Key result
Neuronal Na+ channel inhibition reduces EADs, DADs, aberrant Ca2+ release, and VT in murine models.
Why the study?
Does nNav inhibition with riluzole or 4,9-anhydro-tetrodotoxin reduce triggered arrhythmias in murine models of LQT and CPVT-LQT overlap phenotypes?
Does nNav inhibition with riluzole or 4,9-anhydro-tetrodotoxin reduce triggered arrhythmias in murine models of LQT and CPVT-LQT overlap phenotypes?
Inhibition of neuronal sodium channels reduces triggered arrhythmias in murine models of LQT and CPVT-LQT overlap, providing a basis for a mechanistically driven antiarrhythmic strategy.
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Hypothesis-generating for nNav inhibition in LQT/CPVT models; leaves open human translation pending clinical studies.
Koleske et al. (2018) studied Long QT and CPVT-LQT overlap phenotypes. nNav inhibition (riluzole or 4,9-anhydro-tetrodotoxin) was evaluated on Incidence of EADs, DADs, aberrant Ca2+ release, and ventricular tachycardia. Neuronal Na+ channel inhibition with riluzole or 4,9-anhydro-tetrodotoxin reduced the incidence of early and delayed afterdepolarizations, aberrant Ca2+ release, and VT in murine models.
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