© 2005 The European Society of Cardiology. Published by Elsevier Ltd. All rights reserved.
CASE REPORT
Cardiac resynchronisation therapy versus dual site right ventricular pacing in a patient with permanent pacemaker and congestive heart failure
aNizam's Institute of Medical Sciences Hyderabad, India; bDepartment of Medicine, Second Section of Cardiology, Chang Gung Memorial Hospital, Chang Gung University College of Medicine 199 Tung Hwa North Road, Sung-Shan District, Tao-Yuan, Taipei 111, Taiwan
Manuscript submitted 6 September 2004. Accepted after revision 30 January 2005.
*Corresponding author. Tel.: +886 3 3281200; fax: +886 3 3289134. E-mail address: chcwang{at}adm.cgmh.org.tw (C.-C. Wang).
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Abstract |
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A 46-year-old male patient who had long-term right ventricular (RV) pacing for symptomatic complete heart block, initially by an epicardial, later with an endocardial pacing lead at the RV apex, developed congestive heart failure (CHF) and chronic atrial fibrillation 7 years following the pacemaker implantation and was medically treated. During follow-up, his pacemaker was upgraded to a cardiac resynchronisation therapy (CRT) device, because of uncontrolled CHF symptoms, New York Heart Association (NYHA) functional class IV, while on drugs. The patient's symptomatic status improved to NYHA functional class II with CRT. After 17 months of CRT, the battery became depleted, because of the high capture threshold of the left ventricular lead. The patient was then given dual site RV pacing (RV outflow tract + RV apex) in place of CRT, which showed similar efficacy at 12 weeks follow-up.
Key Words: cardiac resynchronisation therapy, heart failure, complete heart block, pacemaker, atrial fibrillation
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Introduction |
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Cardiac resynchronisation therapy (CRT), a novel pacing therapy for severely symptomatic congestive heart failure (CHF) patients with ventricular conduction delay, is indicated in patients with preserved sinus rhythm [1]
. Few data are available concerning the benefit of CRT in CHF patients with chronic atrial fibrillation (AF) and complete heart block. We report here the benefits and problems associated with CRT in a patient with a permanent pacemaker implantation (PPI) for complete heart block (CHB), who developed chronic AF and CHF during follow-up. The effect of dual site right ventricular pacing in place of CRT, which the patient has subsequently undergone, is also discussed. |
Case report |
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A 46-year-old male patient underwent PPI (VVI, Medtronic Inc, Minneapolis, MN, USA) with an epicardial pacing lead on the right ventricle (RV) (Fig. 2B) at the age of 30 years for symptomatic CHB. The electrophysiological study at that time showed the conduction block to be below the His bundle. Seven years following the PPI, the patient developed symptoms of CHF, New York Heart Association (NYHA) functional class III, and chronic AF. The echocardiographic examination showed dilated cardiac chambers with concentric left ventricular hypertrophy and left ventricular ejection fraction (LVEF) of 27% (Fig. 1A). The patient was managed with diuretics, digoxin, enalapril, amiodarone and oral anticoagulants. Nine years following the initial PPI, the pulse generator (PG) showed impending battery depletion. The patient underwent PPI with an endocardial pacing lead (CapSure Z 5034, Medtronic Inc.,) placed at the right ventricular apex (Fig. 2B) through the right cephalic vein and PG (VVIR, VIGOR 1130, Guidant Inc, St. Paul, MN, USA) positioned in the subcutaneous pocket in the right pectoral region.
