Body Surface Mapping System Research Articles

Signal-averaged body surface mapping for the assessment of low-amplitude potentials. Relation between ventricular depolarization and repolarization in normal subjects.

To examine the relation between ventricular depolarization and repolarization, body surface isopotential maps at the end of the QRS complex were studied in 32 normal subjects using a signal-averaged body surface mapping system. The number of beats averaged was 96-154 (mean 126.2). In this study, there were 8 types of isopotential map patterns at the end of the QRS complex. Mean +/- SD of QRS duration, appearance time of repolarization, and disappearance time of depolarization were 82.0 +/- 8.7 msec, 71.8 +/- 10.5 msec, and 79.7 +/- 9.4 msec, respectively. Time duration of overlapping depolarization and repolarization was 8.6 +/- 6.4 msec. The early repolarization was widely distributed on the left anterior chest and the upper sternal region. These results demonstrated the difference between the appearance time of repolarization and the disappearance time of depolarization for each lead. We concluded that it is difficult to evaluate ECG waves in the terminal portion of the QRS complex with the dipolar theory only.

Mechanism of persistent S-T segment elevation after anterior myocardial infarction

Persistent S-T segment elevation after anterior myocardial infarction, reliably predicts the presence of advanced left ventricular asynergy. The genesis of this persistent S-T elevation is unknown, although recent observations suggest that ischemia within or surrounding the infarct zone might be involved. To explore this possibility, a body surface mapping system was utilized to assess the torso distribution of these repolarization potentials, as well as the responsiveness of the S-T segment elevation to three randomized interventions designed to alter the myocardial oxygen supply/demand ratio (40 percent oxygen, sublingual nitroglycerin and isometric exercise). S-T segment amplitude measured 75 msec after the J point (as well as two measurements from time-normalized ST-T segments) was not significantly altered by any intervention in 11 patients, thus indicating that ischemia was an unlikely cause of the persistent S-T elevation. Moreover, plots of the integrated area of the first three eighths of both the QRS complex (Q wave zone) and the ST-T segment (S-T segment) revealed that the initial repolarization maximum (corresponding to the persistent S-T segment elevation) was spatially concordant with the initial depolarization minimum (reflecting precordial Q waves). Because large Q waves usually indicate transmural scar, this surface distribution supports the conclusion that ischemia is not responsible for persistent S-T segment elevation and suggests that the sources for these repolarization potentials are not located in the infarcted area.