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. 2019 Oct 9;4(7):795–813. doi: 10.1016/j.jacbts.2019.06.004

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© 2019 The Authors

This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).

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Effects of Disopyramide in HCM Cardiomyocytes

(Top) In HCM cardiomyocytes, I_Ca-L and I_NaL are increased, while I_K is markedly decreased, leading to prolonged APs; Na overload impairs NCX, contributing to cytosolic Ca-overload. (Bottom) Disopyramide inhibits I_Na-peak (I_NaP), I_NaL, I_Ca-L and I_K, while also stabilizing ryanodine receptors. These effects lead to shortening of APs. Moreover, normalization of NCX function and I_Ca-L inhibition and RyR stabilization contribute to reduce diastolic Ca and systolic Ca-release, determining negative inotropic effects.

APs = action potentials; HCM = hypertrophic cardiomyopathy; I_Ca-L = L-type Ca current; I_K = delayed-rectifier K current; I_NaL = Late Na current; NCX = Na⁺/Ca²⁺ exchanger; RyR = ryanodine receptor.