A simulation study: electrical alternances during ischemia 1a, 1b and myocardial infarction

Myocardial ischemia and myocardial infarction (MI) are often accompanied by the occurrence of reentrant arrhythmias, which may lead to sudden cardiac death in severe cases. Previous studies show that electrical alternans can occur during myocardial ischemia and MI and may lead to arrhythmias. However, so far, the mechanism of alternans during myocardial ischemia and MI is unclear, so the related study on alternans is particularly important. Based on single-cell models previously modeled by us at three stages: ischemia 1a, 1b, and MI, the mechanism of alternans was revealed by comparing the changes in alternans at three levels: single cells, one-dimensional (1D) tissues, and two-dimensional (2D) tissues. In addition, the main factors inducing alternans were investigated, and the effect of antiarrhythmic drug glibenclamide on alternans was simulated. The simulation results on single cells of ischemia 1a, 1b and MI showed that the electrical alternans on the cell-levels were unstable electrical alternans. Simulation results in tissues showed that stable electrical alternans could occur in both 1D and 2D tissues. Simulation results showed that alternans in ischemia 1a were mainly caused by two factors: inhibition of INa and elevation of [K⁺]ₒ; alternans in ischemia 1b were mainly caused by two factors: inhibition of INaK and elevation of [K⁺]ₒ; alternans in MI were mainly caused by three factors: inhibition of IKr, inhibition of IKs, and elevation of [K⁺]ₒ. And electrical alternans in the tissues result in a 2:1 conduction block. In addition, the simulation results showed that glibenclamide could inhibit electrical alternans in single cells and tissues. Electrical alternans during ischemia 1a, 1b and MI are caused by several currents that directly affect the action potential, and can lead to a 2:1 conduction block in tissues. Glibenclamide inhibits the occurrence of electrical alternans by inhibiting the efflux of potassium ions.