Sudden cardiac death is a major cause of mortality in the United States. In an effort to attach this problem, the concept of a Chain of Survival has been presented as a way to characterized the tasks necessary for successful resuscitation. It is clear that early defibrillation is central to improved survival rates following out-of-hospital cardiac arrest. 1) successful defibrillation of the arrhythmia of the arrhythmia, 2) recurrence if arrhythmias following defibrillation, and 3) poor cardiac function following defibrillation This project will address the first two problems. Very little is known about defibrillation efficacy of spontaneous arrhythmias in the presence of acute ischemia. A much larger shock is needed to halt ventricular fibrillation that occurs spontaneously in the presence of acute is ischemia than to halt electrically induced ventricular fibrillation in the non-ischemic heart. We will study the activation patter following successful and failed defibrillation shocks with the heart in four conditions designed to model different aspects of ischemic ventricular fibrillation shocks the heart in four conditions designed to model different aspects of ischemic ventricular fibrillation: (1) acute regional ischemia causing spontaneous ventricular fibrillation, (2) acute regional ischemia followed by electrically induced ventricular fibrillation, (3) acute regional ischemia causing spontaneous ventricular fibrillation which in turn causes prolonged global ischemia, and (4) acute regional ischemia causing spontaneous ventricular fibrillation in the setting of prolonged global ischemia, and (4) acute regional ischemia causing spontaneous ventricular fibrillation in the setting of an old myocardial infarction. We will test the hypothesis that, in the setting of an ischemically induced spontaneous arrhythmia, a defibrillation shock must do three things: (1) stop all fibrillation wavefronts, (2) not restart fibrillation, and (3) stop the trigger of the original arrhythmia. We will test the hypothesis that a major determinant of whether or not a spontaneous arrhythmia, a defibrillation shock must do three things: (1) stop all fibrillation wavefronts, (2)m not restart fibrillation and (3) stop the trigger of the original. We will test the hypothesis that a major determinant f whether or not a spontaneous arrhythmia caused by acute ischemia can be easily defibrillated depends upon the mechanism of initiation of the arrhythmia and duration of the arrhythmia. We will also test the hypothesis that arrhythmias that occur following the initial fibrillation episode are initiated by focal rather than reentrant mechanisms and will be harder to defibrillate than the initial arrhythmia. To test these hypothesis, we will induce acute ischemia by creating a thrombus in a coronary artery and use electrical mapping techniques to map the initiation of ventricular arrhythmias, and the first few post-shock activations following delivery of a defibrillation shock. By developing an understanding of how a defibrillation shock succeeds or fails under these conditions, we will be in a better position to develop new defibrillation techniques that increase survival rates of patients suffering an episode of sudden cardiac death.
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