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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    ABSTRACT: It is well known that the presence of myocardial ischemia can be observed as a shift in the ST segment of an electrocardiogram (ECG) recording. The question we address in this paper is whether or not ST shift can be used to compute approximations of the size and location of the ischemic region. We begin by investigating a cost functional (measuring the difference between synthetic recorded data and simulated values of ST shift) for a parameter identification problem to locate the ischemic region. We then formulate a more flexible representation of the ischemia using a level set framework and solve the associated minimization problem for the size and position of the ischemia. We apply this framework to a set of ECG data generated by the Bidomain model using the cell model of Winslow et al. Based on this data, we show that values of ST shift recorded at the body surface are capable of identifying the position and (roughly) the size of the ischemia.
    Full-text · Article · Jul 2006 · IEEE Transactions on Biomedical Engineering
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    Preview · Article · Sep 1989 · Journal of the American College of Cardiology
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    ABSTRACT: To determine the ability of initial ST segment elevation and depression to predict infarct size limitation by thrombolytic therapy, data were analyzed in 721 patients with acute myocardial infarction who were admitted to a randomized, placebo-controlled study of intravenous recombinant tissue-type plasminogen activator. Patients with QRS duration of 120 msec or more or with previous history of myocardial infarction were excluded, leaving 322 in the treatment and 333 in the placebo group. Cumulative 72-hour release of alpha-hydroxybutyrate dehydrogenase and global ejection fraction as well as left ventricular wall motion derived from angiography were used as independent measures of infarct size. Electrocardiograms obtained at admission, 6 hours after start of therapy, and before discharge were analyzed. All ST measurements were made by hand at the J point and 60 msec after the J point. Patients with high ST segment elevation at admission (i.e., sum of ST elevation at 60 msec after the J point was 20 mm or more) had significantly larger infarction and higher hospital mortality when compared with those with lower (less than 20 mm) ST elevation. Reciprocal ST segment depression also showed a linear relation with infarct size and mortality, independent from ST elevation, both in anterior and inferior myocardial infarction. The sum of deviations measured at the J point and 60 msec after the J point differed significantly, especially in anterior myocardial infarction at admission (mean, 16 +/- 9 versus 23 +/- 11 mm). The prognostic value of one measurement was not, however, superior over the other. Treatment with recombinant tissue-type plasminogen activator was most effective in those with large ST deviations at admission, but patients with anterior infarction and smaller ST shifts also appeared to benefit from therapy. Results in individual patients were variable, and the overall correlation of initial ST shifts with enzymatic infarct size was rather low. In conclusion, the present study shows that the magnitude of initial ST elevation and also of reciprocal ST depression in the admission electrocardiogram is valuable for the management and assessment of thrombolytic therapy in patients with acute myocardial infarction.
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