Editorial by Pentti M. Rautaharju, MD, PhD, 7 September 2005

The editorial by John Madias in this issue of the Journal of Electrocardiography presents a rather provocative thesis, implying that it is impossible on theoretical grounds to rely upon ST deviations in acute myocardial ischemia to provide insight on the presence or attributes of acute myocardial ischemia and infarction [1]. The editorial offers an explanation why this is so—the ischemic ST-segment counterpoise.

In my dictionary the definition of counterpoise is “any equal and opposing power or force.” This matches the meaning of the term as used in the editorial: ST deviation vectors from the opposite walls of the left ventricle cancel, and occasionally enhance, each other’s effect.

This short commentary presents a differing viewpoint, in a way as a counterpoise to counterpoise. To start with, I submit that it is unnecessary to introduce the term counterpoise. A simple “cancellation” is an adequate, older, and more familiar term used in electrocardiography.

The editorial is on the right track on many points presented, for instance, concerning ischemia induced by exercise stress testing. Ischemia in this situation, presumed to be subendocardial “demand” ischemia, may well be more universal, thus creating a reasonable argument for a substantial cancellation. Extrapolating this concept to acute myocardial injury/infarction is more problematic. The author is correct in stating that using the ECG to assess accurately the presence, age, severity, extent, and evolution of acute myocardial ischemia and infarction may be an impossibility. Accurate prediction is rarely possible in electrocardiography. I would claim, however, that assessing the presence of acute ischemia with a reasonable confidence is a sensible goal. Determination of the presence of acute ischemia is actually clinically more important than all these other aspects of ischemia assessment.

Serious chronic coronary artery disease is often associated with the occlusion of multiple coronary arteries and severe left ventricular dysfunction, indicating large infarction or multiple infarcts [2]. The question is how often myocardial infarction occurs with simultaneous acute total occlusion of multiple coronary arteries producing total cancellation of ST deviations. The editorial does not answer this question.

The schematics of hypothetical extensive acute anterior wall subendocardial and transmural ischemia in Figs. 1 and 2 illustrate possible cancellation effects. In extensive acute subendocardial ischemia, ischemic segments would have to extend to a large portion of the posterior wall before a substantial cancellation of the ST deviations can be expected (Fig. 1). In acute transmural ischemia, only the lateral boundary zones contribute to the ST deviations (Fig. 2). The resulting ST deviations (apparent ST depression in anterior chest leads in acute anterior wall transmural ischemia and ST elevation in posterior transmural ischemia)
are contrary to known clinically observed ST deviations.

The problem we have here is that the exact configuration of the ischemic boundary zone and the injury current return paths are not known. Fiber orientation topology at the lateral boundary may considerably modify injury current strength and flow direction [3]. Consequently, ST deviations may not be what the solid angle concept in a homogeneous model would suggest.

This commentary should not be construed to detract from the value of the editorial. It serves as a useful platform for consideration of this multifaceted issue with many unknown factors. As usual, the truth may lie somewhere in between the viewpoints presented.


[1] Madias JE. Difficulties in assessing the presence, duration, severity,
extent, and evolution of acute myocardial ischemia and infarction:
bIschemic ST-segment counterpoiseQ as a plausible explanation.
J Electrocardiol 2006 [Editorial] [in press].

[2] Startt RH, Selvester RH, Wagner G, Ideker R. Myocardial infarction. In: MacFarlane PW, Lawrie TDV, editors. Comprehensive electro-
cardiology. New York7 Pergamon Books Ltd; 1988. p. 571.

[3] Hopenfeld B, Stinstra JG, MacLeod RS. Mechanism for ST depression
associated with contiguous subendocardial ischemia. J Cardiovasc
Electrophysioil 2004;15:1200.