Advances in Cardiac Pacing Device Implantation

Citation
Asia-Pacific Cardiology 2007;1(1):60-1
DOI
https://doi.org/10.15420/apc.2007:1:1:60

The history of cardiac pacing device implantation began in 1958, when Seymour Furman utilised temporary transvenous pacing as therapy for complete heart block.1 Ake Senning implanted the first pacemaker as an asynchronous ventricular device2 in 1959. The indications for cardiac pacing therapy have been expanding to include patients with different heart rhythm disorders, including sinus node dysfunction, atrial tachyarrhythmias and heart failure with cardiac dyssynchrony.3–5

Deleterious Effects of Right Ventricular Apical Pacing

The right ventricular apex has been the conventional site for pacing lead implantation for reasons of stability and technical ease. Producing an iatrogenic left bundle branch block pattern, right ventricular apical (RVA) pacing is associated with deleterious histological, haemodynamic, mechanical and clinical consequences.6–11 Avoidance of RVA pacing may be accomplished by pacemaker programming techniques or special pacing algorithms in sinus node dysfunction. In patients with intact AV conduction, the percentage of ventricular pacing can be reduced to 19% with a pacing algorithm that allows the AV interval to extend beyond 300ms to promote intrinsic AV conduction.12 Another novel pacing mode-switching algorithm recently became available to further decrease the percentage of ventricular pacing in patients with sinus node dysfunction. During normal operation, the pacing mode remains atrial (AAIR) and the ventricular activity is monitored on a beat-to-beat basis to verify intact AV conduction. With persistent loss of AV conduction, the pacing mode switches temporarily to dual chamber (DDDR). The pacing mode switches back to AAIR as soon as intrinsic AV conduction returns. With this novel pacing algorithm, the cumulative percentage of ventricular pacing can be reduced to 4.1%.13

In AV block (AVB) patients who require a high percentage of RV pacing, avoidance of RVA pacing can be achieved only by pacing alternative ventricular sites. Various sites, including the right ventricular outflow tract (RVOT), right ventricular septum (RVS) and His Bundle and left ventricular and biventricular pacing have been studied, RVOT most extensively. A pooled analysis involving nine prospective studies assessing the haemodynamic effects of RVOT pacing in a total of 217 patients revealed a modest but significant benefit over RVA pacing with an odds ratio of 0.34.14 A study comparing RVA with RVOT pacing in 20 patients with atrial fibrillation and AV-junctional ablation showed that left ventricular systolic function was better preserved by RVOT pacing at 23-week follow-up with radionuclide ventriculogram assessment.15

In another randomised study, 24 patients with complete AVB without coronary artery disease and with normal left ventricular function were randomised to receive RVA or RVOT pacing.10 Interestingly, the regional wall motion abnormalities by radionuclide ventriculography (33 versus 83%) and left ventricular ejection fraction (47 versus 56%) all favoured RVOT over RVA pacing at 18 months but not six. This supports the concept of the time-dependent left ventricular remodelling effect of RVA pacing. However, with a short-term follow-up of three months, RVOT pacing did not improve quality of life compared with RVA pacing in a randomised study including 103 patients with heart failure, chronic atrial fibrillation and impaired left ventricular ejection fraction of <40%.16 The best alternative pacing site is yet to be determined.

