Europace Advance Access originally published online on February 13, 2008
Europace 2008 10(4):502-504; doi:10.1093/europace/eun026
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RESYNCHRONISATION THERAPY
Triangle ventricular pacing in a non-responder to conventional bi-ventricular pacing
1 Cardiovascular Division, Institute of Clinical Medicine, University of Tsukuba, 1-1-1 Tennodai, Tsukuba 305-8575, Ibaraki, Japan; 2 Cardiology Division, Tokyo Medical and Dental University, Tokyo, Japan
Manuscript submitted 28 November 2007. Accepted after revision 14 January 2008.
* Corresponding author. Tel: +81 29 853 3142; fax: +81 29 853 3143. E-mail address: kentaroyo{at}nifty.com
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Abstract |
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A 56-year-old man with cardiomyopathy secondary to myotonic dystrophy and complete atrioventricular block presented to our institution. A cardiac resynchronization therapy (CRT) device (InSync 8040, Medtronic, Inc., Minneapolis, MN, USA) was implanted by a conventional bi-ventricular pacing (Bi-V) technique. However, the patient’s NYHA class did not improve from class IV despite optimized medical therapy. One month after the CRT device implantation, we altered the pacing configuration from that of Bi-V to ‘triangle ventricular pacing’ (Tri-V), i.e. conventional Bi-V from the right ventricular (RV) apex and left ventricle plus additional pacing from the RV outflow tract, using a Y connector to bifurcate the RV bipolar output of the device into an anode and a cathode. In both the acute and 3 month follow-up studies, objective parameters revealed better resynchronization effects with Tri-V, and the patient’s NYHA class immediately improved to class II. Triangle ventricular pacing may have the potential to decrease the number of non-responders to CRT.
Key Words: Resynchronization, Heart failure, Pacing
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Introduction |
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More than 10 years have passed since the introduction of cardiac resynchronization therapy (CRT), but even now, 30–40% of patients remain non-responsive to CRT.1
More suitable inclusion criteria, especially those based on echocardiography, are needed to determine who will best respond to CRT; however, absolute criteria have not yet been discovered. Moreover, although the location of the left ventricular (LV) lead is important for producing an estimated resynchronization effect,2 successful insertion of that lead depends mostly on the individual anatomy of the coronary sinus branches. For this situation, a new method is needed to increase the number of responders to CRT. We present a patient who was not responsive to bi-ventricular pacing (Bi-V) but who did respond clinically to a novel pacing technique ‘triangle ventricular pacing’ (Tri-V).3 |
Case report |
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A 56-year-old man with a history of a DDD pacemaker implantation due to complete atrioventricular (AV) block presented to our hospital with increasing dyspnoea and weakness of his distal limb muscles. The 12-lead electrocardiogram (ECG) on admission showed a wide, paced QRS complex following an atrial complex. A diagnosis of cardiomyopathy secondary to myotonic dystrophy was made on the basis of the pathological findings from an endomyocardial biopsy. In the echocardiographic evaluation, the standard deviation of the time to the peak myocardial contraction in 12 LV segments (Ts-SD)4
was 42 ms at baseline. A CRT device (InSync 8040, Medtronic, Inc., Minneapolis, MN, USA) was implanted according to a conventional Bi-V technique, i.e. pacing from the right ventricular apex (RVA) and LV posterolateral wall. The CRT resulted in a slight decrease in the QRS width (from 210 to 180 ms) and Ts-SD (from 42 to 32 ms) and a slight increase in the systolic blood pressure (from 77 to 81 mmHg). However, the patient’s NYHA class progressively worsened from class III to class IV, and sustained ventricular tachycardias occurred repeatedly.
Therefore, 1 month after the CRT device implantation, we implanted a separate implantable cardioverter-defibrillator (at the time, no CRT-defibrillators were available in Japan), placed an additional lead in the right ventricular outflow tract (RVOT), and revised the pacer lead configuration from that of Bi-V to Tri-V, which consists of conventional Bi-V pacing from the RVA and LV posterolateral wall plus additional pacing from the high RVOT (Figure 1). A detailed haemodynamic study was also performed with temporary jumper cables during the procedure. As described in a previous report from our institution,3 to obtain Tri-V pacing, we modified the pacing circuit with the use of a Y connector (5866-38M, Medtronic Inc.), which allowed bifurcation of the RV bipolar output of the CRT device into an anode and a cathode. The RVA lead was connected to the anode and the RVOT lead to the cathode of the Y connector. Triangle ventricular pacing resulted in an additional decrease in the QRS width (160 ms) (Figure 2) and Ts-SD (22 ms) and an increase in the maximum rate of increase in the pressure (dP/dtmax) (RVA pacing, 560 mmHg/s; Bi-V with RVA and LV pacing, 690 mmHg/s; Bi-V with RVOT and LV pacing, 725 mmHg; Tri-V, 780 mmHg/s) and cardiac output (RVA pacing, 3.5 L/min; Bi-V with RVA and LV pacing, 3.8 L/min; Bi-V with RVOT and LV pacing, 3.7 L/min; Tri-V, 4.5 L/min). Furthermore, the NYHA class immediately improved to class II. Three months after the reconfiguration, the serum BNP level dropped from 968 to 162 pg/mL, LV end-diastolic volume decreased from 236 to 181 mL, and LV ejection fraction increased from 29 to 37% on the echocardiographic study.
