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While acute ischaemia/reperfusion injury primarily leads to ventricular fibrillation, myocardial infarction-related scars and especially the border zone between infarcted and vital myocardium are an important substrate for VT occurrence in ICM: infarct-related changes in excitability and conduction velocity as arrhythmogenic substrates lead to perpetual reentrant VT (see also Fig

(1) Sikiric, Predrag et al

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