In this paper, to analyze the functional influence of ischemia on cardiac cell electrical activity and subsequently on ventricular electrical wave conduction, a human ventricular ischemic model was developed, which took into account three major pathophysiological components of ischemias hyperkalaemia, acidosis, and anoxia. This model simulated the action potential (AP) propagations of endocardial, midmycardial and epicardial cells with different levels of ischemia, and the influence of each factor on cell AP was analyzed. Finally the ECG waveform under ischemia was quantified by using a 2D model of human left ventricular tissue based on the anatomical structure of human heart. The experimental results showed that under ischemia action potential durations (APD) were reduced. In most cases, the larger the size of ischemic region or the more severe the ischemic level, the more dramatic the changes in the amplitude of ST-T wave were observed. For the three components of ischemia, hyperkalaemia was the dominant contributor to ST-T wave changes, which was in agreement with the results obtained on animal models.
Action Potentials ; physiology ; Computer Simulation ; Electrocardiography ; Heart Ventricles ; physiopathology ; Humans ; Hyperkalemia ; physiopathology ; Models, Cardiovascular ; Myocardial Ischemia ; physiopathology

Based on human ventricular single cell mathematical model, a two-dimensional mesh of ventricular wall tissue was constructed. Through the increasing of the concentration of extracellular K+, we simulated the propagation of spiral wave in a condition under the influence of ischemia in 2-D human ventricular tissue. The results showed that along with the increase of ischemic level and size, the instability of spiral waves increased, and under the influence of certain ischemic level and size, spiral waves broke up. Through this simulation study of the effects of ischemia on spiral waves in 2-D human ventricular tissue, we explained the corresponding mechanism of the maintenance of ventricular tachycardia and the cause of ventricular fibrillation under the influence of ischemia.
Arrhythmias, Cardiac ; etiology ; physiopathology ; Computer Simulation ; Heart Ventricles ; Humans ; Models, Cardiovascular ; Myocardial Ischemia ; complications ; physiopathology ; Tachycardia, Ventricular ; etiology ; physiopathology ; Ventricular Fibrillation ; etiology ; physiopathology

Pacemaking dysfunction has become a significant disease that may contribute to heart rhythm disorders, syncope, and even death. Up to now, the best way to treat it is to implant electronic pacemakers. However, these have many disadvantages such as limited battery life, infection, and fixed pacing rate. There is an urgent need for a biological pacemaker (bio-pacemaker). This is expected to replace electronic devices because of its low risk of complications and the ability to respond to emotion. Here we survey the contemporary development of the bio-pacemaker by both experimental and computational approaches. The former mainly includes gene therapy and cell therapy, whilst the latter involves the use of multi-scale computer models of the heart, ranging from the single cell to the tissue slice. Up to now, a bio-pacemaker has been successfully applied in big mammals, but it still has a long way from clinical uses for the treatment of human heart diseases. It is hoped that the use of the computational model of a bio-pacemaker may accelerate this process. Finally, we propose potential research directions for generating a bio-pacemaker based on cardiac computational modeling.