(A) Optical AP records from an NTg heart perfused with solutions containing 3 μM blebbistatin before and after 3 μM EMD. Note that blebbistatin prevents the EMD-induced AP changes shown in Figure 5. (B) Average effect of EMD on murine ventricular APD in the presence of blebbistatin. n = 4 hearts; PCL, 150 ms. (C and D) Isochronal activation maps obtained at a PCL of 60 ms from an NTg heart perfused with solutions containing 3 μM blebbistatin before (C) and after (D) addition of 3 μM EMD to the perfusate. Isolated mouse hearts were stained with the voltage-sensitive fluorescent indicator di-4-ANEPPS and paced at stepwise-shorter PCLs as described in Figure 2. Note that in the presence of blebbistatin, EMD no longer altered ventricular isochronal activation maps. (E) Maximal CV dispersion before and after treatment with blebbistatin. For control conditions, the TnT mutations and the group size follow: NTg, n = 7; WT, n = 6; R278C, n = 6; F110I, n = 8; I79N, n = 8; EMD, n = 6. The group sizes of TnT mutations in the presence of 3 μM blebbistatin follow: NTg, n = 3; WT, n = 7; R278C, n = 5; F110I, n = 7; I79N, n = 7; EMD, n = 3; *P < 0.05, **P < 0.01 by Mann-Whitney U test. (F) Average incidence of sustained VT (>30 s duration) in the different transgenic mice under control conditions and in the presence of 3 μM blebbistatin. For control conditions, the TnT mutations and the group size follow: NTg, n = 8; WT, n = 10; R278C, n = 6; F110I, n = 11; I79N, n = 13; EMD, n = 7. The group sizes of TnT mutations in the presence of blebbistatin follow: NTg, n = 4; WT, n = 8; R278C, n = 5; F110I, n = 7; I79N, n = 8; EMD, n = 4; **P < 0.01, by Fisher’s exact test.