Beat-to-beat detection of ventricular late potentials with high-resolution electrocardiography

To detect dynamic changes of VLPs we developed a low-noise, HR-ECG with a gain of 105–106×. This system allows the beat-to-beat detection of low-amplitude signals at the bedside in a nonshielded room without any averaging process. Analysis was performed in 39 normal subjects (group A: 27 men, 12 women, mean age, 28 ± 8 years), in 98 patients with coronary artery disease without documented sustained ventricular tachycardia (group B: 86 men, 12 women, mean age, 59 ± 10 years) and in 41 patients coronary artery disease with sustained monomorphic ventricular tachycardia (group C: 36 men, 5 women; mean age 63 ± 9 years). Comparison was made with time-domain signal-averaging (SA-ECG) in all cases at the same electrode position and with identical band-pass filtering. In group A no VLPs were detected; the total filtered QRS duration was 84 ± 8 msec (mean ± SD), and the time interval during which the terminal QRS did not exceed 40 μV (I-40) was < 30 msec in all cases (mean, 17 ± 6 msec). In group B, VLPs were detected by HR-ECG in 34 of 98 patients (35%); the total QRS duration was 102 ± 16 msec (mean ± SD, p < 0.01 vs group A), and the I-40 was 29 ± 13 msec (mean ± SD, p < 0.01 vs (group A). In group C, VLPs were detected by HR-ECG in 38 of 41 patients (93%); the total QRS duration was 123 ± 22 msec (mean ± SD, p < 0.01 vs group A and group B), and the I-40 was 40 ± 14 msec (mean ± SD, p < 0.01 vs group A and group B). Concordant results between HR-ECG and SA-ECG were observed in 91% of the cases (59 positive and 103 negative results). Late potentials that exhibited dynamic variations were detected by HR-ECG alone in 13 cases, and very low amplitude VLPs were detected by SA-ECG alone in three cases. In conclusion, the present study demonstrates the feasibility of body-surface recording of VLPs on a beat-to-beat basic, without any averaging process, at the bedside in a nonshielded room. This new approach may allow the study of dynamic changes of VLPs during spontaneous ventricular arrhythmias or ischemia.