Gurbachan S. Sohi

New evidence for inferoposterior myocardial infarction on surface potential maps

Extensive body surface potential recording was performed in 22 patients 2 to 4 weeks after an acute inferoposterior myocardial infarction. Serial isometric projection maps were viewed millisecond by millisecond throughout ventricular excitation, and a second series of maps were examined after removal of the expected range of normal potential distribution. Three major findings outside the normal range appeared: (1) In 6 patients, an early zone of abnormal positivity developed in the left anterior chest at xiphoid level between 15 and 30 msec after onset of the QRS complex; (2) in 13 other patients, a large zone of positivity developed high on the left anterior chest (subclavicular region) between 30 and 60 msec after QRS onset; and (3) in 8 patients the long-lasting rim of negativity about the lower chest was strictly abnormal compared with the expected range. Thus, in 19 of 22 patients the potential map expression was outside the normal range, whereas only eight standard electrocardiograms revealed persistent Q waves with a duration greater than 30 msec. We believe the mid and late activation changes are related to ischemically induced alterations in the temporal sequence of ventricular excitation, not easily appreciated by conventional means of recording but obvious with the departure map technique.

The pathologic correlates of the electrocardiogram: complete left bundle branch block.

To assess whether gross pathologic differences exist between hearts with left bundle branch block (LBBB) and left-axis deviation (LAXD) and those with LBBB and a normal frontal plane axis, we examined 70 hearts with LBBB in a series of 1410 sequential dissections (5%). Thirty-two hearts had LAXD and 34 had normal axes on the correlative ECG. Left ventricular enlargement occurred frequently (93%). No significant differences were found in age distribution, left ventricular weight, coronary anatomy or infarct location. Quantitative analysis revealed larger inferoposterolateral and apical infarcts in hearts with LBBB and LAXD (p < 0.01). The accuracy of various electrocardiographic signs of left ventricular enlargement and myocardial infarction in the presence of LBBB was assessed. Voltage criteria and QRS duration poorly define anatomic chamber enlargement. Anterior infarction is suggested by a q or pathologic Q wave in lead I, a q wave in leads I, V5 and V6 or notched S waves in V3 or V,. Pathologic Q waves or ST shifts in the inferior leads have high diagnostic specificity but low sensitivity for inferior infarction.

Comparison of total body surface map depolarization patterns of left bundle branch block and normal axis with left bundle branch block and left-axis deviation.

Total body surface maps from 15 subjects with left bundle branch block and normal axis (LBBB-NA) and 10 subjects with left bundle branch block and left axis (LBBB-LA) were analyzed and compared with maps from normal subjects. In 19 of the 25 subjects with LBBB, the timing of early upper sternal positivity was similar to that of normal subjects, indicative of timely but oppositely directed septal activation.The right ventricular breakthrough was normally located in all, but was earlier after the onset of QRS than expected in some. The initial portion of the positivity produced by left ventricular activation was located in the upper anterior chest in both LBBB-NA and LBBB-LA, but its onset was generally delayed compared with that in normal subjects, presumably because of the time taken by the right-to-left septal activation. Also, the total duration of this positivity was longer than in normal subjects and extended considerably beyond 90 msec, indicating prolonged activation of the anterior free wall of the left ventricle. In LBBB-NA, this upper anterior positivity remained anterior throughout depolarization, but in LBBB-LA it moved toward the left shoulder and the left upper back, presumably due to the posterior orientation of the terminal portion of depolarization. This terminal orientation in patients with LBBB-LA was thought to be due to the additional delay in the activation of the anterobasal portion of the left ventricle caused by selective involvement of the left anterior fascicle.

Analysis of PR subintervals in normal subjects and early studies in patients with abnormalities of the conduction system using surface his bundle recordings

Utilizing several different approaches to noise reduction, satisfactory beat by beat His bundle activity was recorded from the chest surface in 41 (80%) of 52 normal subjects. Surface atrial to His intervals (PAH) and His to ventricular intervals (HV) were measured in this group and compared with subintervals of the PR segment recorded endocardially from 47 persons with normal electrophysiologic findings. A recent modification in the selection algorithm allows on-line identification of the four of five possible recording sites for utilization in a spatial summation. The ability to record in less favorable circumstances has been improved to the extent that records of suitable clarity for measurement were also obtained in 17 (77%) of 22 individuals with conduction system abnormalities. Comparison of the surface and endocardially acquired data in the normal group reveals no statistically significant difference in the surface acquired PAH and endocardially acquired high right atrial to His (HRAH) intervals, nor in the HV intervals. In a small subset of patients data were acquired by both techniques and no significant differences were found. Thus, when programmed stimulation or endocardial mapping is not required to answer specific clinical questions, in the majority of persons it is possible to record meaningful subintervals from the body surface from each cardiac cycle. Additionally, in instances in which surface P wave activity is obscure in the routine electrocardiogram, this technique enhances atrial electrical activity.

