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Europace 2007 9(1):34-40; doi:10.1093/europace/eul131
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© The European Society of Cardiology 2007. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org

CRT

Evidence of left ventricular dyssynchrony resulting from right ventricular pacing in patients with severely depressed left ventricular ejection fraction

Martin Schmidt*, Jürgen Brömsen, Christian Herholz, Kai Adler, Florian Neff, Carsten Kopf and Michael Block

Department of Cardiology, Stiftsklinik Augustinum, München, Bavaria 80469, Germany

Manuscript submitted 18 May 2006. Accepted after revision 27 August 2006.

* Corresponding author. Tel: +49 408970975032. E-mail address: mschmidtmuc{at}t-online.de


   Abstract
Top
 Abstract
Introduction
 Methods
 Results
 Discussion
 References
 
Aims Cardiac resynchronization therapy (CRT) has recently emerged as an effective treatment for patients with moderate-to-severe systolic heart failure and left bundle branch block (LBBB). Right ventricular pacing (RVP) leads to an LBBB-like pattern in the electrocardiogram. The aim of this study was to evaluate the frequency of ventricular mechanical dyssynchrony in patients induced by RVP.

Methods and results The study included 33 patients with a conventional single or dual chamber pacemaker, 18 with ejection fraction (EF) > 35% and 15 with EF ≤ 35%. In all patients, an intrinsic rhythm without intraventricular conduction delay (QRS ≤ 120 ms) was present without RVP. Two-dimensional and Doppler echocardiographic criteria for mechanical dyssynchrony [aortic pre-ejection delay (APE), interventricular mechanical delay (IVMD), delayed activation of the posterior left ventricular wall (PD), septal-to-posterior wall motion delay (SPWMD)] were evaluated in all patients with and without RVP. QRS duration showed no difference between the two EF-groups without RVP (93 ± 10 vs. 96 ± 9 ms), but was significantly longer in patients with low EF with RVP (152 ± 18 vs. 181 ± 18 ms; P < 0.001). In patients with EF > 35%, only APE was slightly prolonged by RVP (111 ± 20 vs. 129 ± 17 ms; P = 0.03), whereas in patients with EF ≤ 35% marked pathological differences in APE (118 ± 29 vs. 169 ± 24 ms; P < 0.001), IVMD (22 ± 17 vs. 58 ± 14 ms; P < 0.001), SPWMD (103 ± 28 vs. 125 ± 29 ms; P = 0.004), and PD (–21 ± 25 vs. – 39 ± 25 ms; P = 0.005) were found. A significant correlation between QRS duration and mechanical ventricular dyssynchrony was only found for two echocardiographic parameters (IVMD, APE) with RVP.

Conclusion In patients with a conventional pacemaker, mechanical dyssynchrony with RVP was shown exceptionally in patients with preserved or moderately depressed systolic left ventricular (LV) function, but in nearly all patients with severely depressed systolic LV function. These patients might benefit from CRT when frequent RVP is required.

Key Words: Right ventricular pacing, Left bundle branch block, Left ventricular dyssynchrony, Reduced ventricular function, Cardiac resynchronization therapy


   Introduction
Top
 Abstract
 Introduction
Methods
 Results
 Discussion
 References
 
Left ventricular (LV) dyssynchrony is a common problem in heart failure patients. QRS prolongation in left bundle branch block (LBBB) is associated with dyssynchronous ventricular contraction and a depressed left ventricular ejection fraction (LVEF).1Go There is increasing evidence supporting the routine use of cardiac resynchronization therapy (CRT) to improve severe heart failure, despite optimal medical treatment in patients with electrocardiographic ventricular dyssynchrony (LBBB) and low EF (≤35%).2Go–7Go Two large randomized multicentre trials with mortality from all causes as a secondary endpoint showed that CRT reduces mortality with and without backup defibrillation.6Go,7Go

In patients with a conventional indication for a single or dual chamber pacemaker, the usual way of ventricular pacing is from the right ventricular apex. Right ventricular apical pacing (RVP) creates an artificially induced intraventricular conduction delay and impairs ventricular function.8Go Right ventricular pacing has been found to generate a higher number of hypocontractile regions within the LV wall compared with LV lateral wall pacing.9Go In patients with low EF (≤40%), RVP might have a causal relationship to morbidity and hospitalization for congestive heart failure.10Go,11Go In patients with severe heart failure and low EF, echocardiographic markers of mechanical dyssynchrony have been identified as a better predictor of response to CRT than QRS duration.12Go,13Go It is unknown how often RVP introduces mechanical dyssynchrony and if patients with preserved or moderately suppressed LV function also show mechanical dyssynchrony due to RVP.

