Abstract

Cardiac arrhythmias and Epilepsy, at first glance, seemingly have nothing in common besides the fact that they both conditions that are characterized by a sudden onset of irregular activity in the heart and brain, respectively, and that current treatments are not optimal at controlling onset.

Epilepsy affects 3-5% of the population worldwide, affecting persons indiscriminately of age, sex or race. In the vast majority of cases, seizures arise from medial temporal structures that have been damaged months to years before onset of seizures. By characterizing the latent development of epilepsy from traumatic insult to onset in the chronic limbic epilepsy rat model (a realistic animal model for human temporal lobe epilepsy and epileptogenesis), essential relationships between onset pathology and remodeling of the neural tissue can be determined. It has been found that the 0-200 Hz inter-hemispherical communication is supressed in stimulated, but not non-stimulated animals.

Sudden cardiac death is a major health issue. It accounts for more than 300,000 deaths annually in North America and is the leading cause of death in people aged 20 to 64 years. In one sense, sudden cardiac death can be considered an electrical accident, representing a tragic interplay between anatomic and functional substrates modulated by the transient events that perturb the balance. Most such incidents involve ventricular fibrillation (VF) with electrical defibrillation its only therapy. The events surrounding the onset of fibrillation in humans, even after 50 years of study, remain fairly opaque. Using cardiac optical mapping, we experimentally record defibrillation failure on perfused porcine hearts to understand the underlying dynamics and develop a method of assessing orderedness for a lower energy successful defibrillation shock.

Lastly, cardiac ablation is being increasingly used to interdict the complex propagation of excitatory waves during atrial fibrillation. While such procedures are clearly useful, they can often fail. In order to understand this failure, we use optical methods to observe the electrical activity of an ablated porcine heart. We find that ablation lines do attenuate cardiac waves, but the attenuation is not complete. Instead a remnant of the wave incident upont the ablation barrier survives passage through it, albeit as a subthreshold signal. More importantly we have found that these subthreshold signals may add constructively and thereby dynamically reduce the effective attenuation, an effect which we call dynamic transmurality. We suspect this as a factor in the persistence of arrhythmia after ablative procedures.