Dr.-Ing. Gunnar Seemann

Mathias Wilhelms

Ischemia is the most common cause of cardiovascular diseases worldwide. Cardiac ischemia stands for inadequate blood supply of the heart muscle. Consequences of ischemia are short-age of oxygen and nutrients as well as deficient removal of metabolites. Hallmarks of ische-mia are hyperkalemia, acidosis and hypoxia. The electrophysiological changes observed dur-ing ischemia are increased resting voltage of the cell membrane, shortening of the action po-tential (AP), prolongation of the effective refractory period, decrease in the electrical conduc-tion velocity (CV), and changes in excitability. Two temporal stages with increasing ischemia effects have been classified: 5–7 min. after onset of coronary occlusion, the so-called stage 1 (S1) is reached. Stage 2 (S2) represents 10–12 min. after onset of coronary occlusion. Typi-cally, a specific region of the cardiac muscle is affected by ischemia leading to spatial and temporal heterogeneous electrophysiological properties. In a previous work, a framework was presented in order to simulate temporal and spatial processes during ischemia including the effects of hyperkalemia, acidosis and hypoxia.
Aim of this work is to investigate the relation between the location of the ischemic region and ST segment changes in the body ECG as well as to support the understanding on how the ischemia increase the arrhythmogenic potential in the ventricles. Furthermore, a semi-implicit approach to calculate the monodomain equation is implemented in order to optimize the simu-lation times.