This study investigated the frequency and magnitude of ventricular mechanical dyssynchrony due to RVP in patients with conventional pacemakers and EF > 35 or ≤ 35%.


   Methods
Top
 Abstract
 Introduction
 Methods
Results
 Discussion
 References
 
Patients
The study included 33 patients with a conventional single or dual chamber pacemaker including a ventricular pacing lead in the right ventricular apex, in whom all echocardiographic markers of ventricular dyssynchrony could be evaluated. In all patients, an intrinsic rhythm without intraventricular conduction delay (QRS duration ≤ 120 ms) was present without RVP. The patients baseline characteristics are outlined in Table 1. Using current criteria for CRT, patients were divided into groups with an EF > 35% (n = 18; EF: 55 ± 6%; range 45–70%) or an EF ≤ 35% (n = 15; EF: 31 ± 4%; range 25–35%).


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  		Table 1 Baseline characteristics of patients (n = 33)

 
Electrocardiogram
The electrocardiogram (ECG) was performed (ECG recorder, Schwarzer, Germany) at a speed of 50 mm/s and 1 mV/cm standardization. All patients had 12-lead surface resting ECG with and without RVP. QRS duration was measured from the first to the last sharp vector crossing the isoelectric line in all leads, and the maximum value was used.

Echocardiography
Echocardiography recordings were made using a 2.5–3.5 MHz transducer interfaced with a diagnostic ultrasound system (Aplio SSA-700A, Toshiba). The patients were examined in the left lateral recumbent position using standard parasternal, short- and long-axis, and apical views. LVEF was measured using the two-dimensional-echo-derived Simpson method on the four-chamber view. In all patients, the ventricular criteria of dyssynchrony used in the CARE-HF study.14Go,15Go [the aortic pre-ejection delay (APE), the delayed activation of the posterior wall (PD), the interventricular mechanical delay (IVMD)] and additionally the septal-to-posterior wall motion delay (SPWMD) were evaluated with and without RVP (Figures 1–4).12Go,16Go For evaluation without RVP, in all patients, the pacemaker was switched to backup mode (VVI programmed to 30 bpm). The ECG was simultaneously recorded.


Figure 1311
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  		Figure 1 Aortic pre-ejection delay. It is the time from QRS onset to aortic flow onset determined from pulsed-wave Doppler velocity signals proximal to the aortic valve in the LV outflow tract. Intraventricular dyssynchrony is defined by an APE of more than 140 ms.

 


Figure 1312
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  		Figure 2 Interventricular mechanical delay. It is the time difference between APE (Figure 1) and pulmonary pre-ejection delay. Interventricular dyssynchrony is defined by an IVD of more than 40 ms.

 


Figure 1313
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  		Figure 3 Septal-to-posterior wall motion delay. It is the interval between maximal posterior and septal displacement of left posterior and septal wall in a mono-dimensional short-axis view at the papillary muscle level. Intraventricular dyssynchrony is defined by an SPWMD of more than 130 ms.

 


Figure 1314
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  		Figure 4 (A and B) Delayed activation of the posterior LV wall. It is the time difference between QRS onset to onset of the E-wave in the pulsed Doppler transmitral flow signal and time from QRS onset to peak systolic movement of the posterior wall in a mono-dimensional long-axis view. Intraventricular dyssynchrony is defined by a PD < 0.

 
Statistical analysis
Statistical analysis was performed with SPSS software (version 11.5) (SPSS Inc., Chicago, IL, USA). Results are presented as mean ± standard deviation. Paired Student's t-test was used for comparisons between no pacing and RVP. For comparisons of parameters between the two groups, the unpaired t-test was used. Correlations between variables were assessed using Pearson's linear correlation, since there was a normal distribution of data. P < 0.05 was considered significant for all tests.


