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Circulation, Vol 61, 1227-1238, Copyright © 1980 by American Heart Association

ARTICLES

Epicardial and endocardial activation during sustained ventricular tachycardia in man

LN Horowitz, ME Josephson and AH Harken

Ventricular activation during ventricular tachycardia was studied by intraoperative epicardial and endocardial mapping in 21 patients with coronary artery disease and previous myocardial infarction who underwent operation for recurrent ventricular tachycardia. Twenty-nine morphologically distinct tachycardias were mapped; 18 tachycardias had a right bundle branch block morphology and 11 had a left bundle branch block morphology. After cannulation for bypass, the tachycardias were induced and electrograms were recorded at 55-75 epicardial sites. After starting cardiopulmonary bypass, the infarction was incised and electrograms were recorded at 28-55 left ventricular endocardial sites during ventricular tachycardia. All mapping data were analyzed with three simultaneously recorded ECG lead and two reference electrograms. Earliest activation in all tachycardias occured on the endocardial surface of the infarction. In each tachycardia, endocardial electrical activity was recorded before the onset of the QRS complex. Earliest epicardial activation in the 29 tachycardias occurred 10 msec after the onset of QRS complex. Epicardial breakthrough occurred on the right (19 tachycardias) as well as the left ventricle (10 tachycardias). We conclude that ventricular tachycardia associated with ischemic heart disease originates near the endocardial surface of the left ventricle along the border of the infarction and that epicardial mapping alone is insufficient to identify the site of origin of these tachycardias.

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