Search

Vectorcardiograms (VCGs) of 44 patients with a Wolff-Parkinson-White (WPW) syndrome have been analyzed with the aim to correlate the QRS loop patterns with specific preexcitation sites. The VCG QRS loops were analyzed to determine whether conduction abnormalities and myocardial infarction (MI)-like patterns observed in the WPW syndrome could be related to specific preexcitation sites identified by surgery as well as by body surface potential mapping (BSPM). Left bundle branch block pattern was observed with anteroseptal (AS) preexcitation, anterior MI pattern was seen with lateral right ventricle (LRV) preexcitation, left anterior fascicular block was observed with posterior right ventricle (PRV) preexcitation, inferoposterior and strictly posterior MI pattern was found with posteroseptal (PS) and posterior left ventricle (PLV) preexcitation, right bundle branch block was seen in lateral left ventricle (LLV) preexcitation, and right bundle branch block was observed with left posterior fascicular block in anterior left ventricle (ALV) preexcitation. These VCG criteria seem to identify accurately the preexcitation sites as observed by delta wave BSPM and at surgery investigations. Consequently, they could be useful in localizing the preexcitation site in cases of ambiguous delta vector orientation.

Isoarea maps during the PQRST sequence were computed in 22 healthy subjects and 48 patients with Wolff-Parkinson-White (WPW) syndrome. Thirty-eight patients with WPW were on no medication and 10 were treated with class I, II, or III antiarrhythmic drugs. Seventeen isoarea maps were recorded before and 17 were recorded after accessory pathway ablation. One patient had intermittent preexcitation. Body surface maps from all healthy subjects were similar, although the magnitudes of the maxima and minima showed significant variability. In all patients with WPW who were on no medication and in those on class I and II agents, PQRST maps were normal. Two patients taking amiodarone had abnormal PQRST maps, as did patients early after surgery. In the patient with intermittent preexcitation, PQRST maps were very similar during normal and preexcited beats. In conclusion, our results support the theory that the PQRST time integral reflects intrinsic recovery properties of the heart and is independent of the activation sequence.

In 35 subjects with typical or atypical angina and/or documented myocardial infarction (MI), body surface potential maps (BSPMs), ECG, VCG and rest Thallium-201 (T1-201) have been compared to left ventriculography (LVG). BSPMs were recorded with 26 ECGs, and BSPM abnormalities for MI cases were considered to be areas of normally positive potentials that have become negative. Subjects with MI were classified according to the segmental localization and degree of asynergy on LVG. Moderate anterolateral and apical asynergy were found to correlate with BSPM diagnosis of anterolateral MI and ischemia, severe anterolateral and apical asynergy with BSPM diagnosis of anterolateral MI and ischemia, and moderate diaphragmatic and/or posterobasal asynergy with BSPM diagnosis of posterior MI. Simultaneous anterior and posterior asynergy were found for BSPM diagnosis of anterior with posterior MI. Subjects with no LVG asynergy had normal BSPMs. BSPM diagnosis had the highest correlation coefficient with the LVG diagnosis (r = 0.88). ECG and VCG showed similar results with r = 0.65 and 0.71 respectively, while T1-201 had r = 0.55. The examination of our BSPMs, as well as the ECG, VCG and T1-201, did not permit to detect apical damage in presence of anterior MI, and posterobasal damage in the presence of inferoposterior MI. It is concluded that BSPMs are slightly superior to ECG and VCG for diagnosis of MI.

The accuracy of different computation techniques for the non-invasive localization of cardiac ectopic activity was evaluated. Body surface potentials were recorded from 63 leads in 14 patients with implanted pacemakers. The location, orientation and magnitude of a single moving dipole (SMD) were computed from the first eight terms of a truncated multipole expansion estimated from the body surface potentials. The SMD trajectories obtained during the QRS complex were plotted along with the heart outlines and pacing leads obtained independently from chest x-rays. The origin of the SMD trajectories was compared to the position of the pacing lead to evaluate the accuracy of the SMD. The optimum computation technique used a least-squares (LS) estimation of the multipole expansion truncated at 15 multipoles, in conjunction with a torso model that included regions of lower conductivity representing the lungs. With this method, the SMD trajectories originated near the pacing lead (25 +/- 12 mm) and adequately represented the progression of the ectopic wavefront across the entire heart silhouette. With the LS techniques using 8 or 24 multipoles, the spans of the trajectories were respectively too short, or too long to cover the heart, and the average distance between the SMD at QRS onset and the pacing lead was larger. With a surface integration technique, the SMD-pacing lead distances were similar, both for a finite homogeneous torso model with a fixed geometry, as well as for torso models adapted to the torso geometry of each patient. The SMD was found adequate to represent the progression of an ectopic wavefront, and to localize its origin in man.