Cardiac Pacing in Atrial Fibrillation

Atrial fibrillation (AF) may be prevented by cardiac pacing through different mechanisms: namely overdrive suppression of atrial ectopic beats, reduction of global atrial activation time and dispersion of refractoriness and suppression of compensatory pauses. Cardiac pacing for AF prevention can be delivered by special pacing algorithms or multisite/alternative-site atrial pacing. In a single-blind, randomised, controlled study, 319 patients with sick sinus syndrome and AF were randomised to DDDR pacing with a special algorithm on or off.17 The algorithm aims to maintain atrial pacing most of the time by increasing the pacing rate when the native rhythm emerges and periodically reduces the rate to search for intrinsic atrial activity. The AF burden was significantly lower at one, three and six months when the algorithm was turned on. Biatrial pacing can be delivered by pacing the left atrium through a lead in the coronary sinus (CS) and the right atrium simultaneously. In 86 patients with drug-refractory atrial tachyarrhythmias, P-wave duration was significantly reduced and 32.6% of patients were free from AF recurrence with biatrial pacing.18 However, the benefit of biatrial pacing on suppression of AF was not reproduced in the Synchronous Biatrial Pacing for Reduction of Paroxysmal Permanent AF (SYNBIPACE) study. Dual-site atrial pacing can be delivered by pacing the right atrial appendage and a region in the low interatrial septum (IAS) just outside the CS ostium. Twenty-two patients without pacemaker indication had AF recurrence despite sotalol, and underwent cross-over periods of 12 weeks with DDDR pacing and sotalol treatment or continuation of sotalol alone.19 Patients in the pacing group had a significant reduction of atrial ectopics, prolongation of time to first documented AF recurrence and a reduction in AF burden.

Alternative site atrial pacing can be achieved using the conventional screwin pacing lead at the low or high IAS. Leads can also be implanted using special tools such as a steerable stylets or sheaths.20 Forty-six patients with paroxysmal AF were randomised to right atrial appendage (RAA) or low IAS pacing.21 Low IAS pacing was superior to RAA pacing in AF burden reduction over a three-month period. In another study, 120 patients with sinus node dysfunction and paroxysmal AF were randomised to RAA or high IAS (Bachmann’s bundle) pacing.22 High IAS pacing significantly delayed the onset of permanent AF. Ongoing studies are being performed to define the potential benefits and clinical application of IAS pacing in AF prevention.

Cardiac Pacing in Heart Failure

In the past decade, cardiac resynchronisation therapy (CRT) has evolved as a new treatment modality for patients with heart failure and cardiac dyssynchrony. CRT can be delivered by atrial-synchronised biventricular pacing. Apart from implantation of a right atrial and a right ventricular lead in the conventional positions of RAA and RVA, an additional lead is implanted into one of the cardiac veins through the coronary sinus to pace the left ventricle. In a landmark study, 453 patients with moderate to severe heart failure symptoms and poor left ventricular ejection fraction (LVEF) of 35% or less and a QRS interval of 130ms or more were randomised to CRT or the control group.23 Patients in the CRT group experienced an improvement in the six-minute walk test, functional class, quality of life and LVEF. The mortality benefit of CRT in heart failure patients was subsequently confirmed by the Comparison of Medical Therapy, Pacing and Defibrillation Therapy in Heart Failure (COMPANION) and the Cardiac Resynchronisation Therapy in Heart Failure (CARE-HF) studies. The COMPANION study was a randomised, placebo-controlled trial24 in which 1,520 patients with New York Heart Association (NYHA) functional class III or IV heart failure due to ischaemic or dilated cardiomyopathy and QRS duration of >120ms were randomly assigned in a 1:2:2 ratio to optimal pharmacological therapy (OPT), CRT or CRT with defibrillator (CRT-D). Time to all-cause mortality was reduced by 24% with CRT and by 36% with CRT-D compared with OPT. In CARE-HF, 813 patients with NYHA functional class III and IV heart failure and cardiac dyssynchrony were randomised to receive CRT or medical therapy.25 A significant reduction in all-cause mortality was achieved in the CRT group. Despite the success of CRT in the treatment of patients with heart failure, around 20–30% of patients who receive CRT do not respond to the treatment.

