Underestimation of duration of ventricular activation by 12-lead ECG compared with direct measurement of activation duration derived from implanted pacemaker leads.

AIM: To determine extent to which 12-lead ECG QRS duration (QRSd) reflects ventricular activation duration compared with time relations from unpaced ventricular myograms in cardiac resynchronisation therapy (CRT) patients.

METHODS: Left (LV) and right ventricular (RV) myograms were recorded during spontaneous rhythm from in-situ pacemaker leads in 77 patients receiving CRT; 14 'normal activation' (unpaced QRSd <12 ms), 10 'simple left bundle branch block' (LBBB, QRSd 120-149 ms), 40 'advanced LBBB' (QRS ≥ 150 ms) and 13 right bundle branch block. Delay in onset (Q-LV, Q-RV) and duration (dur-LV, dur-RV) of activation were measured. Interventricular delay (ΔT: Q-LV minus Q-RV) and 'LV-overrun' (time between end 12-lead QRS and Q-end LV myogram) were calculated.

RESULTS: 'Normal activation': Neither Q-LV, Q-RV (38 ± 6 ms, 39 ± 11 ms), nor dur-LV, dur-RV (66 ± 9 ms, 81 ± 25 ms) differed. ΔT (-1 ± 11 ms) was not different from zero, nor was Q-end LV (104 ± 10 ms) different from QRSd (p=0.09). 'Simple LBBB': Q-LV (102 ± 28 ms) was longer than 'normal activation' (p<0.001), but Q-RV, dur-LV, and dur-RV were no different. ΔT (54 ± 23 ms) was increased (p<0.001) and Q-end LV (187 ± 48 ms) was longer than QRSd (p=0.005). 'Advanced LBBB': Q-LV (115 ± 52 ms) was longer than 'normal activation' (p<0.001) but Q-RV was no different, so ΔT (72 ± 47 ms) was increased (p<0.001 compared to normal, p=0.04 compared to simple LBBB). Dur-LV (102 ± 27 ms) was also prolonged, so Q-end LV (218 ± 48 ms) was longer than QRSd (p<0.001). Longer LV-overrun was associated with longer ΔT (p<0.001).

CONCLUSIONS: Prolonged LV myopotential duration, associated with interventricular delay, is electrically silent on 12-lead QRSd. Unpaced surface QRSd underestimates true duration of native LV activation in CRT patients.