SLOW CONDUCTION, FRACTIONATION, AND SIGNAL-AVERAGED ECG

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Ventricular arrhythmias are a major source of morbidity and mortality in this country. Most are caused by reentry, one prerequisite for which is slow conduction. Characterizing slow conduction may help in the understanding and treatment of ventricular arrhythmias. Fractionated epicardial electrograms are often detected in patients with ventricular arrhythmias, and they may arise from slowly-conducting myocardium. Recently, abnormal QRS/ST potentials have been detected with signal-averaged ECG on the body surface of patients with ventricular arrhythmias, and these may also arise from slowly-conducting myocardium. Abnormal QRS/ST potentials may in the future provide a noninvasive characterization of slow conduction in individual subjects. However, the relationships among slow conduction, fractionated epicardial electrograms, and abnormal body surface QRS/ST potentials need to be confirmed and quantitated. This application proposes to study three specific hypotheses in a canine model of chronic myocardial infarction: (1) fractionated electrograms arise from areas of slowly-conducting myocardium, (2) abnormal QRS/ST potentials are the body surface manifestation of fractionated electrograms, and (3) there is a correlation between the epicardial location of fractionated electrograms and the body surface location of abnormal QRS/ST potentials. Several novel techniques will be used in this proposal. First, local conduction velocity in the right ventricular free wall will be estimated using local activation times recorded simultaneously from 64 unipolar epicardial leads. Second, the spatial distribution of fractionated electrograms will be derived from the same 64 epicardial leads. Third, multiple simultaneous unipolar ECG's will be used for detection and localization of abnormal body surface QRS/ST potentials.