Body surface map patterns of altered depolarization and repolarization in right bundle branch block.

Surface maps from 14 patients with right bundle branch block were analyzed throughout depolarization and repolarization. The abnormalities in depolarization found in all the subjects were 1) epicardial breakthrough that was delayed and shifted to the left, and 2) development of right upper anterior positivity during the midportion of depolarization. In eight patients, this positivity manifested as multiple peaks, suggesting a fragmented spread of depolarization. We believe these findings result not only from the delayed engagement of the right ventricle by the conduction process, but also from its nonuniform and dyssynchronous spread.The recovery phase displayed five abnormal patterns: 1) simultaneous negativity on the right and positivity on the left of the midline in six patients; 2) only negativity on the right of the midline in four; 3) only positive potentials in the left upper chest in two; 4) only negative potentials on the left side of the midline in one; and 5) negative potentials spread diffusely over the precordium in one. The different degrees of this altered repolarization, we believe, depend upon the degrees of altered sequence of activation of the heart in addition to the changes produced by the underlying disease process.

Cibenzoline for high-frequency ventricular arrhythmias: a short-term comparison with quinidine and a long-term follow-up.

Cibenzoline, a new class I antiarrhythmic drug, was compared with quinidine in an open crossover study of 20 patients with frequent (> 30/hr) premature ventricular depolarizations (PVDs). Eight patients treated with cibenzoline experienced more than 75% reduction in PVD frequency. Cibenzoline completely suppressed ventricular couplets in eight of 17 patients and inhibited ventricular tachycardia (VT) in four of 13 patients. Only four patients (20%) responded to quinidine with a similar reduction in PVDs. Quinidine completely suppressed ventricular couplets in eight of 17 patients and episodes of VT in six of 13 patients. Cibenzoline prolonged PR, QRS, and QTc intervals. Eight patients who had shown more than a 75% reduction of PVDs were treated with cibenzoline for an extended period. At the end of three months, only five of eight patients continued to have 75% or greater reduction of PVDs. At the end of six and 12 months, four of five patients continued to have 75% or greater reduction of PVDs. Cibenzoline was similarly effective in suppressing complex arrhythmias. Thus, cibenzoline was only slightly superior to quinidine in suppressing ventricular arrhythmias. With long‐term use of cibenzoline, significant PVD suppression was noted at the end of three months but not afterward.

Effects of left anterior fascicular block on the depolarization process as depicted by total body surface mapping

To examine the effects of left anterio fascicular block (LAFB) on the depolarization process as manifested on the body surface, 142 lead maps were recorded in 25 subjects with LAFB. Three abnormalities were detected: (1) In the early and mid portion of QRS, twenty of 25 subjects showed abnormal anterior superior positivity, starting in the precordial area and proceeding toward the left subclavicular area. The explanation was thought to be the relatively delayed, dysynchronous, and superiorly directed altered sequence of depolarization of the anterior left ventricle. (2) All the subjects showed left lower abnormal negativity. This was thought to represent the unopposed receding activation front after the left ventricular breakthrough posteroinferiorly and also the negative aspect of the abnormally directed superior positivity. (3) Eleven subjects showed abnormal negative potentials at the right lower chest. This was thought to represent the partially unopposed activation fronts of the right ventricular free wall seen after right ventricular epicardial breakthrough, because of the absence of the usually cancelling normal forces from the anterior portion of the left ventricle. Additionally, the surface manifestation of the septal depolarization was found to be indistinguishable from nornal. This study further enhances our understanding of the altered sequence of depolarization in LAFB, as manifested on the body surface instant-by-instant.

The determination of the human ventricular gradient from body surface potential map data

We have analyzed the Wilson ventricular gradient in terms of body surface potential maps and of the reduction of such surface patterns to equivalent dipoles or vectors. While the ventricular gradient traditionally was treated as first a scalar, then a vector concept, we found that the three entities (QRS area, T area, QRST area) did not reduce to vectors with a common location. However, conventional vector addition (QRST area = QRS area + T area) did precisely apply. Further we found considerable more-than-vector or extra-dipolar information remaining for all three entities after removal of the dipole effect. This suggests that maps of these entities should be considered the boundaries of complex electrical fields rather than simple surface effects of vectors.

Total Occlusion of the Left Main Coronary Artery

An extremely rare case with total occlusion of the left main coronary artery is described. The role of collaterals from the right coronary artery in the maintenance of adequate left ventricular function and in the patients survival is discussed. The need for emergency aortocoronary bypass surgery, once the lesion is discovered, is stressed. An excellent clinical result of aortocoronary bypass surgery in a patient followed for more than 2 years with a usually fatal condition is shown.