   Results
Top
 Abstract
 Introduction
 Methods
 Results
Discussion
 References
 
QRS-duration
Without RVP, the QRS duration showed no difference between EF > 35 and ≤ 35% (93 ± 10 vs. 96 ± 9 ms). With RVP, the QRS duration was significantly prolonged in both groups (EF > 35%: 152 ± 18 ms; P < 0.001, EF ≤ 35%: 181 ± 18 ms; P < 0.001). The QRS duration with RVP was significantly longer in patients with an EF ≤ 35% than in patients with an EF > 35% (P < 0.001).

Mechanical dyssynchrony
Without RVP, the mean values showed no significant mechanical dyssynchrony in patients with EF > 35% (APE 111 ± 20 ms; IVMD 17 ± 13 ms; SPWMD 91 ± 28 ms, and PD 1 ± 28 ms) or EF ≤ 35% (APE 118 ± 29 ms; IVMD 22 ± 17 ms; SPWMD 103 ± 28 ms) except for PD (–21 ± 25 ms).

With RVP, in patients with EF > 35%, only APE was significantly prolonged (111 ± 20 vs. 129 ± 17 ms; P = 0.03). The other markers of mechanical dyssynchrony showed no significant difference with RVP vs. without RVP (Table 2, Figure 5 A–D).


Figure 1315
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  		Figure 5 Comparison of echocardiographic markers of ventricular dyssynchrony with and without RVP. Individual values of (A) APE, (B) IVMD, (C) SPWMD, and (D) PD in patients with EF > 35% are shown. Cut-off levels of each echocardiographic parameter are indicated.

 


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  		Table 2 Left ventricular dyssynchrony with and without RVP

 
In contrast, patients with EF ≤ 35% showed significant differences of APE (118 ± 29 vs. 169 ± 24 ms; P < 0.001), IVMD (22 ± 17 vs. 58 ± 14 ms; P < 0.001), SPWMD (103 ± 28 vs. 125 ± 29 ms; P = 0.004), and PD (–21 ± 25 ms vs. – 39 ± 25 ms; P = 0.005) with RVP (Table 2, Figure 6 A–D).


Figure 1316
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  		Figure 6 Comparison of echocardiographic markers of ventricular dyssynchrony with and without RVP. Individual values of (A) APE, (B) IVMD, (C) SPWMD, and (D) PD in patients with EF ≤ 35% are shown. Cut-off levels of each echocardiographic parameter are indicated.

 
Without RVP, no significant correlation between duration of QRS and APE (r = –0.057), IVMD (r = 0.049), PD (r = –0.187), or SPWMD (r = –0.060) was found. With RVP, APE (r = 0.61; P < 0.001) and IVMD (r = 0.67; P < 0.001) were significantly correlated with QRS duration. This correlation was found in patients with EF ≤ 35% (APE: r = 0.61, P = 0.01; IVMD: r = 0.80, P < 0.001) and in patients with EF > 35% (APE: r = 0.58, P = 0.02; IVMD: r = 0.54; P = 0.02). No significant correlation with QRS duration was found for SPWMD (r = 0.21) and PD (r = –0.27). No significant correlation was also found for QRS duration in patients with EF ≤ 35% with SPWMD (r = 0.46; PD: r = –0.02) and in patients with EF > 35% with SPWMD (r = 0.17; PD: r = 0.10).

With RVP, 14 of 15 patients (93%) with EF ≤ 35%, 3 of 18 patients (16%) with EF > 35%, and one patient of each group without RVP met two of three pathological CARE-HF echo-criteria for mechanical dyssynchrony (Table 3).


