Six new concepts in electrocardiography: Theoretical considerations, and applications in ECG diagnosis

J. E. Madias, M.D.
Mount Sinai School of Medicine/Cardiology Division,
Elmhurst Hospital Center,79-01 Broadway, Elmhurst, NY 11373 USA

Abstract: Voltage modification and often complete cancellation of parts of the ECG curve take place in situations when potentials generated by myocardial territories opposite each other interact. Such changes can occur in the resting ECG or during stress testing, they can affect both the depolarization and repolarization phases, and thus result in stable or transient alterations in the QRS complexes or ST and T waves. Accordingly we have observed, and attributed to the above mechanism, falsely negative stress ECG, disappearance of infarctional Q-waves in patients with thallium-based proof of ischemia, and positive stress ECGs associated with falsely negative thallium tests in patients with ischemia and severe 3-vessel coronary artery disease, proven by coronary arteriography. Also the diagnosis of ventricular aneurysm, consequent to an old myocardial infarction, in patients with left and right bundle branch blocks has been made employing the concept of potential modification. Finally, an unrelated to the above detailed mechanism phenomenon, that of attenuation of ECG voltage due to peripheral edema has been recently the focus of  studies by our group.

INTRODUCTION

Our laboratory has been working for the past few years on six new ideas in electrocardiography, five of which are based on the concept of electrical cancellation or voltage modification of electrical activity generated by cardiac regions, situated opposite each other. It is well known that only a fraction of the heart’s activity is manifested as epicardial electrograms or surface electrocardiograms, with the vast majority undergoing cancellation. These alterations of the ECG potentials due to modification or even cancellation affect both the QRS complexes and the ST-segment and the T wave. Changes may be manifest in both the resting and the exercise ECGs. The resulting electrocardiographic patterns are non-conventional, in the sense that certain feature appear incompatible with the apparent underlying pathology (i.e elevated ST-segments in the lateral precordial leads with predominantly positive QRS complexes in the presence of left bundle branch block). Such modifications of potentials are not only interesting for delineating electrophysiological mechanisms, but they are useful in being translated to diagnostic signs heretofore unknown.

METHODS

1) We have compared serial ECGs in patients undergoing exercise stress testing in reference to the changes in the amplitude of QRS complexes, infarctional Q-waves, and ST-segment depressions, and have correlated them with the corresponding thallium-201myocardial perfusion scintigraphy, its extent and distribution. 2) We have correlated the standard ECGs of patients with ventricular aneurysm with the non-ECG based evidence (contrast ventriculography/and or echocardiography) for such a diagnosis. 3) We have correlated amplitude measurements from daily standard ECGs in patients with peripheral edema, developed in the context of critical care illnesses, with weight changes.

RESULTS / DISCUSSION

We have observed the following:

1) Areas of ischemia in territories opposite each other may cancel out, rendering the exercise ECG falsely negative, while the associated thallium-201 myocardial scintigram is grossly positive in more than one myocardial region ("ischemic ST- segment counterpoise") [1-3].

2) A Q-wave due to an old myocardial infarction can decrease in amplitude, or even disappear transiently during the exercise testing, if there is severe
ischemia present in the contralateral to the infarcion myocardial territory [4]. This is due to the "deficient voltage" genetated by the transiently ischemic region,
which in the absence of ischemia is responsible for the inscription of the infarctional Q-wave. Accordingly, patients with fixed defects due to a previous myocardial infarction in the thallium scintigram, and no ischemia in the contralateral to the infarction territory retain their Q-waves in the exercise ECG. 

3) The apical myocardial region, when ischemic, is the only myocardial region which cannot be opposed by another ischemic territory, as it happens for the
other cardiac regions, due to its place opposite the non-muscular valve rings; as a result ischemia of the apex has a decisive role in rendering the exercise ECG positive. This explains the occasional occurrence of a true positive stress ECG associated with a false negative myocardial scintigram due to uniformly distributed severe ischemia [5].

4) Stable ST-segment elevation in precordial lead V5 in the presence of left bundle branch block suggests ventricular aneurysm consequent to an old myocardial infarction; this is due to a primary repolarization disturbance "overwhelming" the secondary ST- segment depression of the of left bundle branch block [6,7]. The above-described ECG sign of   ventricular aneurysm was abolished following aneurysmectomy in one patient, although it was sought after by precordial multi-lead ECG mapping.

