| dc.description.abstracteng | Sudden cardiac death, caused by ventricular fibrillation, is a leading cause of mortality. To date, the only treatment is the delivery of a high-energy electrical shock through the heart, either externally or through implanted devices. Although potentially life- saving, these shocks can be painful and traumatic for patients, especially when delivered due to diagnostic errors or device malfunctions. A promising new method to terminate ventricular fibrillation more gently is Low Energy Antifibrillation Pacing (LEAP). LEAP applies a series of pulses at low electric field strengths, thereby exciting the heart muscle locally at many different locations and synchronizing the tissue. In this work I show that this excitation takes place at the cardiac vasculature and that LEAP leads to substantial energy reductions. With the use of a micro-CT scanner, I obtained three- dimensional data of cardiac vasculature of dogs and pigs and quantified the vessel sizes with a custom-developed algorithm. I found that the size distribution of the coronary vasculature follows a power law that can be transformed into a prediction of the dynamic behavior of cardiac tissue. To assess the efficiency of LEAP in clinically relevant settings, I performed in vivo and ex vivo experiments on porcine and canine hearts. On average, the defibrillation energy using LEAP could be decreased by up to 70 % compared to the respective single shock energy. Pacing slower than the dominant fibrillatory frequency was more efficient than faster pacing, which supports the hypothesis that direct access to fibrillation vortex cores via heterogeneities is essential to LEAP success. | de |