Dual-Site Left Ventricular Pacing Improved Quality of Life in a Patient with End-Stage CHF and Incessant VT

L. Bing Liem, DO, FACC, James D. Joye, DO, FACC, Benjamin Potkin, MD, FACC
El Camino Hospital
Mountain View, California

L. Bing Liem, DO, FACC, James D. Joye, DO, FACC, Benjamin Potkin, MD, FACC
El Camino Hospital
Mountain View, California

In this article, Dr. Liem and colleagues provide a case study on dual-site LV pacing.This patient was an example of a non-responder to the traditional CRT method who became a partial responder and benefitted from freedom of ICD shocks.

Case Report

A 67-year-old male was referred to El Camino Hospital for further management of his progressive ischemic cardiomyopathy and frequent ventricular tachycardia (VT), which resulted in multiple, nearly daily shocks from his implanted cardiac resynchronization therapy defibrillator (CRT-D). He had extensive coronary artery disease with multiple remote myocardial infarctions and non-revascularizable coronary anatomy, as well as peripheral vascular disease, underlying severe obesity, diabetes mellitus, hypertension, dyslipidemia, hypothyroidism, and chronic obstructive pulmonary disease (COPD). He has become progressively disabled by his status of congestive heart failure (CHF), going from a NYHA functional class III to IV despite CRT-D upgrade from a standard implantable cardioverter defibrillator (ICD) a year prior. He had been declined for cardiac orthotropic transplantation and destination left ventricular assist device due to his numerous and advanced co-morbidities. Both the patient and his wife were well aware that his prognosis was quite poor, with an expected longevity of less than six months. Their predominant concern was the numerous ICD shocks he received over the previous weeks.

His echocardiogram at the time of his transfer to El Camino Hospital showed four-chamber enlargement with a markedly enlarged left ventricle with left ventricular (LV) internal diastolic and systolic diameters of 8.39 cm and 7.86 cm, respectively, and LV ejection fraction (EF) estimated at 13%. His medical therapy for CHF had been optimized, which included an angiotensin-receptor inhibitor, double diuretics, digoxin and outpatient intravenous milrinone. Beta blockers could not be provided due to his severe COPD. For his VT, he had been on high-dose amiodarone of 400 mg twice daily.

The patient was taken to the cardiac electrophysiology laboratory for catheter ablation of his VT. Numerous VT morphology was inducible as well as occurred spontaneously, although a predominant morphology (right bundle branch block with right axis at 150 bpm) was identified. An early site was identified at the lateral wall, and numerous ablations were applied at sites with fractionated electrogram and mid-diastolic potential (Figure 1). Nonetheless, at the end of the procedure, VT remained inducible; furthermore, he had more clinical recurrences the ensuing day.

We then postulated that, given his markedly enlarged LV size and the apparent inefficacy of standard CRT, he might benefit from dual-site LV pacing. Therefore, we proceeded with further upgrading of his CRT-D system. His pre-existing LV lead was already in a traditionally desirable location: at a basal portion of the posterior vein (Figure 2). A repeat coronary sinus venography showed that as the only traditionally desirable tributary. There was only a rudimentary lateral vein, and the typically small anterior and anterolateral veins (Figure 2). The pre-existing LV lead was removed, and two new LV leads were inserted into a deep posterior vein position and in the anterior vein, respectively. Deep positioning was achieved by utilizing the distally-tapered LV lead (QuickFlex, St. Jude Medical, St. Paul, MN). The final positions are shown in Figures 3 and 4 (30-degree right anterior oblique [RAO] and left anterior oblique [LAO] views, respectively). Two LV-lead delivery sheaths were put in place in this case as to allow for maneuvering of both LV leads to the desired positions.

The patient reported improved symptoms afterward. He had less dyspnea on exertion, his NYHA functional class improved to class III, and most importantly to him, he no longer had VT recurrence. A repeat echocardiogram performed two days after the implementation of dual-site LV pacing showed an improved LV internal diastolic and systolic diameter to 7.8 cm and 6.8 cm, respectively, and an improved LVEF of 26%. He maintained these subjective and objective parameters for one year until he developed combined cardiopulmonary failure.


Prior studies have shown the additional benefit of dual-site LV pacing in patients with progressive mechanical and electrical remodeling,1-3 and this method was applied to patients who remained refractory to the standard CRT pacing using single-site LV pacing. For dual-site LV pacing, previous studies deliberately placed the two LV pacing sites as far as possible from one another.2 In the two studies comparing dual- versus single-site LV pacing, a significant improvement in rate of responder2 or hemodynamic parameters3 was noted and hence, this modality was postulated as a potential alternative to patients who are non-responders to the traditional CRT (single-site LV pacing). We elected to offer our patient this modality because of the failure to respond to the standard CRT clinically, continuous mechanical and electrical remodeling (the latter was evidenced by progression into incessant VT), and the apparent paucity of area LV stimulation site using traditional single-site pacing, mainly due to his marked LV dilatation.

The management of patients with incessant VT should at least include an attempt at catheter ablation of the “culprit” VT; we performed a comprehensive VT ablation using three-dimensional mapping with the Array catheter (St. Jude Medical) and were able to identify the critical ablation site for the culprit VT, but still failed to suppress the VT clinically. In patients with advanced CHF, electrical remodeling is associated with increasing VT episodes resulting in frequent ICD shocks, which in turn, can further cause deterioration of LV function (“the-chicken-and-the-egg” phenomenon). Our patient might have been an example of such, and hence, we seriously considered any attempt at improving his CHF status.

Placing an additional LV lead was not associated with a significant difficulty or complexity in this case. With current availability of many types of LV leads, positioning into sites which provide “comprehensive” distribution of pacing can be easily achieved.

Although the improved electrical remodeling, as evidenced by greater freedom from VT episodes, might have been the result of delayed ablation efficacy from maturation of ablation scar formation, the improved LV parameters (diastolic and systolic dimensions and EF) were quite convincing after the implementation of dual-site LV pacing. With this anecdotal experience, and with the emerging data showing the salutary effects of dual-site LV pacing, we believe that this modality should be more broadly implemented, especially in those patients who are non-responders to traditional CRT pacing with single-site pacing.

Our patient was an example of a non-responder to the traditional CRT method who became a partial responder and benefitted from freedom from ICD shocks for the last 12 months of his life.


  1. Pappone C, Rosanio S, Oreto G, et al. Cardiac pacing in heart failure patients with left bundle branch block: Impact of pacing site for optimizing left ventricular resynchronization. Ital Heart J 2000;1:464-469.
  2. Leclercq C, Gadler F, Kranig W, et al. A randomized comparison of triple-site versus dual-site ventricular stimulation in patients with congestive heart failure. J Am Coll Cardiol 2008;51:1455-462.
  3. Niazi I, Kiemen JO, Yong P, et al. Hemodynamic superiority of dual-site left ventricular stimulation over conventional biventricular stimulation in heart failure patients. The Journal of Innovations in Cardiac Rhythm Management 2011;2:412-418.