Joseph A. Vassallo

Endocardial catheter mapping was performed in 18 patients with left bundle branch block (LBBB). Four patients had no organic heart disease (group I), six had cardiomyopathy (group II), and eight had coronary artery disease and previous infarction (group III). Twelve patients had one septal site of left ventricular endocardial breakthrough, while six had two left ventricular endocardial breakthrough sites, with one site always being septal. There was no significant difference among the groups with respect to time of left ventricular breakthrough (group I, 44 msec after the onset of the QRS complex; group II, 58 msec; and group III, 51 msec). Total left ventricular endocardial activation time was significantly longer in group III (119 msec) than group I (81 msec; p less than .05) and group II (61 msec; p less than .001). Duration of total right ventricular endocardial activation was 36 msec (seven patients). The final site of right ventricular activation was at 44 msec after the onset of the QRS complex. We conclude that (1) right ventricular activation occurs before initiation of left ventricular activation in patients with LBBB, (2) left ventricular endocardial activation in patients with LBBB most likely occurs as a result of right-to-left transseptal activation, (3) left ventricular endocardial activation sequence in patients with LBBB is heterogeneous, and (4) patients with coronary artery disease and LBBB have significantly longer total left ventricular endocardial activation times than patients with no organic heart disease or those with cardiomyopathies.

We assessed the value of endocardial catheter mapping in 52 patients in sinus rhythm and with 102 morphologically distinct ventricular tachycardias. The local bipolar electrograms from various regions of the left ventricle were assessed and quantitatively classified with respect to the characteristics of amplitude and duration. With the use of this assessment we found that electrograms from the site of origin were of significantly lower amplitude and longer duration; however, because such an overlap occurred with electrograms that were not from sites of origin, this does not serve as a useful clinical marker. Various types of electrograms, including normal, abnormal, fractionated, abnormal late, fractionated late, and longest, were evaluated with respect to sensitivity, specificity, and positive predictive value. None of these types possessed the ability to reliably localize the site of origin of ventricular tachycardia. We therefore conclude that endocardial catheter mapping during sinus rhythm is not useful as a guide in localized surgical therapy of ventricular tachycardia. Surgery guided only by the results of mapping during sinus rhythm would result in a more extensive excision than that directed by maps obtained during ventricular tachycardia and in some cases would result in the exclusion of the area considered to be the site of origin of the tachycardia.

Catheter mapping during sinus rhythm was performed in 132 patients with coronary artery disease and 26 patients with congestive noncoronary cardiomyopathy. Each of the patients had a clinical history of one of the following: no ventricular arrhythmia, nonsustained ventricular tachycardia, cardiac arrest, or sustained ventricular tachycardia. The characteristics of the endocardial electrogram and other measured indexes of slow endocardial conduction were compared between patients with different types of disease and in different arrhythmia groups to determine if differences existed. The cardiomyopathic group had a higher percent of normal endocardial electrograms than the coronary artery disease group, with no evidence of slow endocardial conduction. The sustained ventricular tachycardia group exhibited a greater percent of abnormal endocardial electrograms and more evidence of slow endocardial conduction, distinguishing this group from the three other arrhythmia groups. We conclude the following: The underlying electrophysiologic substrate varies in patients with different ventricular arrhythmias. It is therefore inappropriate to analyze all patients with ventricular arrhythmias as a single group. Patients with congestive noncoronary cardiomyopathy, regardless of the type of their arrhythmia, have a relatively normal endocardium. Those patients with serious ventricular arrhythmias should not be considered candidates for surgery directed at removing abnormal endocardium.

Endocardial catheter mapping was performed in 15 patients in sinus rhythm who had no evidence of structural heart disease and normal left ventricles. Mapping was performed with the use of 10 mm interelectrode distance from various left ventricular endocardial sites. In 10 patients a quantitative analysis of electrographic amplitude, duration, and amplitude/duration ratio was performed. The normal left ventricular bipolar electrograms had an amplitude of greater than 3 mV, a duration of less than 70 msec, and an amplitude/duration ratio of greater than 0.045. Local activation times were also assessed in the 15 patients. This analysis revealed two endocardial breakthrough sites, one on the midinferior septum and a second on the anterior wall near the insertion of the anterior papillary muscle. We therefore have defined normal quantitative characteristics of left ventricular bipolar electrograms and the normal left ventricular activation sequence in the intact normal human left ventricle.