A theoretical analysis of acute ischemia and infarction using ECG reconstruction on a 2-D model of myocardium

We developed a two-dimensional ventricular tissue model in order to probe t he determinants of electrocardiographic (ECG) morphology during acute and c hronic ischemia, Hyperkalemia was simulated by step changes in [K+](out), w hile acidosis was induced by reducing Na+ and Ca2+ conductances. Hypoxia wa s introduced by its effect on potassium activity. During the initial moment s of ischemia, ECG changes were characterized by increases in QRS amplitude and ST segment shortening, followed in the advanced phase by ST baseline e levation, T conformation changes, widening of the QRS and significant decre ases in QRS amplitude in spite of an enlarged Q, During each phase, potenti al proarrhythmic mechanisms were investigated. The presence of unexcitable regions of simulated myocardial infarction led to polymorphic EGG. We also observed a nonuniform deflection of the ST segment from beat to beat, We us ed similar protocols to explore the responses of infarcted myocardium after impairment resolving. We found that despite irreversible uncoupling of the necrotic region, the restored normal ionic concentrations produced an isop otential ST segment and monomorphic ECG complexes, while an enlarged Q wave was still visible. In summary, these numerical experiments indicate the po ssibility to track in the ECG pathologic changes following the altered elec trophysiology of the ischemic heart.