Goldberger A L, Bhargava V, Froelicher V, Covell J, Mortara D
J Electrocardiol. 1980 Oct;13(4):367-71. doi: 10.1016/s0022-0736(80)80089-6.
Studies based on analysis of QRS notching and slurring have suggested an increase in high frequency QRS potentials following myocardial infarction (MI). We investigated the sensitivity and specificity of an indirect, but easily quantitated index of high frequency potentials--the peak-to-peak amplitude of the high frequency signal. A commercially-available micro-processor ECG system was employed with a QRS-averaging program to reduce random noise and an 80-300 Hz filter to selectively record higher frequency potentials. High frequency ECGs were recorded in leads II, III and aVF in 40 normal men and 41 patients with prior inferior MI. Peak-to-peak amplitude of the high frequency signal was less than or equal to 35 micro V in one or more of these leads in 18 of 41 MI patients (44%) compared with only 1 of 40 normals (2.5%) (P < 0.001). In the infarct group, reduced peak amplitude of the high frequency signal was also noted in some leads where the standard ECG did not show pathologic Q waves. This diminution in peak amplitude probably reflects a reduction in high frequency voltage. Therefore, contrary to previous theory, MI may actually cause a decrease in high frequency potentials as part of an overall loss of electromotive force or a slowing of conduction associated with myocardial necrosis. Quantitative high frequency QRS measurements may be of critical value in selected cases.
