Derived epicardial potentials differentiate ischemic ST depression from ST depression secondary to ST elevation in acute inferior myocardial infarction in humans

Department of Medicine, University of Tasmania, Australia.
Journal of the American College of Cardiology (Impact Factor: 16.5). 10/1989; 14(3):695-702; discussion 703-4. DOI: 10.1016/0735-1097(89)90112-5
Source: PubMed


It was hypothesized that in acute inferior wall myocardial infarction, an additional ischemic area in the subendocardium of the noninfarcting territory would produce a selective current dipole between the infarcting and ischemic regions. A resistance network model to calculate epicardial potentials from body surface electrocardiographic potentials was developed and used to examine the hypothesis in 219 patients with acute inferior myocardial infarction. In the learning set of 110 patients, two characteristic dipole patterns were observed, each associated with a high mortality rate in the ensuing 15 months when compared with that in the remaining patients. In the test set of 109 patients, a double-blind analysis of the patterns showed that the 34 patients with a dipole pattern had a collective mortality rate of 35% at 15 months compared with a 15 month rate of 5% in the remaining patients. In the total group of 219 patients, the magnitude of ST segment elevation and both the magnitude and integral of the area voltage of ST depression on the epicardium were significantly correlated with the mortality rate (p less than 0.0002 for all variables against death at 15 months). This study strongly suggests that ST depression due to ischemia can be differentiated from ST depression secondary to the ST elevation in acute inferior infarction by the examination of epicardial potential distributions.

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    • "Here, we capitalize on the efficiency of the stationary model for use with the inverse problem of identifying the size and position of the ischemia. Using the stationary model, which is based on the well-known Bidomain model for cardiac tissue [14], [15], distinguishes our approach from others, like [16], that use very different forward models to localize ischemia, or those like [17]–[21], which discuss the relation between inverse calculations of the epicardial potential and the location of ischemia and infarction. "
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