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Long Term Effects of RV Pacing

Long Term Effects of RV Pacing. Tehran Arrhythmia Center April 2006. To Pace or not to Pace?. Pacing the right ventricle. Deleterious Effects of RV Apical Pacing. Altered left ventricular electrical and mechanical activation Altered ventricular function Less work produced for given LVEDV

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Long Term Effects of RV Pacing

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  1. Long Term Effects of RV Pacing Tehran Arrhythmia Center April 2006

  2. To Pace or not to Pace? Pacing the right ventricle

  3. Deleterious Effects of RV Apical Pacing • Altered left ventricular electrical and mechanical activation • Altered ventricular function • Less work produced for given LVEDV • Delayed papillary muscle activation  Valvular insufficiency • Remodeling • Modified regional blood flow patterns • Increased oxygen consumption without increase in blood flow • 60% change in blood flow between early and later activated regions • Abnormal thickening of LV wall • Cellular disarray • Fibrosis (away from pacing lead location) • Fat deposition • Calcification • Mitochondrial abnormalities

  4. Altered left ventricular mechanical activation • Potential detrimental effect of RV apical pacing in the form of pacing-induced LV dyssynchrony secondary to the abnormal activation sequence • Pacing-induced abnormalities of myocardial blood flow • RV apical pacing alters LV papillary muscle function, changing the timing sequence of the mitral valve apparatus, thus causing MR.

  5. Altered LV Electrical Activation Pattern • Two break-out locations on LV endocardium • Inferior border of the mid-septum • Superior basal aspect of free wall • Latest activation • Base of the inferior posterior wall • Muscular conduction (less Purkinje fiber density) Normal Sinus Rhythm Right Ventricular Apical Pacing Cassidy DM, et al. Circ 1984;70:37-42 Vassallo JA, et al. JACC 1986;7:1228-33 • Single break-out location on LV endocardium • Similar to left bundle branch block • Latest activation • Similar to intrinsic • Inferioposterior base

  6. Apical Pacing Histopathology • Karpawich (1990) – PediatricCanine Model • LV myofibril disarray was found after 4 months of pacing from RV apex • 90 degree misalignment of adjacent fibers (stress related?) • Also noted appearance of prominent Purkinje cells in subendocardium, variable-sized mitochondria, and dystrophic calcification • Karpawich (1999) – Pediatric Patients • Myofibril hypertrophy, intracellular vacuolation, degenerative fibrosis, and fatty deposits in the LV after more than 3 years RV apical pacing • Independent of paced time, patient age, epi- or endocardial electrode placement, and mode • Adomain (1986) • Myofibril disarray was found in 75% of canine hearts after 3 months of pacing from RV apex • Greatest at base of left ventricular free wall 25X: Karpawich PP, et al. Am Heart J 1990;119:1077-83

  7. Clinical Studies of Adverse Effects of RV Pacing Pace,Vol.29, March 2006

  8. Clinical Studies of Adverse Effects of RV Pacing Heart Rhythm, Vol 2, No 2, January 2005

  9. Danish StudyOverview • Hypothesis: • In patients with SND, atrial pacing (AAI) will result in less atrial fibrillation, thromboembolism, heart failure and overall mortality than ventricular pacing (VVI). • Study Design: • Single center, prospective, randomization of patients referred for first pacemaker implant

  10. Danish Study Endpoints • Primary: • -Mortality • -Cardiovascular death • Secondary: -Atrial fibrillation -Thromboembolic events -Heart failure -AV block

  11. Danish StudyPatient Characteristics

  12. Danish StudyPatient Characteristics * P = 0.04, atrial versus ventricular group

  13. 1-0 0-8 Atrial pacing 0-6 p = 0.045 0-4 Ventricular pacing 0-2 0 0 2 4 6 8 10 Number of patients at risk during follow-up Atrial Ventricular Time (years) 110 115 102 103 97 96 92 91 86 85 82 80 59 56 38 29 13 12 Danish Study Overall survival by pacing mode Andersen H, et al. Lancet 1997; 350: 1210-16.

  14. 110 115 102 103 97 96 92 91 86 85 82 80 59 56 38 29 13 12 Danish Study Cardiovascular death by pacing mode 1-0 Atrial pacing 0-8 p = 0.0065 0-6 Cumulative survival Ventricular pacing 0-4 0-2 0 Time (years) 0 2 4 6 8 10 Number of patients at risk during follow-up Atrial Ventricular Andersen H, et al. Lancet 1997; 350: 1210-16.

