The electrical treatment of arrhythmias includes cardioversion, defibrillation, stimulation to prevent arrhythmias and ablation of arrhythmogenic tissue. Little is known about the basic mechanisms of how electric stimulation halts or prevents arrhythmias and ablates tissue. Experimental techniques have been developed by us to study these basic mechanisms by determining the potential gradient and current density fields created throughout the heart by the electrical stimulus as well as by mapping the activation sequences immediately before and after the stimulus. These techniques will be used to accomplish the following specific aims.
Specific Aim #1 : To determine the basic mechanism by which a chock halts ventricular tachycardia and the shock field strength needed to halt ventricular tachycardia in animals. The mechanism by which cardioversion inadvertently induces fibrillation will also be determined. The optimum cardioversion electrode configurations will be determined for tachycardias arising from different cardiac regions.
Specific Aim #2 : To determine the mechanism and field characteristics with which a shock halts ventricular fibrillation in humans. High shock fields adjacent to cardiac defibrillation electrodes will be investigated to see if they cause post-shock conduction disturbances.
Specific Aim #3 : To determine the mechanisms by which inhibition and stimulation during the protective zone can prevent arrhythmias. An array of stimulating electrodes will be developed to create the required electrical field to prevent arrhythmia induction.
Specific Aim #4 : To determine if the amount and location of tissue necrosis during electrical ablation is a function of the electrical field strength. If so, the field strength causing ablation will be determined as a function of stimulus duration. Modeling and experimentation will be used to develop a multi-electrode catheter probe for insertion into the left ventricular cavity to create focused fields for ablating predictable known locations and amounts of myocardium. The effects of fiber orientation and shock waveform, e.g., monophasic, biphasic, and triphasic, will be determined as part of all four specific aims. Accomplishing these specific aims will be a large step forward in understanding the fundamental principles governing the response of the myocardium to externally applied electric fields and should lead to better therapies to halt and prevent ventricular tachyarrhythmias.
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