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Circulation Research. 1999;85:959-964

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(Circulation Research. 1999;85:959.)
© 1999 American Heart Association, Inc.


Integrative Physiology

Epicardial ST Depression in Acute Myocardial Infarction

Danshi Li, Chuan Yong Li, Ah Chot Yong, Peter R. Johnston, David Kilpatrick

From the Discipline of Medicine, University of Tasmania, Hobart, Australia.

Correspondence to D. Kilpatrick, The Discipline of Medicine, University of Tasmania, 43 Collins St, Hobart, 7000, Australia. E-mail d.kilpatrick{at}utas.edu.au

Abstract—The presence of electrocardiographic ST depression in acute infarction remains controversial and poorly explained. A combined animal and modeling study was performed to evaluate the source of ST changes in acute infarction. In anaesthetized sheep, small infarcts showed uniform ST elevation over the infarction whereas larger infarcts showed marked ST depression over the normal myocardium in addition to the ST elevation. These findings were replicated by bidomain models of the heart. A hollow sphere was used to model a gradually increasing infarct, and this showed that there was a decrease in the ratio of ST elevation to ST depression as the infarct was increased. The current flowing out of the heart must be identical to the current flowing back into the heart. This means that any infarction will produce ST depression as well as ST elevation, the ratio between the two being related to the size of the infarction. Small infarction is associated with a small region of ST elevation and minor ST depression of the remaining myocardium, and as the infarct region increases, the amplitude of the epicardial ST elevation falls and the amplitude of the ST depression increases. Infarction size is proportional to both the height of the ST depression on the epicardium and the strength of the epicardial ST segment dipole.


Key Words: electrocardiography • epicardial potential • acute infarction • bidomain model • ST depression




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