Effects of DHA on action potential duration ex vivo. (A) Representative examples of recorded MAPs before (in grey) and after administration of DHA in perfused WT (black), LQT1 (green), LQT2 (red), LQT2–5 (violet), and LQT5 (blue) rabbit hearts. The APD shortening appears during phase 3, which corresponds to the phase in which I_Ks is conducted. (B) Left panel: APD₇₅ in WT, LQT1, LQT2, LQT2–5, and LQT5 rabbits before and after DHA administration. Right panel: changes in APD₇₅ in the different genotypes are indicated as ΔAPD₇₅. (C) Comparison of APD₇₅ in LQTS rabbits treated with DHA vs. baseline QTc in WT animals (grey) indicates a normalization in LQT2 (lack of differences between LQT2+DHA and WT at baseline). Grey bars are repeated to better show the difference to WT for each individual genotype. (D) Representation of DHA-induced APD₇₅ changes in the individual rabbits (left: APD₇₅ values before; right: after administration of DHA). (B–D) Sample numbers: LQT1 (green) n = 7, LQT2 (red) n = 6, LQT2–5 (violet) n = 9, LQT5 (blue) n = 9, and WT rabbits (grey) n = 7. Differences are indicated as * for P-value < 0.050, ** for P-value < 0.010, and *** for P-value < 0.001. All data are presented as mean ± SEM. DHA, docosahexaenoic acid; LQTS, long QT syndrome; LQT1, long QT Type 1; LQT2, long QT Type 2; LQT5, long QT Type 5; LQT2–5, combined form of long QT Types 2 and 5; MAP, monophasic action potential; SEM, standard error of the mean; WT, wild type.