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. Author manuscript; available in PMC: 2015 Sep 1.
Published in final edited form as: J Mol Cell Cardiol. 2014 May 10;74:53–63. doi: 10.1016/j.yjmcc.2014.04.024

Figure 4. Propensity for ventricular arrhythmias in αMHC-miR130a mice.

Figure 4

In panel (A), representative P-QRS complexes in control and αMHC-miR130a mice at 6 and 10 weeks after doxycycline removal. In panel (B), representative programmed electrical ventricular stimulation studies in control mice (top panel) and αMHC-miR130a transgenic mice (bottom panel). In the control mouse, pacing stimulus could not induce VT. In contrast, sustained VT is seen in the αMHC-miR130a mouse following pacing stimulus. In (C), summary of programmed electrical stimulation studies with the number of inducible VT episodes in control (C) and miR-130a transgenic (Tg) animal cohorts at 4, 6, and 10 weeks. Sustained ventricular arrhythmias could not be induced in any of the controls. Beginning at 6 weeks after doxycycline removal, αMHC-miR130a mice could be induced into monomorphic VT. In panel (D), simultaneous intracardiac and surface ECG in αMHC-miR130a mice during VT episode. Atrial electrogram (top panel) demonstrates a slower atrial signal with a regular cycle length. Ventricular electrogram (middle panel) demonstrates a rapid high amplitude signal corresponding with the rapid wide QRS complexs on surface ECG. Arrows indicate potential atrial signal and corresponding surface ECG location within the QRS complex consistent with atrioventricular dissociation. These findings are supportive of VT. Shown in panel (E), an example of spontaneous VT initiated after premature ventricular complexes in αMHC-miR130a mice during ambulatory ECG monitoring 10 weeks after removal of doxycycline. Five animals in each group was studied for both stimulation studies and ambulatory ECG monitoring. * indicates p=0.026. NSVT: nonsustained ventricular tachycardia; A: atrial signal; VT: ventricular tachycardia; Tg: transgenic; C: control littermate.