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The physiological basis of serial T-wave abnormalities associated with myocardial infarction was studied. After coronary artery ligation in dogs, ventricular functional refractory periods (FRPs) were measured at five to eight epicardial, intramural, and endocardial sites. FRPs measured during acute ischemia shortened an average of 26 msec. FRPs measured 24 to 72 hr after coronary ligation were 24 msec longer at ischemic than at nonischemic sites. Alterations of recovery times were analyzed in terms of a repolarization model which related the form of the action potential downstroke to the form of the T wave of the body surface ECG. Observed FRPs were used to infer action potential duration and T waves were derived. Shortening FRPs in the anterolateral wall of the ventricle increased the amplitude of derived T waves in the X lead and caused T-wave inversion in the Z lead. Prolonging FRPs in the same area caused T-wave inversion in lead X and increased T amplitude in lead Z. The form of derived T waves qualitatively corresponded to serial T-wave abnormalities seen in patients with myocardial infarction.
Mandel et al. (Mon,) studied this question.