Figure 1
From: The mitochondrial calcium uniporter promotes arrhythmias caused by high-fat diet

MCU KO hearts are protected from ventricular tachycardia and repolarization dispersion after HFD. (A) Examples of telemetry from control mouse, with QT at baseline on chow and QT prolongation after 4 weeks of HFD. Both images have the same time scale. (B) Two examples of heart rhythm from control hearts on chow or HFD, showing rapid ventricular pacing (at different rates) followed by non-sustained VT in the HFD heart. Time scale: each vertical thick line is 500 ms, each thin line is 100 ms. (C) Two examples of heart rhythm from MCU KO heart on chow or HFD, showing that rapid ventricular pacing does not cause VT. Time scale is the same as panel (B). (D) Graph of number of episodes of VT from control and MCU hearts induced by rapid ventricular pacing. N = hearts 5–7 per group. The differences between groups are statistically significant by nonparametric Kruskal–Wallis test, p = 0.0018, *indicates significantly different by post-hoc test. E. Graphs of action potential duration 50% (APD50) and 80% (APD80). The means are significantly different by ANOVA, *indicates significantly different from control by post-hoc test. F. Examples of optical mapping showing APD50 duration, both hearts were paced from the ventricular apex at 10 Hz. False color shows the gradient of APD50 from 20 ms (dark blue) to 40 ms (dark red). Note the increased repolarization dispersion in the control HFD heart compared to MCU KO HFD. G. Graph of APD dispersion in milliseconds, mean + SEM, n = 6–7 hearts per group. The means are significantly different by ANOVA, *indicates significantly different by post-hoc test.