No abstract

Endocardial catheter mapping of the left ventricle was performed in 40 patients during right ventricular pacing to determine the effect of underlying myocardial infarction on endocardial activation. Group I comprised 18 patients without infarction, Group II 12 patients with inferior infarction and Group III 10 patients with anteroseptal infarction. Thirty-nine of the 40 patients had only a single left ventricular breakthrough site located on the midseptum in 33 cases, apical septum in 4 cases and basal septum in 2 cases. The earliest left ventricular local activation time during right ventricular pacing was earlier in Group III (40 +/- 11 ms) than in Group I (55 +/- 17 ms) and Group II (60 +/- 15 ms) (p less than 0.01). Total endocardial activation time was significantly longer in Group III (118 +/- 30 ms) than in Group I (76 +/- 14 ms) and Group II (72 +/- 20 ms) (p less than 0.001). The latest left ventricular site of activation during right ventricular pacing was the inferoposterior base in 14 (77%) of the 18 Group I patients, and 10 (83%) of the 12 Group II patients. The latest site of activation in Group III patients was variable. It is concluded that: left ventricular endocardial activation patterns and conduction times are influenced by the site of previous infarction. Longer total endocardial activation in Group III suggests that specialized conducting tissue in the septal and anterior walls may play an important role in left ventricular activation during right ventricular pacing.(ABSTRACT TRUNCATED AT 250 WORDS)

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 LI), 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 111 (1 19 msec) than group 1 (81 msec; p < .05) and group 11 (61 msec; p < .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 heterogenous, 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. Circulation 69, No. 5, 914-923, 1984. OUR PRESENT UNDERSTANDING of ventricular activation in man is based on data derived from studies involving preparations in vitro and canine preparations and from intraoperative epicardial mapping of the human heart in a small number of patients. standing of ventricular activation in the human heart with left bundle branch block (LBBB) in vivo is therefore limited by several factors. These include differences between the anatomic and functional properties

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: (1) No. 4, 645452, 1986. LEFT VENTRICULAR mapping in individuals in sinus rhythm has been performed in a variety of patient groups, including those with a normal left ventricle,'-' conduction defects,8-14 coronary artery disease with or without ventricular tachycardia,'2-22 and hypertrophic cardiomyopathy.23 These studies primarily described activation patterns only, although a few attempted to quantitatively and qualitatively characterize local elec-

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 ittuscle. 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. Circulation 70, No. 1, 37-42, 1984. NORMAL left ventricular endocardial activation and electrographic characteristics in man have not previously been described in vivo. It is imperative to establish normal guidelines if this technique is to be used to evaluate conduction defects, infarction, or arrhythmias. Our study was designed to characterize the electrograms and sequence of ventricular activation obtained during sinus rhythm by catheter endocardial mapping of the normal human left ventricle. MethodsPatient population. Fifteen patients referred to the Hospital of the University of Pennsylvania for electrophysiologic evaluation underwent sinus rhythm endocardial mapping during the course of their examinations. There were eight male and seven female subjects with a mean age of 30 years (range 17 to 64).In no patient was there evidence of structural heart disease. All had normal M mode and two-dimensional echocardiograms. Ten of the 15 patients had normal left ventricular radionuclidegated blood pool scans and in 10 (including five who did not undergo radionuclide-gated blood pool scanning) of the 15 patients results of left heart catheterization and coronary angiographic examination were normal. All patients had normal PR and QRS intervals and normal electrical axes. In two patients intermittent long QT intervals were documented (one drug-related and the other idiopathic). Electrocardiograms of both patients were normal at the time of endocardial mapping. There was no evidence of a preexcitation syndrome in any patient, as determined clinically and by laboratory testing. Electrophysiologic studies were performed to determine the presence or absence of a variety of arrhythmias. Three patients had sustained ventricular tachycardia in the absence of structural heart disease.Electrophysiologic study. Studies were performed in patients in the nonsedated, postabsorptive state after informed written consent had been obtained. Antiarrhythmic drug therapy was discontinued at least five half-lives before endocardial mapping. ...

The purpose of this study was to determine left ventricular activation, dispersion of refractoriness, and total recovery time in patients with coronary artery disease and ventricular tachycardia and in patients with the long QT syndrome and to compare these patients with a group of normal patients. Left Patients and Methods Patient PopulationThe study population consisted of 18 patients. The mean age was 46 years with a range from 17 to 72 years. There were 10 men and eight women.

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.

Plasma immunoreactive atrial natriuretic factor was measured in 10 patients with chronic atrial fibrillation before and after cardioversion to sinus rhythm, and in 14 patients during electrophysiologic evaluation of paroxysmal supraventricular tachycardia. The mean plasma concentration of atrial natriuretic factor in atrial fibrillation was 138 +/- 48 pg/ml and decreased to 116 +/- 45 pg/ml 1 hour after cardioversion to sinus rhythm (p less than 0.005). The mean plasma concentration of atrial natriuretic factor increased from 117 +/- 53 pg/ml in sinus rhythm to 251 +/- 137 pg/ml during laboratory-induced supraventricular tachycardia (p less than 0.005). Right atrial pressures were recorded in 12 patients; the baseline atrial pressure was 4.3 +/- 1.9 mm Hg and increased to 7.4 +/- 3.6 mm Hg during supraventricular tachycardia (p less than 0.005). A modest but significant linear relation was noted between the changes in plasma atrial natriuretic factor and right atrial pressure measurements during induced supraventricular tachycardia (r = 0.60, p less than 0.05). In conclusion, changes in atrial rhythm and pressure may be an important factor modulating the release of atrial natriuretic factor in the circulation and raised levels of this hormone may be a contributing factor for the polyuria and the hypotension associated with paroxysmal supraventricular tachyarrhythmias.