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  		Table 3 Pathological echocardiographic parameters in patients with EF ≤ 35% and > 35%

 

   Discussion
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
References
 
In this study, RVP caused mechanical dyssynchrony in all but one patient with severely depressed LV function and a conventional pacemaker according to the criteria used by the CARE-HF trial. Using the criterion of the delay of contraction of the posterolateral wall to the septum (SPWMD), all but six patients showed mechanical dyssynchrony. Thus the frequency of mechanical dyssynchrony introduced by RVP in patients with severely depressed LV function seems to be at least as high as in patients with LBBB without pacing. In the CARE-HF trial, only 62% of patients had interventricular dyssynchrony defined by IVMD compared with 87% of our patients.5Go Left intraventricular dyssynchrony measured by SPWMD was only described in CARE-HF in 55% of patients with current indication for CRT compared with 60% of our patients.13Go

The magnitude of interventricular dyssynchrony caused by RVP was at least as large in our patients due to RVP as reported for patients currently receiving CRT, 58 ± 14 (our patients) vs. 48 ± 18 ms (CARE-HF patients).17Go The magnitude of intraventricular dyssynchrony measured by SPWMD seems to be less in our patients due to RVP than for patients currently receiving CRT (125 ± 29 vs. 147 ± 96 ms).13Go As left intraventricular dyssynchrony, but not interventricular dyssynchrony, seems to predict response to CRT, the impact of biventricular pacing compared with RVP might be less impressive than in current CRT patients.4Go However, the feasibility and reproducibility of SPWMD measurements and the correlation of SPWMD with clinical response to CRT has been discussed controversially,13Go,18Go and more sophisticated techniques as tissue Doppler imaging or strain rate imaging might be needed to determine left intraventricular mechanical dyssynchrony.19Go But with improvements in practicability, three-dimensional analysis of ventricular dyssynchrony might make two-dimensional echocardiographic parameters obsolete. Collection of sufficient data by tissue Doppler imaging covering multiple myocardial segments is currently time consuming and the clinical applicability of strain rate imaging might be operator-dependent and limited by artefacts.14Go,20Go

In patients with an LVEF > 35%, who are currently not candidates for CRT, RVP only caused mechanical dyssynchrony according to the criteria used by the CARE-HF trial in three patients, interventricular dyssynchrony according to IVMD in only one patient, and left intraventricular dyssynchrony according to SPWMD in only two patients. The incidence of inter- and intraventricular delay in patients with LBBB and preserved LV function is comparably low.21Go This suggests that patients with an EF > 35% will not benefit from upgrading from RVP to biventricular pacing. But due to data that long-standing LBBB may be a reversible cause of cardiomyopathy22Go and dual chamber pacing but not single-chamber atrial pacing decreases LV fractional shortening in patients with sick sinus syndrome,23Go further studies are required to analyse mechanical dyssynchrony in patients with RVP during long-term follow-up.

Alternative RVP sites have been evaluated and the right ventricular outflow tract is the most feasible alternative to RVP. A review evaluating the haemodynamic effects of right ventricular outflow tract pacing including prospective studies and measurement of systolic LV function showed only a modest benefit over RVP.24Go The only randomized trial comparing right ventricular outflow tract pacing with RVP did not show a consistent improvement in the quality of life.25Go

A QRS duration ≥ 190 ms due to RVP has been described as a predictor of developing congestive heart failure.26Go As 20–30% of heart failure patients did not respond to CRT, despite long QRS durations in multicentre randomized CRT-trials, electrical dyssynchrony due to RVP might not be the ideal predictor for upgrading from RVP to biventricular pacing.2Go,5Go,27Go Previous data showed that the underlying pathophysiology of heart failure may lead to inter- and LV intraventricular dyssynchrony in RVP by mechanisms other than electrical conduction delay.11Go We only found a significant correlation between the QRS duration and the degree of mechanical ventricular dyssynchrony for two parameters (APE, IVMD) with RVP, which was independent of EF. Thus, consistent with the previous findings,26Go,28Go a paced QRS duration of ≥ 190 or ≥ 200 ms should not be considered as a strict criterion for upgrading patients from RVP to biventricular pacing.

In conclusion, we showed that in patients with a conventional pacemaker, significant ventricular mechanical dyssynchrony with RVP was present exceptionally in patients with preserved or moderately depressed systolic LV function, but in nearly all patients with severely depressed systolic LV function. The latter patients might benefit from CRT when RVP is frequent (high percentage of the time).


