UC Irvine

Through the creation of in silico and in vitro models of discontinuous electrical propagation,data can be generated and collected about the stress output of electrically discontinuous cardiac tissues. Diseased and malformed cardiac tissue can cause an improper spread of action potentials, causing a decrease in cardiac contractility. Building different types of models can help to investigate the effect of tissue discontinuity on cardiac stress output. In both models, discontinuity is introduced by creating gaps between the tissue. The formation of the computational model based on the probability of cell firing events is explained, along with the generated simulation. The in vitro model was also created to collect contractile force data in discontinuous engineered cardiac tissues. Together, these two models validate the theoretical prediction that as the number of electrically independent segments (N) of tissue increases, the maximum contractile stress (σ) decreases in proportion to 1/√N.