More importantly, it has been estimated that fewer than half of patients with heart failure have a prolonged QRS duration (currently the index of cardiac dyssynchrony listed in treatment guidelines).26,27 Other novel implantable device therapies for heart failure are in development. Cardiac contractility modulating (CCM) signals are non-excitatory signals applied during the absolute refractory period using a pacemaker-like device. Acute studies carried out in animals and humans with heart failure suggest that CCM signals can enhance left ventricular contractility.28,29 In 23 patients with idiopathic or ischaemic cardiomyopathy and poor LVEF, CCM improved functional class, quality of life and LVEF.30

Implantable Device Monitoring

The presence of an implantable device offers a unique opportunity for the monitoring of a patient’s condition. Revelation of new or previously undiagnosed arrhythmias such as AF by the device may facilitate better patient management. Heart rate variability, which is a powerful predictor of the risk of death due to progressive heart failure,31 can also be monitored by some implantable devices. Intrathoracic impedance, which correlates with pulmonary capillary wedge pressure and fluid status, can be measured by some implantable devices. In 11 patients with a total of 26 hospitalisations due to worsening heart failure over a mean follow-up of 20 months, a decline in intrathoracic impedance preceded symptom onset by a mean lead time of 11.2 days.32 A multicentre, randomised, controlled study is being conducted to further explore the clinical benefits.

Future Perspectives

The optimal ventricular or atrial pacing sites will be further explored in ongoing and future studies. The simultaneous advances in the new delivery systems for pacing leads will facilitate the technical need for implanting a lead in an alternative site to the RVA or RAA. Novel electrical therapies for heart failure patients who are non-responders to CRT are being developed. As well as monitoring the physiological ‘result’ of fluid accumulation by intrathoracic impedance, haemodynamic parameters such as intracardiac pressures will be directly measured by future implantable devices.

