Using a translational porcine model, the structural basis for post myocardial infarction ventricular tachycardia was assessed using in-vivo cardiac magnetic resonance imaging. High-resolution LGE imaging was acquired under contrast steady state in order to allow detailed tissue characterisation. Arrhythmia was induced and assessed under haemodynamic support to allow the unambiguous identification of arrhythmogenic tissue involved in these scar mediated VT circuits. The electrophysiological and imaging data was then registered to establish the structural features of tissue involved in these rhythms. It was identified that tissue participating in the diastolic phase of post-MI VT was thinner, had non-transmual scar or intermediate signal intensity and had higher gradients in tissue thickness.
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