Potential pro-arrhythmic effect of cardiac resynchronization therapy
Osama Tayeh1, Waleed Farouk, Abdo Elazab
1Critical Care Department, Faculty of Medicine, Cairo University.
Insights
Cardiac resynchronization therapy (CRT) may prolong corrected QT interval (QTc) and Tpeak-end (Tp-e) intervals, potentially predicting major arrhythmogenic events and premature ventricular contractions (PVCs). Further research is needed to explore these pro-arrhythmic effects.
Area of Science:
- Cardiology
- Electrophysiology
- Medical Devices
Background:
- Cardiac resynchronization therapy (CRT) reduces heart failure mortality but its impact on sudden cardiac death and ventricular arrhythmias is debated.
- Investigating potential pro-arrhythmic effects of CRT using electrocardiogram (ECG) markers is crucial.
Purpose of the Study:
- To evaluate the pro-arrhythmic potential of CRT by analyzing ECG markers.
- To determine if CRT influences the occurrence of major arrhythmogenic events (MAE) and premature ventricular contractions (PVCs).
Main Methods:
- Seventy-five patients undergoing CRT were studied.
- Surface ECGs were used to measure corrected QT interval (QTc), Tpeak-end (Tp-e) interval, QT dispersion (QTd), and Tpeak-end dispersion before and after pacing.
- Arrhythmias were monitored via ECG, Holter, and pacemaker event recorders.
Main Results:
- CRT significantly prolonged the QTc interval post-procedure (P=0.0001).
- Patients experiencing MAE and increased PVCs showed significantly prolonged QTc (P=0.043) and Tp-e intervals (P=0.049) compared to those without arrhythmias.
- QTd and Tp-e dispersion did not significantly differ between groups.
Conclusions:
- Prolonged QTc and Tp-e intervals after CRT may predict the occurrence of MAE and PVCs.
- QTd and Tp-e dispersion are not reliable predictors of arrhythmia post-CRT.
Unlabelled:
A decline in mortality due to pump failure has been clearly documented after cardiac resynchronization therapy (CRT), however the impact on sudden cardiac death and the development of malignant ventricular arrhythmias remains questionable. Our study aims to investigate this alleged pro-arrhythmic effect of CRT using surface electrocardiogram (ECG) markers of pro-arrhythmia.
Methods:
Seventy five patients, who received CRT were included in this study. Manual measurement of corrected QT interval (QTc), Tpeak-end (Tp-e) interval, QT dispersion (QTd) and Tpeak-end dispersion during baseline 12 lead surface ECG and after applying atrial-biventricular pacing were done. Arrhythmias post CRT was recorded from ECG, 24 h holter monitoring or pacemaker programmer event recorder.
Results:
QTc interval showed significant prolongation after CRT (498.9 ± 50.8 vs. 476.2 ± 41.6 msec, P = 0.0001). Comparing patients with major arrhythmogenic events (MAE) and increased frequency of premature ventricular contractions (PVCs) post CRT pacing to those patients without arrhythmias, there was a significant prolongation of the QTc interval (527 ± 63.29 vs. 496.95 ± 45.2 msec, P = 0.043) and Tp-e interval (94.16 ± 9 vs. 87.41 ± 16.37 msec, P = 0.049). While in the arrhythmogenic group, there was an insignificant decrease in QTd and Tpeak-end dispersion.
Conclusion:
QTc and Tp-e intervals are a potential predictor of occurrence of MAE and PVCs. On the other hand, Tp-e dispersion and QTd did not show a predictive potential for arrhythmia.
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