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The patient's symptoms of heart failure worsened (NYHA functional class IV), despite adequate medical therapy, requiring repeated hospital admissions. When the second PG showed battery depletion after 5 years, CRT was selected. Under local anaesthesia, the right subclavian vein puncture gave access to the right heart and the coronary sinus (CS) was cannulated with some difficulty using a deflectable tip 7F quadripolar electrode catheter, allowing a guiding sheath to be tracked over it. With a 6F balloon tipped catheter (Arrow International Inc. Reading, PA 19605, USA) a CS venogram was performed, to delineate its anatomy. Posterolateral cardiac vein (PLCV) was chosen for left ventricular (LV) lead placement as it was the only suitably large vein (Fig. 2A). The CS venogram also revealed dissection of the ostium with contrast staining of the surrounding epicardial fat, probably due to damage during cannulation. However, echocardiographic examination did not show any evidence of haemopericardium. The left ventricular (LV) lead (Attain 4189, Medtronic Inc.,) with stylet support was advanced through the guiding sheath into the CS, then into the target vein. In the middle and distal part of the PLCV, the lead had a satisfactory LV capture threshold (1.2 V at 0.50 ms pulse duration (PD)), but there was also left phrenic nerve stimulation. Thus, it was necessary to select the proximal portion of the PLCV where the LV capture threshold was very high (7.0 V at 0.50 ms PD) but stable and without phrenic nerve stimulation (Fig. 2B). Epicardial placement of the LV lead by surgical approach was avoided because of the high risk associated with thoracotomy and general anaesthesia in a patient with severe CHF (NYHA functional class IV). The cardiac output (L/min) and cardiac index calculated with thermodilution technique during RV, LV and biventricular pacing (BVP) were 3.0/1.7, 3.5/1.9 and 3.8/2.1, respectively. LV lead was connected to the atrial port and RV lead (implanted during the previous PPI) to the ventricular port of the pulse generator (PG) (Meridian DR 1276, Guidant Inc, St. Paul, MN, USA). The PG was programmed with RV lead output of 2.0 V (PD 0.50 ms) and LV lead output of 7.0 V (PD 1.5 ms) with interventricular delay of 10 ms thus initiating CRT. The ECG with CRT showed AF with a QRS duration of 0.16 s in the limb leads with superior axis (Fig. 3A). The patient had significant improvement in his symptoms of heart failure (NYHA functional class II) following the procedure. Echocardiography at 6 months showed LVEF 39% (Fig. 1B). However, the LV lead capture threshold remained high. By 17 months of CRT, the PG reached elective replacement.
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In view of the high capture threshold of the LV lead, dual site RV pacing was selected. Another active fixation endocardial pacing lead (CapSureFix Novus 5076, Medtronic Inc.,) was positioned through the right subclavian vein on the high septum of the RV, near the outflow tract (RVOT) (Fig. 2B). The lead had a capture threshold of 0.6 V at 0.50 ms PD and R wave sensing was 14 mV. The RVOT lead was connected to the atrial port and the lead at the RV apex (implanted during the previous procedure) was connected to the ventricular port of the PG (INSIGNIATM I Entra DR 1294, Guidant Inc.). The LV lead was capped and anchored to the subcutaneous tissue in the PG pocket. Pacing with an intraventricular delay of 10 ms, the surface ECG showed AF with a QRS duration of 0.12 s in the limb leads with inferior axis (Fig. 3B). After 12 weeks of follow-up, the patient has maintained the same NYHA functional class (II). The LVEF was estimated by echocardiography to be 40% (Fig. 1C) at 12 weeks of follow-up.
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Discussion |
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CRT can be delivered either by simultaneous or sequential pacing of LV and RV (BVP) or pacing the LV alone after sensing or pacing the atrium at a given delay. Both methods can re-time the delayed activation of the left ventricle, thereby resynchronising the LV and RV contractions, resynchronising regional LV wall motion and maximising the preload by shortened atrioventricular delay [2,
3].
Pronounced anatomical variations in the CS from patient to patient cause considerable difficulty at times, in choosing the optimal site for LV lead implantation. Even though middle and great cardiac veins are constantly present, posterior or lateral branches can be absent in 1% of patients. In addition, the diameter of the branches and angles they make with the CS may vary between patients, making access to these branches difficult [4]. In our patient only the PLCV was of sufficient size to position the LV lead. Alonso et al. in their six-year experience of CRT in 102 patients noted an 88% success rate of implantation and CS dissection in 2%. LV lead repositioning was required because of increased threshold in 15% and phrenic nerve stimulation in 3% of their patients [5]. In our patient during the LV lead implantation, apart from the CS dissection, the problem of phrenic nerve stimulation was also found in the middle and distal portion of the PLCV, where there was also a good capture threshold. This forced us to position it in the proximal part of the PLCV, despite the high threshold, which led to rapid depletion of the battery.
