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(Circulation. 1999;100:1250-1252.)
© 1999 American Heart Association, Inc.

Correspondence

Misdiagnosis of New Bifascicular Block

John E. Madias, MD

Cardiology Division Elmhurst Hospital Center, Elmhurst, NY

	Introduction

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To the Editor:

I enjoyed the contribution of Kaji et al¹ in the "Images in Cardiovascular Medicine" section of the journal. I have found an error, and because I believe that this part of Circulation is very popular and is read by a large number of physicians, it would be an opportunity to call attention to a frequently committed misdiagnosis. I am referring to the characterization of the ECG made by the authors as showing "a new bifascicular block." Apparently the authors made this diagnosis on the basis of the widened QRS complex in lead V₁ (which they interpreted as a right bundle-branch block) and the leftward shift of the frontal QRS axis well depicted in leads aVL and aVF (which they attributed to left anterior hemiblock).

However, the ECG features noted in their case and the precipitating clinical circumstances are typical of the "giant R waves syndrome" noted in the hyperacute phase of transmural ischemic injury.^{2 3 4 5 6} ECG patterns identical to the one depicted in the case under discussion are seen in the setting of the very early phase of transmural myocardial infarction and coronary vasospasm (Prinzmetal's angina) and immediately after acute coronary occlusion in the animal laboratory.^{2 3 4 5 6}

The diagnostic particulars of the ECG include an increase in the R amplitude of waves and the decrease or disappearance of S waves (vide leads aVL, V₂, and V₃ of the authors case), ST-segment elevation merging with the R waves (V₂), and widening of the QRS complex (VL, 3, VF, V₂), often indistinguishable from ventricular tachycardia, in which the P waves are obscured and the rate is fast.

The mechanism of this ECG syndrome has nothing to do with a compromise of conduction at 1 or more sites of the conduction system and is believed to constitute a "focal" block or delay in conduction in an area of severe transmural ischemic injury. In such a territory, late slow conduction produces delayed enhanced (due to lack of opposition) depolarization vectors, pointing toward the ECG leads reflecting the particular region involved (vide, positive potentials in aVL, V₂, and V₃ and negative in 3 and aVF in this case).^{1 2 3 4 5}

	References

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1. Kaji EH, Bednarz J, Spencer KT, Lang RM. Left main coronary artery disease: cardiac arrest following stress echocardiography. Circulation. 1998;98:1038.[Free Full Text]
   
2. Madias JE. The earliest electrocardiographic sign of acute transmural myocardial infarction. J Electrocardiol. 1977;10:193–196.[Medline] [Order article via Infotrieve]
   
3. Madias JE, Krikelis EN. Transient giant R waves in the early phase of acute myocardial infarction: association with ventricular fibrillation. Clin Cardiol. 1981;4:339–349.[Medline] [Order article via Infotrieve]
   
4. Madias JE. The "giant R waves" ECG pattern of hyperacute phase of myocardial infarction. J Electrocardiol. 1993;26:77–82.[Medline] [Order article via Infotrieve]
   
5. Ekmekci A, Toyoshima H, Kwoczynski JK, Nagaya T, Prinzmetal M. Angina pectoris, V: giant R and receding S wave in myocardial ischemia and certain nonischemic conditions. Am J Cardiol. 1961;7:521–532.[Medline] [Order article via Infotrieve]
   
6. Prinzmetal M, Ekmekci A, Kennamer R, Kwoczynski JK, Shubin H, Toyoshima H.. Variant form of angina pectoris: previously undelineated syndrome. JAMA. 1960;174:1794–1800.
   

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