Overthrow! The Demon Queen 1


Overthrow! The Demon Queen 1

This putrid filthy feminine slave race seeks freedom of the flesh so they can have no soul to please, no divine purpose except to be used by these infernal beast men as they please.Sudden cardiac death is a major health problem in the United States, affecting more than 200,000 people annually. Recent evidence suggests that abnormalities in cardiac autonomic function play a significant role in the pathogenesis of this condition. It has long been established that the control of heart rate and blood pressure in the sinus node and the peripheral arterial and venous vascular beds are under powerful, tight neural regulation. Autonomic dysfunction has been implicated in a variety of cardiac arrhythmias, from ventricular fibrillation to atrial fibrillation. It is our hypothesis that disturbances in cardiac neural control also underlie a unique form of ventricular tachycardia, called ventricular fibrillation “coupled,” in which there is a regular sinus rhythm on the surface EKG with simultaneous ventricular fibrillation on the intracardiac electrograms. The main goal of the present grant application is to investigate the concept that coupled ventricular fibrillation is a distinct pathophysiological entity, and a set of fundamental changes in the normal cardiac autonomic control of ventricular function that are specific to this arrhythmia. To this end, we plan to study a group of patients with ventricular fibrillation, a group of patients with ventricular arrhythmias of unknown origin, and a group of normal control subjects by the following specific aims: 1) To examine the pathophysiologic mechanisms responsible for abnormal intracellular electrophysiologic repolarization that may trigger coupled ventricular fibrillation; 2) To test the hypothesis that coronary artery disease plays an important role in the maintenance of coupled ventricular fibrillation; 3) To examine the relationship between abnormalities of cardiac neural control and changes in ventricular automaticity that occur in cases of coupled ventricular fibrillation; 4) To test the hypothesis that coupled ventricular fibrillation results from the spontaneous development of polymorphic ventricular tachycardia, induced in the intact heart and in the isolated perfused heart; 5) To test the hypothesis that alterations in the intracellular environment and cell-to-cell electrical coupling properties of cardiomyocytes provide a substrate for the development of coupled ventricular fibrillation; and 6) To examine whether changes in intrinsic cell properties and in the electrophysiologic properties

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