Remodeling of repolarization and arrhythmia susceptibility in a myosin-binding protein C knockout mouse model

In conclusion, decrease in repolarizing K+ currents in MyBPC KO ventricular myocytes contributes to AP and corrected QT interval prolongation and could account for the arrhythmia susceptibility.
NEW & NOTEWORTHY Ventricular myocytes isolated from the myosin-binding protein C knockout hypertrophic cardiomyopathy mouse model demonstrate decreased repolarizing K+ currents and action potential and QT interval prolongation, linking cellular repolarization abnormalities with arrhythmia susceptibility and the risk for sudden cardiac death in hypertrophic cardiomyopathy.

Source: AJP: Heart and Circulatory Physiology - September 12, 2017 Category: Cardiology Authors: Toib, A., Zhang, C., Borghetti, G., Zhang, X., Wallner, M., Yang, Y., Troupes, C. D., Kubo, H., Sharp, T. E., Feldsott, E., Berretta, R. M., Zalavadia, N., Trappanese, D. M., Harper, S., Gross, P., Chen, X., Mohsin, S., Houser, S. R. Tags: RESEARCH ARTICLE Source Type: research