More deaths occur in the United States each year due to heart attacks than from cancer, stroke, and accidents combined. At least half of these sudden cardiac deaths result from ventricular fibrillation which develops prior to the patients receiving any medical aid. Despite vigorous investigation, the reason that some hearts fibrillate and others do not is very poorly understood. Major efforts have been applied to protect ischemic myocardium in order to reduce the mortality from heart attacks; an equally important approach is to prevent electrical deaths due to ventricular fibrillation. The role of infarct size and the distribution of myocardial ischemia and infarction on the susceptibility to ventricular fibrillation is important to understand. The present investigations will employ two new canine infarction models. The first model is produced using a two-stage occlusion of the left anterior descending coronary artery modified by a reperfusion stage. In this chronic canine infarct model the infarcts are mottled with regions of normal, abnormal and necrotic myocardium interspersed. Three days and up to five months after occlusion all animals demonstrate sustained VT/VF which can be reproducibly initiated and terminated using the same techniques of programmed electrical stimulation as used in the clinical electrophysiology lab. The second canine infarct model is a coronary embolization model employing a rapidly hardening vinyl latex solution which can be injected into the coronary artery to eliminate collateral circulation. The latex injection produces a transmural infarct which closely resembles many human infarcts. We will use both microelectrode and extracellular stimulating and recording techniques to evaluate the importance of infarct size and distribution of ischemia and infarction on the susceptibility to tachyarrhythmias. Mottled infarcts will be switched into transmural infarcts by injecting the vinyl latex solution at the same LAD site previously subjected to the occlusion/reperfusion technique. These studies should provide new answers concerning the role of infarct size and distribution in influencing the development of ventricular tachycardia and ventricular fibrillation.
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