High resolution electrocardiography (HRECG) is used to record electrical activity from diseased and/or damaged regions of the myocardium. These potentials are at the end of the QRS and extend into the ST segment. These "late potentials" have been studied primarily in humans, post-infarction, and are an independent marker for identifying those at risk for ventricular tachycardia. Optimization of the technology used to record and analyze the HRECG is an ongoing theme in our clinical and animal laboratories. The animal laboratory affords the use of invasive means to substantiate the observations of the body surface HRECG and to allow each animal to serve as its own control in cases of intervention. The HRECG has been adopted in many laboratories as a clinical tool, but, several problems remain in which our new approaches may be ideally tested in the animal laboratory. The first problem will focus on the evolution of late potentials following infarction. Secondly, the distribution of late potentials on the body surface will be examined. Current approaches rely on XYZ leads but preliminary data suggest that this may not be adequate. And finally, new frequency domain methods will be used to identify late potentials in the presence of bundle branch block in an effort to provide insights into this long standing problem. There are three key questions being asked: #1. Are there consistent and identifiable characteristics of late potentials which are associated with the degree of severity of arrhythmias following an infarction? #2. What is the spatial distribution on the body surface of cardiac late potentials following myocardial infarction? #3. Are there frequency domain measurements of the signal averaged ECG which improve the detection and identification of late potentials over time domain measurements? Answers to these questions will be obtained by studying a canine infarction model. One group of dogs will be studied four-days post infarct. The intervening period is when late potential characteristics and varying degrees of arrhythmias are evolving. Specially designed Holter recorders will provide an ambulatory HRECG from which late potential measurements can be correlated with the evolving arrhythmic state (question #1). The distribution of late potentials on the thorax will be examined with a 128 channel mapping system which is able to perform body surface signal averaging and record epicardial activation maps. Quantifying the signal and noise levels in each lead should provide answers for question #2. In the acute phase we will examine changes in frequency domain characteristics in dogs with the effects of induced bundle branch to answer question #3.