In the present proposal we will use programmed electrical stimulation and endocardial catheter mapping of the heart to: 1) evaluate the electrophysiologic substrate in terms of abnormalities of conduction and/or refractoriness which characterize patients prone to develop ventricular tachycardia and/or sudden death; 2) assess the electrophysiologic determinants to inducibility of ventricular arrhythmias; 3) evaluate abnormal electrical signals in the early QRS as noted on the signal averaged surface electrocardiogram in patients with anterior infarction and ventricular tachycardia; and 4) evaluate the time course of the development of fractionated electrograms following acute infarction and assess whether the appearance of this abnormality of conduction reflects a propensity to the development of spontaneous sudden death or ventricular tachycardia. It is our general hypotheses that patients prone to develop malignant arrhythmias will have a specific electrophysiologic substrate characterized by abnormalities of conduction and refractoriness that can be determined by programmed stimulation and endocardial mapping. The specific hypotheses which will be evaluated will determine whether the number and duration of abnormal electrograms and/or the dispersion of refractoriness and recovery of excitability identify a substrate characteristic of patients at risk for sustained ventricular tachycardia and sudden death. We believe that such a substrate may be able to select out patients with nonsustained arrhythmias and coronary artery disease who are at risk for sudden death. In patients suffering cardiac arrest these abnormalities, if present, will suggest a fixed substrate which is not amenable to coronary artery bypass grafting. In this case therapy, whether surgical or medical, would be directed towards the arrhythmogenic substrate. We also plan to identify an arrhythmogenic substrate in patients with dilated cardiomyopathy, who are at high risk for sudden death so that these patients may be appropriately treated. These studies will also identify which patients will have inducible arrhythmias and those in whom pharmacologic therapy will be successful or make the arrhythmia incessant. In addition, these studies will help select patients early post-infarction, particularly anterior infarction, who are at risk for sudden death and have not been detected by noninvasive techniques. In sum, our studies are aimed at identifying substrates for malignant ventricular arrhythmias. Defining such a substrate might help identify patients at risk for lethal arrhythmias and help select the most appropriate form of therapy to prevent their occurrence.
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