1. 1. There is a current difference of opinion regarding the interpretation to be placed upon the RS-T junction displacements caused by myocardial infarction. 2. 2. When an electrical situation similar to that which exists with certain varieties of direct subepicardial damage is applied to the ordinary varieties of infarction, according to the laws which determine the flow of electric currencs in homogeneous volume conductors, the predicted electrocardiographic effects prove to be the inverse of those which are known to occur clinically and experimentally in association with infarction. 3. 3. Inasmuch as these laws have been shown to apply to problems of the kind herein considered with sufficient accuracy to be useful, it appeared highly probable that the electrical situations caused by direct damage and by infarction, although fundamentally similar, must differ considerably in pattern detail. 4. 4. A summary of the pathologic changes is presented, together with the requirements deduced from a critical analysis of the electrocardiographic changes associated with infarction. The data led to a reasonable definition of the source and sink distribution of the electrical field of injury and of the neighboring zone of ischemia which are associated with infarction. Moreover, an explanation for the occurrence in sequence of the RS-T junction displacements and the primary T-wave changes is regarded as an integral part of the problem. This sequential relationship, together with heretofore unexplained QRS changes, is thus accounted for incidentally. The RS-T junction displacements in the extremity leads are regarded as the result of the development and subsequent decay of the spatial axis of injury-î. The primary T-wave changes have been ascribed elsewhere to a diversion and subsequent reversion of the spatial gradient of duration of the excited ventricular state. In general, the injured zone caused by recent infarction is perifocal or semiperifocal with respect to the dead zone, depending upon whether the infarct is essentially subendocardial or transmural. The ischemic zone is at first small and semiperifocal with respect to the injured zone. Later, as the injured zone diminishes in the direction of the dead zone and finally disappears, the ischemic zone necessarily undergoes an inward expansion and becomes directly perifocal with respect to the dead zone of a subendocardial infarct, or directly semiperifocal with respect to the dead zone of a transmural infarct. The changes are ascribed chiefly to improvement in the local circulation. 5. 5. The explanation offered for the RS-T junction displacements and the sequential occurrence of T-wave changes as a result of infarction has the additional advantage of being directly applicable to similar but more transient serial changes which are observed in certain patients during and immediately after an attack of angina pectoris. 6. 6. A summary of certain electrocardiographic interpretations is presented which is regarded as tentatively acceptable for curves that reflect the complex combination of infarction and pericarditis.
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