Durrer et al reported that ventricular
Durrer et al.  reported that ventricular depolarization begins in the LV septum, which suggests that initiating pacing from regions close to this area (e.g., RV septum) may produce a physiologic contraction pattern. In contrast, the free wall of the RV is the last zone to be depolarized. Thus, it is important to distinguish septal positioning from other RV sites. Although a number of studies describe RVS pacing [18,19], they do not provide specific details regarding the position of the leads or confirmation of septal site placement. In this study, we clearly demonstrated right ventricular septal pacing anatomically under fluoroscopy. The pacing of this site produces a narrower QRS than the pacing of the right ventricular apex. These findings suggest that right ventricular septal site may be more optimal than the right ventricular apex in patients who need continuous ventricular pacing. Moreover, the difference in QRS interval between the 2 groups became significant at different times after purchase GSK343 in this study.
The negative remodeling effects of RVA-pacing may take years to manifest. Thus, results from acute studies of RVA-pacing cannot be generalized to outcomes in patients undergoing chronic pacing. Xue-Hua Z  reported that RVA pacing with >90% ventricular pacing was associated with HF in 26% of patients over a median follow-up period of 7.8 years. They also reported that an elderly age at the time of implantation predicted new onset of HF. Our study found that 27.2% of RVA-paced patients had HF only 2 years after implantation. The 2 studies differed in the age of patients at the time of implantation. The mean age was 76.0±13 years in our study, while it was 68.2±14.9 years in that of Xue-Hua et al. Therefore, an elderly age may predict HF after implantation.
The use of RVS pacing has been limited by concerns regarding procedural complication and long-term electrical performance, such as R-wave sensing and stimulation threshold. Most studies of RVS pacing have had a relatively small sample size, limited follow-up duration, and include relatively few data concerning the electrical performance and complications associated with these septal pacing sites . Lead dislodgment was the most common adverse event in previous studies of RVS pacing, even when RV apex pacing was employed. In order to further explore these issues, prospective long-term comparative studies should be conducted that include strict definitions of RVS pacing and that exclude patients with atrial fibrillation. The present study is the first study to meet these criteria.
Conflict of interest statement
Introduction Cardiac resynchronization therapy (CRT) has been proven to decrease morbidity and overall mortality in heart failure patients with cardiac dyssynchrony [1–5]. While several randomized studies (COMPANION study, CARE-HF study) have demonstrated that biventricular pacing results in an improvement of interventricular synchronization, systolic function, exercise tolerance, and quality of life [1–4], the effect of this therapy on the incidence of ventricular arrhythmias is less clear. Several studies have suggested that CRT suppresses the incidence of major arrhythmic events (MAEs), citing reduced wall stress (as a result of reverse remodeling) and decreased repolarization dispersion (as a result of dual depolarization wavefronts) as potential mechanisms [6–8]. Other studies, however, have demonstrated a proarrhythmic potential [9–13]. It remains unclear why certain rare patients develop MAEs after CRT therapy. Recent reports [10–12] suggest that left ventricular (LV) epicardial pacing can be proarrhythmic, leading to polymorphic ventricular tachycardia (VT) by reversal of the normal activation sequence, prolongation of the QT interval, and creation of transmural dispersion of repolarization (TDR). LV epicardial pacing reverses the natural activation sequence from endocardium to epicardium. This reduces the repolarization time of the already short epicardial action potentials, thereby increasing repolarization time differences compared with the longer underlying action potentials of the midmyocardial and endocardial layers. Thus, TDR may contribute to ventricular arrhythmias . We hypothesize that the increase of Tpeak–end after CRT may be a good predictor of ventricular tachyarrhythmia if it reflects transmural dispersion in the LV.