Magnetocardiography and 32-lead potential mapping: repolarization in normal subjects during pharmacologically induced stress.
Signals from 37 magnetocardiographic sensors and simultaneously recorded 32 ECG leads were obtained in three healthy male subjects (including two reinvestigations). After recordings at rest, the heart rate was increased by pharmacologic stress (117 to 142 beats/min). Comparison of the repolarization of rest and stress showed substantial changes in the magnetocardiogram (MCG) up to T wave inversions during stress. In the ECG only junctional ST-T segment shifts were present. For quantification, correlation coefficients between pairs of rest and stress MCG and rest and stress ECG distributions were calculated for the same time instant at the beginning of T wave under rest and stress conditions. In addition, equivalent electrical current dipole moment and magnetic dipole moment vectors were calculated from the MCG, and their change from rest to stress evaluated. Correlation coefficients for MCG comparison ranged from 0.3 to 0.5; ECG comparison suggested much less change from stress, ranging from 0.7 to 1.0. Current dipole moment changes at T wave onset were marginal; in contrast, the magnetic dipole moment changed substantially. Since the magnetic dipole reflects vortex currents, changes in its intensity and/or orientation during repolarization suggest this as the biophysical basis of the striking difference in the response of the MCG and ECG to pharmacologic stress. Normal ECG findings at rest and under stress in healthy subjects support the conclusion that the repolarization changes in the MCG were of nonpathologic origin.
Brockmeier
K
K
Department of Pediatric Cardiology, Virchow Medical Center, Humboldt Universität Berlin, Germany.
Schmitz
L
L
Bobadilla Chavez
J D
JD
Burghoff
M
M
Koch
H
H
Zimmermann
R
R
Trahms
L
L
D000328:Adult; D018780:Body Surface Potential Mapping / Q000379:methods*; D004562:Electrocardiography / Q000379:methods*; D006801:Humans; D008280:Magnetics; D008297:Male; D013312:Stress, Physiological / Q000139:chemically induced / Q000503:physiopathology*