This project will explore four electrocardiographic problems of clinical and basic significance. Canine models of acute ischemia, and acute and chronic infarction will be studied using quantitative as well as qualitative body surface mapping techniques. First, the quantitative relationship between body surface ECG changes during transient myocardial ischemia and regional myocardial blood flow will be determined to provide a physiologic basis for clinical exercise electrocardiography. Ischemia will be produced by atrial pacing after implantation of an ameroid constrictor about a selected coronary artery, flow will be measured by serial radiolabelled microsphere injections, and ECG consequences will be quantitated using an 84 electrode torso array. Effects of localized and of global primary S-T segment shifts produced by nontransmural infarction and digoxin or potassium infusions, respectively, upon the ischemic ECG response will likewise be investigated. Second, electrocardiographic consequences of acute myocardial infarction will be studied to develop techniques based upon conduction delay and disparate repolarization for the prediction of post-occlusion and post-reperfusion ventricular tachyarrhythmias. ECG parameters to be computed during and after acute arterial occlusion include QRST area and Q-T interval spatial distributions. A statistical model relating these ECG parameters as well has lesion size to arrhythmia vulnerability will be attempted. Third, anatomic and functional determinants of mid and late QRS changes after chronic transmural and nontransmural myocardial infarction will be explored. These will be studied in relation to lesion location and activation timing as well as to size and transmural extent. Lesions will be produced by transient occlusion or embolization of the anterior descending or circumflex artery, and infarct size will be quantitated by computer-assisted planimetry of histochemically stained tissue sections. Last, electrophysiologic properties of the previously utilized ameroid constrictor model will be explored to evaluate its utility as an analog of clinical sudden cardiac death. The incidence of spontaneous and inducible arrhythmias in relation to the high incidence of sudden death in this noninfarction, stress-induced ischemic model will be examined. Spontaneous ectopy will be recorded using ambulatory ECG methods, and arrhythmia induction will be attempted with multiple extrastimuli at rates that do and do not cause subendocardial underperfusion as determined by microsphere injection.
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