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Discussion |
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We have previously reported that in an acute haemodynamic and echocardiographic study conducted during a CRT device implantation procedure, the technique of Tri-V produced a better resynchronization effect than did the conventional Bi-V technique because of the better resynchronization of the LV anterior free wall resulting from the addition of the RVOT pacing site.3
However, that data were obtained in the laboratory, and the potential clinical benefit of Tri-V compared with that of Bi-V remains uncertain. The patient reported herein, who underwent reconfiguration from Bi-V to Tri-V, has shown that Tri-V may have the potential to produce direct clinical benefit in patients non-responsive to Bi-V.
The activation pattern of the LV during Tri-V was more similar to the activation pattern of the normal heart than that during Bi-V with a short AV delay, especially for the activation of the anterior free wall.3 In regard to the number of pacing sites, more is theoretically better, but a previous study had reported that both LV single-site pacing and Bi-V were associated with almost equivalent improvement in subjective and objective parameters.5 We hypothesized that CRT with LV single-site pacing also uses the intrinsic conduction system through the AV node and that such ‘hidden’ conduction contributes to the early depolarization and contraction of the LV septum or anterior wall, as does the additional RVOT pacing of Tri-V. The previous studies reasoned that the AV delay influences the contribution of the intrinsic conduction to the total ventricular activation by fusing the intrinsic activation wave with the activation wave originating from pacing sites in LV single-site pacing or Bi-V.6–8 If candidates for CRT have a normal PR interval on 12-lead ECG and an intermediate or long AV delay is selected, it is possible that ‘hidden’ conduction through the AV node exists also during Bi-V. Such hidden conduction may latently contribute to the resynchronization of the LV in some patients referred for LV single-site pacing or Bi-V.
The hidden conduction should not remain constant, however. When a patient’s heart rate increases due to exercise, alternation in the autonomic nervous system, or atrial pacing in the clinical situation, the AV conduction may be delayed, resulting in a breakdown in the electrical synchrony of the LV, especially in a severely failing heart requiring CRT. Therefore, LV single-site pacing and Bi-V may not be able to produce stable resynchronization effects when following a fluctuating heart rate in the clinical situation. Garrigue et al.9 reported that LV single-site pacing can provide a haemodynamic and clinical improvement similar to that of Bi-V at rest; however, LV single-site pacing is inferior to Bi-V during exercise. We believe that our RVOT pacing method is superior to the ‘hidden’ conduction in that it is not affected by the fluctuations of heart rate.
For these reasons, patients with disturbances in AV conduction, such as complete AV block, may obtain a greater benefit from Tri-V, just as the patient in this case report did. Because myotonic dystrophy is a progressive disease, we cannot evaluate the long-term benefit of Tri-V to this patient. Moreover, an extensive clinical study is necessary to confirm our hypothesis. However, the results from our patient indicate that Tri-V may have the potential to decrease the number of non-responders to CRT.
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Acknowledgements |
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We wish to thank John Martin and George B. Powell for their review of this manuscript.
Conflict of interest: none declared.
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References |
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[1] Abraham WT, Fisher WG, Smith AL, Delurgio DB, Leon AR, Loh E, et al. Cardiac resynchronization in chronic heart failure. N Engl J Med (2002) 346:1845–53.
[2] Rossillo A, Verma A, Saad EB, Corrado A, Gasparini G, Marrouche NF, et al. Impact of coronary sinus lead position on biventricular pacing: mortality and echocardiographic evaluation during long-term follow-up. J Cardiovasc Electrophysiol (2004) 15:1120–5.[CrossRef][Web of Science][Medline]
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[4] Yu CM, Fung WH, Lin H, Zhang Q, Sanderson JE, Lau CP. Predictors of left ventricular reverse remodeling after cardiac resynchronization therapy for heart failure secondary to idiopathic dilated or ischemic cardiomyopathy. Am J Cardiol (2003) 91:684–8.[CrossRef][Web of Science][Medline]
[5] Touiza A, Etienne Y, Gilard M, Fatemi M, Mansourati J, Blanc JJ. Long-term left ventricular pacing: assessment and comparison with biventricular pacing in patients with severe congestive heart failure. J Am Coll Cardiol (2001) 38:1966–70.
[6] Vernooy K, Verbeek XA, Cornelussen RN, Dijkman B, Crijns HJ, Arts T, et al. Calculation of effective VV interval facilitates optimization of AV delay and VV interval in cardiac resynchronization therapy. Heart Rhythm (2007) 4:75–82.[CrossRef][Web of Science][Medline]
[7] Verbeek XA, Auricchio A, Yu Y, Ding J, Pochet T, Vernooy K, et al. Tailoring cardiac resynchronization therapy using interventricular asynchrony. Validation of a simple model. Am J Physiol Heart Circ Physiol (2006) 290:H968–H977.
[8] Verbeek XA, Vernooy K, Peschar M, Cornelussen RN, Prinzen FW. Intra-ventricular resynchronization for optimal left ventricular function during pacing in experimental left bundle branch block. J Am Coll Cardiol (2003) 42:558–67.
[9] Garrigue S, Bordachar P, Reuter S, Jais P, Kobeissi A, Gaggini G, et al. Comparison of permanent left ventricular and biventricular pacing in patients with heart failure and chronic atrial fibrillation: prospective haemodynamic study. Heart (2002) 87:529–34.
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