Recent reports suggest that long-term RV pacing after ablation of atrioventricular junction may be responsible for the onset or aggravation of CHF symptoms [6,7]. Chronic RV pacing may induce changes of ventricular volume, geometry and abnormal ventricular regional loading, thus favouring adverse remodelling and CHF [8]. RV pacing causes asynchronous activation of the LV, which may mimic the abnormal activation sequence of left bundle branch block, that is present in most patients currently receiving CRT [9]. In the case under discussion, CHF occurred 7 years following RV pacing and the patient received CRT for uncontrolled CHF symptoms with optimal medical management.
In the only randomised crossover study (on the clinical effect of BVP in patients with AF) between BVP and RV pacing, there were no significant differences between the two modes of therapy, when assessed in an intention to treat manner. However, in patients with effective therapy there was a small benefit of BVP, in terms of greater mean walking distance, decreased hospitalisations and increase in peak O2 uptake [10]. In the MUSTIC study, CRT benefit in 131 patients who were either in sinus rhythm or AF was examined. There was a similar degree of improvement in 6-min walking distance, O2 consumption, quality of life, NYHA class, LVEF and decrease in mitral regurgitation in both groups [10,11]. These data suggest that it may be useful to have CRT even in patients with AF. In our patient also, CRT improved the LVEF from 27% to 39% and the symptomatic status from NYHA class IV to II. Because of the rapid battery depletion due to the high pacing threshold on the LV lead, it was felt that CRT could not be maintained.
Pachon et al. in their study of 39 patients with dilated cardiomyopathy and indication for PPI for CHB found remarkable improvement in systolic, diastolic LV function together with reduction of QRS duration, when pacing was instituted simultaneously from the RV apex and RVOT [12]. Recently, the beneficial effects of dual site RV pacing (RVOT + RV apex) in a small group of patients, in whom CS lead implantation failed because of the technical difficulties during CRT, has been reported. The author speculated that the wide separation of the electrodes in the RV apex and RVOT at base, results in simultaneous activation of the apex and base. The proximal LV is activated by conduction of the electrical impulse through the thin part of the upper septum. This synchronous activation pattern of both ventricles may produce the similar clinical response to that of CRT [13]. In our patient, with dual site RV pacing (RVOT + RV apex) with intraventricular delay of 10 ms, the QRS was narrow (0.12 s) and the patient maintained symptomatic improvement with LVEF of 40%, similar to CRT at 12 weeks of follow-up. Pacing in the RVOT is usually associated with good capture threshold and R wave sensing as was found in this patient. This will improve the longevity of the PG.
In conclusion, we have presented the efficacy and difficulties of CRT in a patient with CHF and chronic AF who had long-term RV pacing for CHB and the benefits of dual site RV pacing as an alternative to CRT in the same patient at 12 weeks of follow-up.
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References |
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[1] Gregoratos G, Abrams J, Epstein AE, et al. ACC/AHA/NASPE 2002 guideline update for implantation of cardiac pacemakers and antiarrhythmia devices – summary article: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (ACC/AHA/NASPE committee to update the 1998 pacemaker guidelines). J Am Coll Cardiol 2002; 40: 1703–1719.
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[10] Leclercq C, Walker S, Linde C, et al. Comparative effects of permanent biventricular and right-univentricular pacing in heart failure patients with chronic atrial fibrillation. Eur Heart J 2002; 23: 1780–1787.
[11] 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: 111–118.
[12] Pachon JC, Pachon EI, Albornoz RN, et al. Ventricular endocardial right bifocal stimulation in the treatment of severe dilated cardiomyopathy heart failure with wide QRS. Pacing Clin Electrophysiol 2001; 24: 1369–1376.[CrossRef][Medline]
[13] Vlay SC. Alternate site biventricular pacing: Bi-V in the RV – is there a role? Pacing Clin Electrophysiol 2004; 27: 567–569.[CrossRef][Medline]
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