Abstract
The major hypothesis guiding our studies of arrhythmias in experimental healed myocardial infarction is that during the evolution and subsequent healing of experimental myocardial infarction, some tissues exposed to ischemic injury heal, but persisting abnormalities in the healed tissues influence the characteristics of electrophysiologic responses to future events. A subordinate premise is that mechanisms for electrophysiologic disturbances in hearts with healed myocardial infarction extend beyond the structural and geometric abnormalities created by the presence of a scar with surrounding or intertwining bands of muscle. There are data demonstrating that long-term changes in patterns of repolarization and response to antiarrhythmic agents may result from either uncoupling or long-term changes in membrane properties; that persistent changes in adrenergic receptors and the adenylate cyclase-cyclic AMP axis are present in hearts with healed infarction; and that neurophysiologic abnormalities may result from nerve damage, membrane responses to sympathetic stimulation, or both. AH of these changes are quantitatively and/or qualitatively regional in distribution. The consequence of regional alterations in properties of hearts with healed infarction becomes most obvious during subsequent acute ischemia and may explain, in part, why the heart with healed myocardial infarction is more susceptible to potentially lethal arrhythmias.