Influence of patient-specific acute myocardial ischemia maps on arrhythmogenesis: A computational study

The early phase of acute myocardial ischemia is associated with an elevated risk of ventricular reentrant arrhythmias. After partial or total occlusion of a coronary artery, some regions of the heart experience a reduction in myocardial blood flow. This causes metabolic and cellular processes, such as hypoxia, hyperkalemia and acidosis, which lead to changes in the transmembrane ionic dynamics. The effect of such alterations may result in the formation of electrical loops and reentries. In this context, computational approaches based on differential multiscale models may serve to predict patient-specific arrhythmic propensity in a given scenario. Specifically, they could assess the arrhythmic risk by simulating the generation of reentrant episodes, possibly persistent, triggered by ectopic beats and in presence of acute myocardial regions. Since quantitative information (extent, localization, …) about acute ischemic regions are hardly available from medical imaging, to date, in computational models such regions are either arbitrarily drawn or inspired by chronic infarcted information. In both the cases, this does not represent a patient-specific condition of acute ischemia. This work aims to overcome this limitation by introducing a novel patient-specific electrophysiological model, based on Myocardial Blood Flow (MBF) maps acquired during stress-CTP acquisitions of stable Coronary Artery Diseased (CAD) patients in hyperemic conditions. Indeed, during such an acquisition, CAD may destabilize and acute ischemic events may occur, allowing to obtain measured MBF maps representative of patient-specific acute ischemic regions. First, we aim to numerically investigate the induction and sustainment of reentrant drivers in different patients, in order to assess their arrhythmic propensity. Secondly, we perform an intra-patient sensitivity analysis, where different levels of acute ischemia are virtually depicted for the most arrhythmogenic patient. Our results suggest that the amount of ischemic regions seems to have less influence on arrhythmogenesis rather than their pattern.