   References
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 Abstract
 Introduction
 Methods
 Results
 Discussion
 References
 
[1] Grines CL, Bashore RC, Boudoulas H, Olson S, Shafer P, Wooley CF. Functional abnormalities in isolated left bundle branch block. The effect of interventricular asynchrony. Circulation 1989; 79: 845–53.[Medline]

[2] Cazeau S, Leclercq C, Lavergne T, et al. for the Multisite Stimulation in Cardiomyopathies (MUSTIC) Study Investigators. Effects of multisite biventricular pacing in patients with heart failure and intraventricular conduction delay. N Engl J Med 2001; 344: 873–80.[Abstract/Free Full Text]

[3] Saxon LA, De Marco T, Schafer J, Chatterjee K, Kumar UN, Foster E. for the VIGOR Congestive Heart Failure Investigators. Effects of long-term biventricular stimulation for resynchronization on echocardiographic measures of remodeling. Circulation 2002; 105: 1304–10.

[4] Auricchio A, Stellbrink C, Sack S, et al. for the Pacing Therapies in Congestive Heart Failure (PATH-CHF) study group. Long-term clinical effect of hemodynamically optimized cardiac resynchronization therapy in patients with heart failure and ventricular conduction delay. J Am Coll Cardiol 2002; 39: 2026–33.[Abstract/Free Full Text]

[5] Abraham WT, Fisher WG, Smith AL, et al. for the MIRACLE Study group. Multicenter InSync randomized clinical evaluation. Cardiac resynchronization in chronic heart failure. N Engl J Med 2002; 346: 1845–53.[Abstract/Free Full Text]

[6] Bristow MR, Saxon LA, Boehmer J, et al. for the Comparison of medical therapy pacing and defibrillation in heart failure (COMPANION) investigators. Cardiac resynchronization therapy with or without an implantable defibrillator in advanced chronic heart failure. N Engl J Med 2004; 350: 2140–50.[Abstract/Free Full Text]

[7] Cleland JG, Daubert JC, Erdmann E, et al. for the Cardiac Resynchronization-Heart Failure (CARE-HF) study investigators. The effect of cardiac resynchronization on morbidity and mortality in heart failure. N Engl J Med 2005; 352: 1539–49.[Abstract/Free Full Text]

[8] Sweeney MO, Hellkamp AS, Ellenbogen KA, et al. 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: 2932–7.

[9] Prinzen FW and Peschar M. Relation between the pacing induced sequence of activation and left ventricular pump function in animals. Pacing Clin Electrophysiol 2002; 25: 484–98.[CrossRef][Medline]

[10] Sharma AD, Rizo-Patron C, Hallstrom AP, et al. for the Dual chamber and VVI implantable defibrillator trial investigators. Percent right ventricular pacing predicts outcomes in the DAVID trial. Heart Rhythm 2005; 2: 830–4.[CrossRef][ISI][Medline]

[11] Wilkoff BL, Cook JR, Epstein AE, et al. Dual-chamber pacing or ventricular backup pacing in patients with an implantable defibrillator: the Dual chamber and VVI implantable defibrillation (DAVID) trial. JAMA 2002; 288: 3115–23.[Abstract/Free Full Text]

[12] Pitzalis MV, Iacoviello M, Romito R, et al. Cardiac resynchronization therapy tailored by echocardiographic evaluation of ventricular asynchrony. J Am Coll Cardiol 2002; 40: 1615–22.[Abstract/Free Full Text]

[13] Pitzalis MV, Iacoviello M, Romito R, et al. Ventricular asynchrony predicts a better outcome in patients with chronic heart failure receiving cardiac resynchronization therapy. J Am Coll Cardiol 2005; 45: 65–9.[Abstract/Free Full Text]

[14] Cleland JG, Daubert JC, Erdmann E, et al. for the Cardiac Resynchronization-Heart Failure (CARE-HF) study Steering Committee and Investigators. The CARE-HF (Cardiac Resynchronization in Heart Failure study): rationale, design and end-points. Eur J Heart Fail 2001; 3: 481–9.[CrossRef][ISI][Medline]

[15] Cleland JG, Daubert JC, Erdmann E, et al. for the Cardiac Resynchronization-Heart Failure (CARE-HF) study Steering Committee and Investigators. Baseline characteristics of patients recruited into the CARE-HF study. Eur J Heart Fail 2005; 7: 205–14.[CrossRef][ISI][Medline]

[16] Porciani MC, Puglisi A, Colella A, et al. for the In Sync Italian registry investigators. Echocardiographic evaluation of the effect of biventricular pacing: InSync Italian registry. Eur Heart J 2000; 2:Suppl. J, 23–30.

