expression of key genes involved in endosome trafficking.

Ex vivo, in vitro, and computational modeling studies indicate a persistence of myofibroblast senescence in the infarct border zone with age which can disrupt conduction and promote arrhythmias via senescent myofibroblast-cardiomyocyte coupling.

Personalized virtual-heart technology for arrhythmia risk assessment could transform the management of hypertrophic cardiomyopathy patients, eliminating many unnecessary primary-prevention defibrillator deployments while ensuring patients at high risk for arrhythmia are adequately protected.

4,6-Sulfation of chondroitin sulfate proteoglycans prevents sympathetic nerve regeneration into the infarct after myocardial ischemia/reperfusion, and reducing this sulfation promotes nerve regeneration and decreases arrhythmia susceptibility.

Vigorous endurance training results in prolongation of cardiac repolarization and increased repolarization instability, mild ventricular fibrosis associated with decrease of the transient outward potassium current, and enhanced arrhythmia susceptibility in canine model.

Targeted recruitment of protein kinase A subunits enables distinctive regulation of the functional expression of a potassium channel depending on whether the enzyme is targeted to a pore-forming or auxiliary subunit.

Networked cardiac control, revealed through analysis of extended baseline-state multi-channel recordings, differentiates heart failure and normal regimes highlighting the promise of peripheral neurally based clinical interventions.

Important mechanistic details on Duchenne Muscular Dystrophy arrhythmogenesis are revealed, providing a crucial lead for investigators interested in developing therapeutic solutions for this deadly disease.

In neocortex, Nav1.1 is expressed in neocortical pyramidal tract projection neurons and a minor subpopulation of cortico-cortical projection neurons in addition to its predominant expression in inhibitory neurons, while the majority of cortico-thalamic, cortico-striatal, and cortico-cortical neurons express Nav1.2.