5) Stable ST- segment elevation in precordial leads V1-V3 in the presence of right bundle branch block suggests ventricular aneurysm consequent to an old myocardial infarction; such patients' ECGs also show Q-waves in these leads [8]. The mechanism of this phenomenon is similar to the one outlined in 5 (see above).

6) Severe peripheral edema, regardless of its etiology, leads to marked reduction of the ECG's voltage; a good correlation of the loss of QRS voltage with weight gain is found in such cases [9]. This phenomenon is attributed to the decrease in the resistance offered by the conductive medium surrounding the heart, as per Ohm's law, and is not due to pericardial effusion or other lung or pleural pathology, which has been excluded in the cases we have studied. Reduction in the amplitude of QRS potentials is gradual pari passu with the progressive fluid retention and weight gain. Also patients who have subsequently lost all or part of the gained weight have shown partial or complete “recovery” of the amplitude of ECG potentials.

CONCLUSIONS

The above six new concepts have important theoretical underpinnings, and considerable applicability to the practice of cardiology. They can be reduced to two basic ideas, one of the effects of modification/cancellation of ECG potentials by competing similar (ischemia), or different (aneurism and abnormal repolarization due to a bundle branch block) pathophysiological alterations, and the other of the attenuation of ECG potentials due to peripheral edema altering transfer of cardiac potentials to the body surface by decreasing the volume conduction resistance. Interpretation of the ECG along the ideas expounded here will explain some “ECG aberrations” or inconsistencies encountered in the clinical setting. For example it will explain the apparent low sensitivity of the ECG stress testing, the frequent discordance of findings in the exercise ECG and thallium-201myocardial scintigraphy, and the marked changes in the ECG noted during prolonged hospitalization in patients with critical illness. Another counterintuitive alteration which can be explained by these concepts is the occasional transient and gradual reduction of the amplitude of infarctional Q-waves, or their complete disappearance in the course of exercise testing; as explained above; this phenomenon proves the “plasticity” of the QRS complex, in contrast to the perception of clinicians favoring the notion that the depolarization part of the ECG is stable and unchangeable, while the repolarization portion is unstable volatile and perpetually changing. Finally these concepts can be further extended to explain other ECG aberrations or inconsistencies in the clinical arena; also they can become the springboard for new ventures in laboratory and theoretical electrocardiology.

Acknowledgments:  The author wishes to acknowledge his trainees, too numerous to include in the authorship of this communication, for their contributions in the research activities carried out at the Cardiology Division of the Elmhurst Hospital Center; their names appear in the references cited.

REFERENCES

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[2] J.E.  Madias, M. Mahjoub, J. Valance, The paradox of negative exercise stress ECG/positive thalium scintigram: Ischemic ST-segment counterpoise as the underlying mechanism. J. Electrocardiol 29:243-248,1996. 

[3[ J.E. Madias,  M Khan, B. Manyam, The role of Ischemic ST-segment counterpoise in rendering the response of exercise ECG falsely negative. Clin Cardiol 20:489-92,1997.   

[4] J.E. Madias, B. Manyam, M. Khan, et al, Transient disappearance of Q-waves of previous myocardial infarction due to exercise-induced ischemia of the contralateral noninfarcted  myocardium. J. Electrocardiol 30:97-103,1997.

[5] J.E. Madias, P. Knez, M. Win, True-positive exercise ECG/false negative thallium 201 scintigram: A proposal of a mechanism for the paradox. Clinical Cardiol 23: 625- 629, 2000.

[6] J.E. Madias, A. Kaminetsky, N. Solanki, Myocardial infarction induced ventricular aneurysm in the presence of complete left bundle branch block: A case report suggesting a new electrocardiographic diagnostic criterion. J. Electrocardiol 32: 179-183,1999.

[7]  J.E. Madias, R. Ashtiani, H. Agarwal, et al., Diagnosis of myocardial infarction-induced ventricular aneurysm in the presence of complete bundle branch block. J. Electrocardiol 34: 147-154, 2001.

[8] J. E. Madias, MD, H. Agarawal, R. Ashtiani, et al., Diagnosis of ventricular aneurysm in the presence of right bundle branch block: Non-ECG correlates of a positive ECG diagnosis (submitted).

 [9] J.E. Madias, R. Bazaz H. Agarwal, et al., Anasarca mediated attenuation of the amplitude of electrocardiogram   complexes. A description of a heretofore unrecognized   phenomenon. J Amer Coll Cardiol 38:756-764, 2001.