> 40% Ventricular Paced – is there anything we can do?

It has been widely publicised and accepted that unnecessary Right Ventricular (RV) pacing in patients may adversely affect heart failure morbidity and total mortality. Reducing Right Ventricular pacing as much as possible without compromising haemodynamics is therefore a must. However, not only must RV pacing be reduced, but it must be reduced to below the significant number of 40%, we must also continue until we achieve levels of less than 10% as each 10% reduction equates to a 54 fold decrease in heart failure morbidity. 1

Even with expert device optimisation and the utilisation of advanced hysteresis algorithms most implantable pacemakers and cardioverter defibrillators have available, it is not always possible to reduce RV pacing as much as we require. This can be due to a number of factors including:

• Patients with Complete Heart Block (CHB).

• Progression of AV node disease.

• Development of abnormal ventricular activation

• Advancement to Bi-nodal disease after pacing for SA node disease

• Episodes of Atrial Fibrillation with slow ventricular response

According to the Danish Pacemaker Registry report2, which shows pacing statistics over a 25 year period, Dual chamber pacemaker implantation for patients suffering from CHB was performed for approx. 30% of the observed population, this is a significant quantity of patients that will need permanent RV pacing.

Anderson et al3 described how over an 8 year follow up period, that the incidence of developing CHB in patients receiving pacing therapy for SA node disease = 3.6%, which equated to an annual incidence of 0.6%, again a significant number.

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So what is the answer, how do we treat this conceivably sizeable patient group effectively?

Bailey WM et al4 investigated the concept of Closed Loop Stimulation (CLS). They concluded that pacing using this method improves ejection fraction and NYHA class in patients with congestive heart failure (CHF) and/or ejection fraction <40%. Patients indicated for pacing underwent implant of a CLS device were assessed for NYHA and EF at implant and follow-up. They found the following results:

Of the CLS implants, 13 of 59 had CHF and/or EF < 40%. Average follow-up was 18.5 months. All 7 patients who were NYHA II at implant had an improvement in EF. Of the 6 NYHA III patients at implant, 4 had an improvement in EF, 2 had a reduction in EF. Of the two patients that had a reduction one experienced a 4% reduction and one a 2% reduction in EF. Of the 7 NYHA II patients at implant 6 improved to Class I, 1 remained Class II. Of the 6 patients who were NYHA III at implant 5 improved to Class II, 1 remained Class III. NYHA at implant was 2.5 + 0.52 vs 1.6 + 0.65 at follow-up (p=.001). EF at implant was 34.4% + 4.9% vs 44.6% + 12.8% at follow-up (p=.004).

Conclusion:

CLS pacing improved NYHA and EF in patients indicated for pacing with CHF and/or EF < 40%.

If Bailey et al reached this conclusion for CHF and/or low EF patients, is it conceivable that this could be the case for any patient receiving CLS pacing therapy?

Puglisi et al5 in 2003 studied: Impact of Closed-Loop Stimulation, overdrive pacing, DDDR pacing mode on atrial tachyarrhythmia burden in Brady-Tachy Syndrome (Burden trail).

149 Brady-Tachy Syndrome patients received DDD pacing therapy (72 male, mean age 74±9), who received a dual chamber pacemaker (Philos DR or Inos 2+CLS, Biotronik GmbH, Berlin, Germany) programmed in DDD at 70 min?1. At 1-month follow-up, DDDR, DDD+ or CLS algorithms were activated according to randomization. Follow-up visits for data collection were performed at 4 and 7 months. Non parametric statistical tests (Kruskal–Wallis H-test, Dunn test, Spearman coefficient) were used to analyse not-normally-distributed samples. At 7 months, AT burden was significantly lower in CLS group (20.3±63.1 min/day, P<0.01) compared to DDDR (56.0±184.0 min/ day) and DDD+ group (63.1±113.8 min/day). APP was higher in CLS (89.0±13.2%) and in DDD+ group (97.9±2.7%) than in DDDR group (71.1±26.7%, P<0.001). The correlation found between AT burden and APP was very weak: at 7-month follow-up the Spearman coefficient was ?0.29 (P=NS) in CLS, ?0.52 (P<0.01) in DDD+, ?0.22 (P=NS) in DDDR.4

Conclusions:

CLS pacing was associated with a significantly lower AT burden, compared to the other pacing algorithms. Moreover APP was significantly higher in DDD+ and in CLS mode, than in DDDR. APP weakly correlated with AT burden only in DDD+ mode, though the lowest AT burden level was obtained in the CLS group where no significant correlation was found.

So how does Closed Loop Stimulation (CLS) work?

CLS is a unique algorithm that monitors cardiac contraction dynamics by measuring a localized intra-cardiac impedance signal. This impedance signal provides a direct assessment of myocardial wall motion changes on a beat to beat basis. Geometrical changes around the pacing electrode are influenced by ventricular wall tension, ventricular wall thickness and inotropic state of the surrounding myocardium i.e. impedance change during the cardiac cycle is a reflection of the contraction process over time and therefore used as a surrogate marker of RV contractility. Because CLS detects physiological parameters that directly influence cardiac function it is classed as a primary rate response sensor.

Sub threshold pulses of current are injected down the lead for 250ms after every ventricular sensed or paced event. This produces an impedance waveform that is compared to a reference waveform that is collated during any resting period (avg. 256 cycles), this allows CLS to continuously optimize itself to the patient. The differential area between these two curves is determined and an appropriate pacing rate is calculated.

Closed Loop stimulation has a propensity to be reserved for the treatment of Vasovagal syncope, although this has been highly effective, it has emerged that CLS can offer other benefits in the areas of rate response, Atrial Fibrillation and CHF.

References:

1. Michael O. Sweeney, MD; Anne S. Hellkamp, MS; Kenneth A. Ellenbogen, MD; Arnold J. Greenspon, MD; Roger A. Freedman, MD; Kerry L. Lee, PhD; Gervasio A. Lamas, MD; for the MOde Selection Trial (MOST) Investigators. Adverse Effect of Ventricular Pacing on Heart Failure and Atrial Fibrillation Among Patients With Normal Baseline QRS Duration in a Clinical Trial of Pacemaker Therapy for Sinus Node Dysfunction. Circulation. 2003;107:2932-2937

2. Danish Pacemaker and ICD statistics 2006, Department of Cardiology, Odense University Hospital Denmark.

3. Anderson et al, Long-term follow-up of patients from a randomized trial of atrial versus ventricular pacing for sick-sinus syndrome. The Lancet 1997; 350:1210-1216

4. William M. Bailey, MD and *Denise Hull, RN. Closed Loop Stimulation improves ejection fraction and NYHA class in patients with Congestive Heart Failure and/or ejection fraction <40%. 2005 P5-98

5. A. Puglisi, G. Altamura, F. Capestro, B. Castaldi, G. Critelli, S. Favale, L. Pavia, G. Pettinati, Impact of Closed Loop Stimulation, overdrive pacing, DDDR pacing mode on atrial tachyarrhythmia burden in Brady-Tachy syndrome. European heart journal (2003) 24, 1952-1961