
Slowed Conduction with Antiarrhythmic Drugs Reduces High Frequency Energy of the Signal‐Averaged Electrocardiogram
Author(s) -
Bloomfield Daniel M.,
Freedman Roger A.,
Steinberg Jonathan S.
Publication year - 1998
Publication title -
annals of noninvasive electrocardiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.494
H-Index - 48
eISSN - 1542-474X
pISSN - 1082-720X
DOI - 10.1111/j.1542-474x.1998.tb00346.x
Subject(s) - qrs complex , medicine , cardiology , propafenone , myocardial infarction , signal averaged electrocardiogram , electrocardiography , ventricle , anesthesia , atrial fibrillation
Background: We have previously demonstrated that high frequency QRS energy decreases after experimental myocardial infarction (Ml) and is lower in patients who have had MI compared to controls. The mechanism for this decrease in high frequency QRS energy is unclear. The objective of this study was to evaluate the effect of slowed myocardial conduction on high frequency QRS energy measured on the signal‐averaged SAECG. We hypothesized that slowed conduction in the infarcted ventricle may be responsible for the decrease in high frequency QRS energy. In order to test this hypothesis, we examined antiarrhythmic drug therapy known to slow conduction (propafenone) compared to drug therapy with minimal effects on conduction (sotalol). Methods: In patients with sustained ventricular tachyarrhythmias undergoing serial drug testing, SAECGs were obtained before and after antiarrhythmic therapy. After filtering the leads with a spectral band‐pass (15–40 Hz, 40–80 Hz, and 80–300 Hz) filter, the vector magnitude was con structed, and the energy (in μV sec) was calculated for the entire QRS by integrating the area under the filtered QRS complex. Results: Propafenone significantly prolonged QRS duration (+17%, P > 0.001) and significantly reduced QRS energy (‐16.1% to 21.8%, P > 0.0001) in all three band widths. Sotalol did not have either effect (P = ns). There was a strong correlation between the prolongation of the filtered QRS and the drop in QRS energy for all three band widths (r values ranging from 0.64–0.90, all P > 0.05). When the changes in QRS energy were corrected for QRS duration, the results did not change. Conclusion: The Class IC antiarrhythmic drug propafenone, known to decrease myocardial conduction velocity, significantly reduced QRS energy in all three band widths, whereas the Class III drug sotalol did not. These data are consistent with the hypothesis that decreases in low and high frequency QRS energy after Ml result in part from slowed conduction.