[17] Ghio S, Freemantle N, Serio A, et al. Baseline echocardiographic characteristic of heart failure patients enrolled in a large European multicenter trial (Cardiac Resynchronization Heart Failure study). Eur J Echocardiogr 2006; 7: 373–8.[Abstract/Free Full Text]

[18] Marcus GM, Rose E, Viloria EM, et al. VENTAK CHF/CONTAK-CD Biventricular Pacing Study Investigators. Septal to posterior wall motion delay fails to predict reverse remodeling or clinical improvement in patients undergoing cardiac resynchronization therapy. J Am Coll Cardiol 2005; 46: 2208–14.[Abstract/Free Full Text]

[19] Bax JJ, Bleeker GB, Marwick TH, et al. Left ventricular dyssynchrony predicts response and prognosis after cardiac resynchronization therapy. J Am Coll Cardiol 2004; 44: 1834–40.[Abstract/Free Full Text]

[20] Bax JJ, Ansalone G, Breithardt OA, et al. Echocardiographic evaluation of cardiac resynchronization therapy: ready for routine clinical use? A critical appraisal. J Am Coll Cardiol 2004; 44: 1–9.[Abstract/Free Full Text]

[21] Caso P, DAndrea A, Martiniello AR, et al. Myocardial systolic activation delay in patients with left bundle branch block and either normal or impaired left ventricular function. Echocardiography 2006; 23: 14–23.[CrossRef][ISI][Medline]

[22] Blanc JJ, Fatemi M, Bertault V, Baraket F, Etienne Y. Evaluation of left bundle branch block as a reversible cause of non-ischaemic dilated cardiomyopathy with severe heart failure. A new concept of left ventricular dyssynchrony-induced cardiomyopathy. Europace 2005; 7: 604–10.[Abstract/Free Full Text]

[23] Nielsen JC, Kristensen L, Andersen HR, et al. A randomized comparison of atrial and dual-chamber pacing in 177 consecutive patients with sick sinus syndrome: echocardiographic and clinical outcome. J Am Coll Cardiol 2003; 42: 614–23.[Abstract/Free Full Text]

[24] De Cock CC, Giudici MC, Twisk JW. Comparison of the haemodynamic effects of right ventricular outflow-tract pacing with right ventricular apex pacing. A quantitative review. Europace 2003; 5: 275–78.[Abstract/Free Full Text]

[25] Stambler BS, Ellenbogen K, Zhang X, et al. Right ventricular outflow versus apical pacing in pacemaker patients with congestive heart failure and atrial fibrillation. J Cardiovasc Electrophysiol 2003; 14: 1180–6.[CrossRef][ISI][Medline]

[26] Miyoshi F, Kobayashi Y, Itou H, et al. Prolonged paced QRS duration as a predictor for congestive heart failure in patients with right ventricular apical pacing. Pacing Clin Electrophysiol 2005; 28: 1182–88.[CrossRef][Medline]

[27] Bordachar P, Garrigue S, Lafitte S, Reuter S, Jaïs P, Haïssaguerre M, et al. Interventricular and intra-left ventricular electromechanical delays in right ventricular paced patients with heart failure: implications for upgrading to biventricular stimulation. Heart 2003; 89: 1401–5.[Abstract/Free Full Text]

[28] Linde C, Leclercq C, Rex S, et al. Long-term benefits of biventricular pacing in congestive heart failure: results from the Multisite Stimulation in cardiomyopathy (MUSTIC) study. J Am Coll Cardiol 2002; 40: 111–8.[Abstract/Free Full Text]


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