References
  1. Furman S, Robinson G, The use of an intracardiac pacemaker in the correction of total heart block, Surg Forum, 1958;9:245.
  2. Senning A, Discussion, J Thoracic Surg, 1959;38:639.
  3. Gregoratos G, Abrams J, et al., ACC/AHA/NASPE 2002 guideline update for implantation of cardiac pacemakers and antiarrhythmias devices, 2002; available at: http://www.acc.org/clinical/guidelines/pacemaker/incorporated/index.htm
  4. Fuster V, et al., ACC/AHA/ESC guidelines for the management of patients with atrial fibrillation, JACC, 2006;48:149–246.
  5. Hunt SA, Abraham WT, Chin MH, et al., ACC/AHA guideline update for the diagnosis and management of chronic heart failure in the adult, JACC, 2005;46:1–82.
  6. Tanabe A, Mohri T, Ohga M, et al., The effects of pacinginduced left bundle branch block on left ventricular systolic and diastolic performances, Jpn Heart J, 1990;31:1372–7.
  7. Tantengco MVT, et al., Left ventricular dysfunction after long-term right ventricular apical pacing in the young, JACC, 2001;37:2093.
  8. Karpawich PP, Rabah R, Haas JE, Altered cardiac histology following apical right ventricular pacing in patients with congenital atrioventricular block, PACE, 1999;22:1372–7.
  9. Thambo JB, et al., Detrimental ventricular remodelling in patients with congenital complete heart block and chronic right ventricular apical pacing, Circulation, 2004;110:3766–72.
  10. Tse HF, Yu CM, Wong KK, et al., Functional abnormalities with permanent right ventricular pacing, JACC, 2002;40:1451–8.
  11. Tse HF, Lau CP, Long-term effect of right ventricular pacing on myocardial perfusion and function, JACC, 1997;29:744–9.
  12. Melzer C, Sowelam S, Sheldon TJ, et al., Reduction of right ventricular pacing in patients with sinus node dysfunction using an enhanced search AV algorithm, PACE, 2005;28:521–7.
  13. Sweeney MO, Ellenbogen KA, Casavant D, et al., Multicentre, prospective, randomised safety and efficacy study of a new atrial-based managed ventricular pacing mode (MVP) in dual chamber ICDs, J Cardiovasc Electrophysiol, 2005;16:1–7.
  14. De Cock CC, Giudici MC, Twisk JW, Comparsion of the haemodynamic effects of right ventricular outflow tract pacing with right ventricular apex pacing: A quantitative review, Europace, 2003;5:275–8.
  15. Bourke JP, Hawkins T, Keavey P, et al., Evolution of ventricular function during permanent pacing from either right ventricular apex or outflow tract following AV-junctional ablation for atrial fibrillation, Europace, 2002;4:218–19.
  16. Stambler BS, Ellenbogen KA, Zhang X, et al., Right ventricular outflow versus apical pacing in pacemaker patients with congestive heart failure and atrial fibrillation, J Cardiovasc Electrophysiol, 2003;14:1180–86.
  17. Carlson MD, Ip J, et al., A new pacemaker algorithm for the treatment of atrial fibrillation-results of the atrial dynamic overdrive pacing trial (ADOPT), JACC, 2003;42:627–33.
  18. D’Allonnes GR, et al., Long-term effects of biatrial synchronous pacing to prevent drug-refractory atrial tachyarrhythmia : a nineyear experience, J Cardiovasc Electrophysiol, 2000;11:1081–91.
  19. Lau CP, et al., Dual-site atrial pacing for atrial fibrillation in patients without bradycardia, Am J Cardiol, 2001;88:371–5.
  20. Manolis AS, Sousani E, Simeonidou E, et al., Alternate sites of permanent cardiac pacing: A randomised study of novel technology, Hellenic J Cardiol, 2004;45:147–51.
  21. Paeletti L, Pieragnoli P, et al., Randomised cross-over comparison of right atrial appendage pacing versus interatrial septum pacing for prevention of paroxysmal atrial fibrillation in patients with sinus bradycardia, Am Heart J, 2001;142:1047–55.
  22. Bailin SJ, Adler S, Giudici M, Prevention of chronic atrial fibrillation by pacing in the region of Bachmann’s bundle: results of a multicentre randomised trial, J Cardiovasc Electrophysiol, 2001;12:912–17.
  23. Abraham WT, et al., Cardiac resynchronisation in chronic heart failure, NEJM, 2002;346:1845–53.
  24. Bristow MR, et al., The comparison of medical therapy, pacing and defibrillation in heart failure investigators. Cardiac resynchronisation therapy with or without an implantable defibrillator in advanced chronic heart failure, NEJM, 2004;350:2140–50.
  25. Cleland J, et al., The effect of cardiac resynchronisation on morbidity and mortality in heart failure, NEJM, 2005;352:1539–49.
  26. Sandhu R, Bahler RC, Prevalence of QRS prolongation in a community hospital cohort of patients with heart failure and its relation to left ventricular systolic dysfunction, Am J Cardiol, 2004;93:244–6.
  27. Shenkman HJ, et al., Congestive heart failure and QRS duration: establishing prognosis study, Chest, 2002;122:528–34.
  28. Mohri S, He KL, Dickstein M, et al., Cardiac contractility modulation by electric currents applied during the refractory period, Am J Physiol Heart Circ Physiol, 2002;282:H1642–7.
  29. Pappone C, Rosanio S, et al., Cardiac contractility modulation by electric currents applied during the refractory period in patients with heart failure secondary to ischaemic or idiopathic dilated cardiomyopathy, Am J Cardiol, 2002;90:1307–13.
  30. Stix G, Borggrefe M, et al., Chronic electrical stimulation during the absolute refractory period of the myocardium improves severe heart failure, Eur Heart J, 2004;25:650–55.
  31. Nolan J, Batin PD, Andrews R, et al., Prospective study of heart rate variability and mortality in chronic heart failure. Results of the United Kingdom Heart Failure Evaluation and Assessment of Risk Trial (UK-Heart), Circulation, 1998;98:1510–16.
  32. Yu CM, et al., Device-based intrathoracic impedance correlates with fluid status and provides automated prediction of CHF hospitalisations, J Cardiac Failure, 2004;10(Suppl. 1):S113.