PACING/ICD/CRT
Impact of left ventricular epicardial and biventricular pacing on ventricular repolarization in normal-heart individuals and patients with congestive heart failure
1 Department of Internal Medicine/Cardiology, Tong-Ji Hospital, Tong-Ji Medical College, Huazhong University of Science and Technology, Wuhan 430030, People's Republic of China; 2 Department of Cardiology, National Heart Centre, Singapore 168752, Singapore
Aims Malignant ventricular arrhythmias can arise in a subset of congestive heart failure (CHF) patients after they undergo cardiac resynchronization therapy (CRT), thus counteracting the haemodynamic benefits typically associated with biventricular pacing. This study seeks to assess whether alteration of the ventricular transmural repolarization and conduction due to reversal of the depolarization sequence during epicardial or biventricular pacing facilitate the development of ventricular arrhythmias.
Methods and results ECGs and monophasic action potential (MAP) were recorded during programmed stimulation from right ventricle (RV) endocardium (RV-Endo), left ventricle (LV) epicardium (LV-Epi), or both (biventricular, Bi-V) in 15 individuals without structural heart diseases. In patients with severe CHF and CRT (n=21), ECGs were collected during RV-Endo, LV-Epi, and Bi-V pacing. MAP duration on intracardiac electrogram, the QT, JT, and Tpeak–Tend intervals on ECGs at different pacing sites were measured and compared. In subjects with or without structural heart disease, compared with RV-Endo pacing, LV-Epi and Bi-V pacing resulted in a longer JT (341.78±61.97 ms with LV-Epi, 325.86±59.69 ms with Bi-V vs. 286.14±38.68 ms with RV-Endo in CHF individuals, P<0.0001) or Tpeak–Tend interval (121.55±19.88 ms with LV-Epi, 117.71±42.63 ms with Bi-V vs. 102.28±12.62 ms with RV-Endo in normal-heart subjects, P<0.0001; 199.70±62.44 ms with LV-Epi, 184.89±74.08 ms with Bi-V vs. 146.41±31.06 ms with RV-Endo in CHF patients, P<0.0001), in addition to prolonged myocardial repolarization time and delayed endocardial activation. During follow-up, sudden death and arrhythmia storm occurred in two CHF patients after CRT.
Conclusion Epicardial and biventricular pacing prolong the time and increase the dispersion of myocardial repolarization and delay the transmural conduction. All of these should be considered as potential arrhythmogenic factors in CHF patients who receive CRT.
Key Words: Cardiac resynchronization therapy, Congestive heart failure, Epicardial pacing, Monophasic action potential, Tpeak–Tend interval, Transmural dispersion of repolarization
* Corresponding author. Tel/fax: +86 27 83632827. E-mail address: bairong74{at}yahoo.com.cn