  15. 1-0 Atrial pacing 0-8 0-6 p = 0.012 Proportion without AF 0-4 0-2 Ventricular pacing 0 0 2 4 6 8 10 Time (years) Number of patients at risk during follow-up Atrial Ventricular • 100 92 82 73 69 46 21 9 • 115 99 86 76 61 49 34 10 2 Danish Study Cumulative risk of PAF by pacing mode Andersen H, et al. Lancet 1997; 350: 1210-16.

  16. Atrial pacing 1-0 0-8 p = 0.004 0-6 Proportion without chronic AF 0-4 Ventricular pacing 0-2 0 8 6 10 2 4 0 Number of patients at risk during follow-up Atrial pacing Ventricular pacing Time (years) 110 102 96 91 80 74 49 26 10 115 102 92 84 75 65 41 18 5 Danish Study Cumulative risk of chronic AF by pacing mode Andersen H, et al. Lancet 1997; 350: 1210-16.

  17. 1,00 Atrial pacing p = 0.18 Ventricular pacing Survival without death from CHF ,80 ,60 0 4 2 6 10 8 Time (years) AAI: 110 102 97 92 86 82 59 38 13 VVI: 115 103 96 91 85 80 56 29 12 Danish Study Mortality as a result of CHF Andersen H, et al. Lancet 1997; 350: 1210-16.

  18. Danish Study CHF Analysis • NYHA classification was higher in the ventricular group vs. the atrial group (p=0.010) at long term follow up. • During follow up, NYHA class worsened in the ventricular group vs. the atrial group (p<0.005) • Mean dose of diuretics increased in the ventricular group vs. the atrial group (p=0.033)

  19. Danish StudyConclusions • In patients with SND, atrial pacing is associated with a significantly higher survival, less atrial fibrillation, fewer thromboembolic complications, and less heart failure compared to ventricular pacing.

  20. Canadian Trial of Physiologic PacingCTOPP

  21. CTOPP Study Overview • Hypothesis: • -Physiologic (DDDR or AAIR) pacing is superior to single-chamber (VVIR) pacing because it is associated with lower risks of atrial fibrillation, stroke, and death. • Study Design: • -32 Canadian centers • -Prospective, randomized

  22. CTOPP Study Endpoints • Primary: • -Stroke or death due to cardiovascular causes • Secondary: • -Death from any cause • -Atrial fibrillation • -Hospitalization for heart failure

  23. CTOPP Study Protocol Patients undergoing first IPG implant n=2,568 Ventricular-Based Pacing n = 1,474 Physiologic Pacing n = 1,094 • Follow for an average of 3 years and compare: • Stroke or death due to cardiovascular causes • Death from any cause • Atrial fibrillation • Hospitalization for HF

  24. CTOPP Cumulative Risk of Stroke or Cardiovascular Death 0.4 0.3 Ventricular pacing Cumulative Risk P = 0.33 0.2 Physiologic pacing 0.1 0 0 1 2 3 4 Years after Randomization No. at risk: Ventricular pacing 1474 1369 1259 847 366 Physiologic pacing 1094 1005 954 637 287 Connolly S et al. N Engl J Med 2000; 342: 1385-91.

  25. CTOPP Cumulative Risk of any AF 0.4 0.3 Cumulative Risk Ventricular pacing P = 0.05 0.2 Physiologic pacing 0.1 0 0 1 2 3 4 Years after Randomization No. at risk: Ventricular pacing 1474 1276 1127 731 303 Physiologic pacing 1094 936 857 559 250 Connolly S et al. N Engl J Med 2000; 342: 1385-91.

  26. CTOPP Cumulative Risk of Chronic AF 0.4 0.3 P = 0.016 Cumulative Risk Ventricular pacing 0.2 0.1 Physiologic pacing 0.0 0 1 2 3 4 Years Since Randomization Number V 1474 1317 1180 779 331 At Risk P 1094 975 906 601 269 Skanes A, et al. J Am Coll Cardiol 2001; 38: 167-72.

  27. CTOPPConclusions • Physiologic pacing (dual-chamber or atrial) provides little benefit over ventricular pacing for the prevention of stroke or death due to cardiovascular causes. • Physiologic pacing does provide a reduction in the relative risk of paroxysmal and persistent AF.

