Does late sodium current (I(NaL)) inhibition reverse electromechanical dysfunction in ventricular myocytes and trabeculae from patients with hypertrophic cardiomyopathy?
Inhibition of the late sodium current (I(NaL)) may reverse electromechanical dysfunction in human hypertrophic cardiomyopathy by targeting complex remodeling processes.
We highlighted a specific set of functional changes in human HCM myocardium that stem from a complex remodeling process involving alterations of CaMKII-dependent signaling, rather than being a direct consequence of the causal sarcomeric mutations. Among the several ion channel and Ca(2+)(i) handling proteins changes identified, an enhanced I(NaL) seems to be a major contributor to the electrophysiological and Ca(2+)(i) dynamic abnormalities of ventricular myocytes and trabeculae from patients with HCM, suggesting potential therapeutic implications of I(NaL) inhibition.
Coppini et al. (2012) studied this question.