Background: The changes in ventricular repolarization after cardiac resynchronization therapy (CRT) are poorly understood. Objective: Address this knowledge gap using a multimodality approach including electrocardiographic and echocardiographic measurements in patients and using patient-specific computational modeling. Methods: In 33 patients electrocardiographic and echocardiographic measurements were performed before and at various intervals after CRT, both during CRT-ON and temporary CRT-OFF. T-wave area was calculated from vectorcardiograms, reconstructed from the 12-lead ECG. Computer simulations were performed using a patient-specific eikonal model of cardiac activation with spatially varying action potential duration (APD) and repolarization rate, fit to a patient’s ECG. Results: During CRT-ON T-wave area diminished within a day and remained stable thereafter, whereas QT-interval did not change significantly. During CRT-OFF T-wave area doubled within 5 days of CRT, while QT-interval and peak-to-end T-wave interval hardly changed. Left ventricular (LV) ejection fraction did not significantly increase before 1 month of CRT. Computer simulations indicated that the increase in T-wave area during CRT-OFF can be explained by changes in APD following chronic CRT that are opposite to the change in CRT-induced activation time. These APD changes were associated with a reduction in LV dispersion in repolarization during chronic CRT. Conclusions: T-wave area during CRT-OFF is a sensitive marker for adaptations in ventricular repolarization during chronic CRT that may include a reduction in LV dispersion of repolarization.

Background: Right ventricular (RV) pacing causes delayed activation of remote ventricular segments. We used the UHF-ECG to describe ventricular depolarization when pacing different RV locations. Methods: In 51 consecutive patients, temporary pacing was performed at the RV apex, anterior and lateral wall, and at the RV septum with (cSp) and without direct conductive tissue engagement (mSp) (further subclassified as RVIT and RVOT for septal inflow and outflow positions). The timing of UHF-ECG electrical activations were quantified as: left ventricular lateral wall delay (LVLWd; V8 activation delay), RV lateral wall delay (RVLWd; V1 activation delay), and LV lateral wall depolarization duration (V5-8d). Results: The LVLWd was shortest for cSp (11 ms (95% CI; 5;17), followed by the RVIT (19 ms (11;26) and the RVOT (33 ms (27;40), (p<0.01 between all of them), although the QRSd for the latter two were the same (153 ms (148;158) vs. 153 ms (148; 158); p=0.99). The RVOT caused longer V5-8d (9 ms (3;14) compared to the RVIT (1 ms (−5;8), p<0.05. RV apical capture not only had a worse LVLWd (34 ms (26;43) compared to mSp (27 ms (20;34), p<0.05), but its RVLWd (17 ms (9;25) was also the longest compared to other RV pacing sites (mean values for cSp, mSp, anterior and lateral wall captures being below 6 ms), p<0.001 compared to each of them. Conclusions: UHF-ECG ventricular dyssynchrony parameters show that cSp offers the best ventricular synchrony followed by RVIT pacing, which should be preferred over RVOT and other RV myocardial pacing locations.