Introduction: Reperfusion after myocardial ischaemia can lead to fatal arrhythmias, in part due to heterogeneities in electrophysiology (EP) across affected tissue. Understanding the spatiotemporal dynamics of this pathophysiological cardiac electrical behaviour may improve outcomes. Objective: Elucidate EP mechanisms underlying ischaemia-reperfusion arrhythmias. Methods and Results: In experiments involving panoramic optical mapping of transmembrane voltage of Langendorff-perfused rabbit hearts, a region of the left ventricle was independently perfused by cannulation of the anterior branch of the left circumflex coronary artery with physiological solution, which was switched to and from no-flow ischaemia, simulated ischaemia solution, or a solution that mimicked a specific aspect of ischaemia (hyperkalaemia, hypoxia or acidosis). When local no-flow, simulated ischaemia, hyperkalaemic or hypoxic solution (n = 6, 22, 8, 5, respectively) was switched to physiological perfusion, we observed preferential recovery of electrical excitability of myocardium along the main branch of the perfused coronary vessel (‘perivascular excitation tunnelling’, PVET). In a subset of hearts, PVET resulted in re-entrant arrhythmias. In contrast, local acidosis experiments showed no loss of excitability and subsequently no PVET (n = 5). Assessment of tissue perfusion showed that myocardium closest to major arteries was first perfused and likely underlies the surprisingly fast recovery of excitability in perivascular myocardium. Data were used to inform a computational model of ischaemia-reperfusion to further explore mechanisms of arrhythmia inducibility. The computational model reproduced PVET and illustrated the quantitative plausibility of PVET as a cause for re-entry. Simulations predicted that step-wise reperfusion strategies could reduce EP heterogeneity and thus vulnerability to arrhythmias, however experimentally step-wise or gradual reperfusion (n = 5 and n = 2) increased the heterogeneous period, resulting in increased arrhythmogenesis. Conclusions: We observed a novel PVET-based re-entry mechanism upon coronary reperfusion, suggesting that detrimental reperfusion-induced gradients arise in the myocardium along coronary vessels. Initial step-wise or gradual recovery of normal perfusion tests were not less arrhythmogenic than instant recovery of physiological flow. Further research is required to identify ‘smart reperfusion’ approaches favourable in the clinical setting.