  28. A Mode Selection Trial MOST Sub-StudyEffect of Pacing Mode and Cumulative Percent Time Ventricular Paced on Heart Failure and Atrial Fibrillation in Patients with Sinus Node Dysfunction and Baseline QRS Duration <120 Milliseconds in MOST Michael O. Sweeney, Anne S. Hellkamp, Arnold J. Greenspon, Robert Mittleman, John McAnulty, Kenneth Ellenbogen, Roger Freedman, Kerry L. Lee, Gervasio A. Lamas, for the MOST Investigators Circulation 2003, in press

  29. MOST Sub-Study Background: • DDDR pacing preserves AV synchrony and reduces CHF compared to VVIR pacing in SND. • DDDR pacing results in prolonged QRS durations (QRSd) due to ventricular desynchronization. Hypothesis: • DDDR pacing often results in prolonged QRS duration (QRSd) due to ventricular desynchronization in patients with normal baseline QRSd and may increase risk of heart failure and atrial fibrillation. Sweeney MO, et al. Circulation 2003, in press

  30. MOST Sub-Study Methods: • Baseline QRSd obtained from 12-lead EKG prior to IPG implant in MOST (a 2,010 patient, 6-year randomized trial of DDDR vs. VVIR pacing in SND). • Cumulative % time ventricular paced was determined from stored pacemaker diagnostic data. • Baseline QRSd <120 ms was observed in 1332 patients; 702 were randomized to DDDR; 640 to VVIR. Sweeney MO, et al. Circulation 2003, in press

  31. MOST Sub-Study: Results • Cum%VP was greater in DDDR (90%) vs. VVIR (51%). • The rates of CHF hospitalization increased with Cum%VP: Sweeney MO, et al. Circulation 2003, in press

  32. MOST Sub-study:Risk of HFH Relative to a DDDR Patient with Cum % VP = 0 • Risk of HFH increased between 0% and 40% Cum VP, but was level at Cum%VP above 40%. • Risk can be reduced to about 2% if ventricular pacing is minimized. Sweeney MO, et al. Circulation 2003, in press

  33. MOST Sub-Study: Risk of HFH Relative to a VVIR Patient with Cum % VP = 0 • Risk of CHF was constant between 0% and 80% Cum VP and increased by as much as 2.5-fold when Cum%VP exceeded 80%. • Risk cannot be reduced regardless of minimization of ventricular pacing. Sweeney MO, et al. Circulation 2003, in press

  34. MOST Sub-Study P=0.047 Sweeney MO, et al. Circulation 2003, in press

  35. MOST Sub-Study P=0.0046 Sweeney MO, et al. Circulation 2003, in press

  36. MOST Sub-studyConclusions: CHF • Higher rates of CHF hospitalization were associated with higher Cum% VP: • - Cum % VP<10% was associated with the lowest rates of CHF hospitalization (DDDR 2%, VVIR 7%). • - Cum % VP >90% was associated with the highest rates of CHF hospitalization (DDDR 12%, VVIR 16%). • Ventricular pacing in the DDDR mode more than 40% confers a 3-fold increased risk of heart failure hospitalization but can be reduced to about 2% if ventricular pacing is minimized. Sweeney MO, et al. Circulation 2003, in press

  37. MOST Sub-study: AF Risk Risk of AF increases linearly with Cum%VP up to 80-85% in both DDDR and VVIR Sweeney MO, et al. Circulation 2003, in press

  38. MOST Sub-study: AF Risk Sweeney MO, et al. Circulation 2003, in press

  39. MOST Sub-study: AF Risk Sweeney MO, et al. Circulation 2003, in press

  40. MOST Sub-studyConclusions: AF • Relationship between risk of AF and Cum%VP was similar between pacing modes: • Risk of AF showed a linearly increasing relationship with increased Cum%VP from 0% pacing up to 80-85% pacing in both pacing modes. • Within this range, the risk of AF increased by 1% for each 1% increase in Cum%VP (DDDR hazard ratio 1.01 [1.004, 1.022] p=0.012; VVIR 1.01 [1.001, 1.01], p=0.025). Sweeney MO, et al. Circulation 2003, in press

  41. MOST Sub-Study:Overall Conclusions • The adverse effects of forced ventricular desynchronization probably explain the difficulty in demonstrating a mortality and stroke benefit with physiologic (DDDR) compared to ventricular (VVIR) pacing in randomized trials. • These investigators concluded that RV pacing imposes ventricular dyssynchrony even when AV synchrony is preserved, thereby increasing the risk of heart failure and AF. Sweeney MO, et al. Circulation 2003, in press

  42. Dual-Chamber and VVI Implantable Defibrillator TrialDAVID

  43. DAVID Trial Overview • Hypothesis: • - Aggressive management of LV dysfunction with optimized drug therapy and with dual chamber pacing could improve the combined endpoint of total mortality and hospitalization for heart failure, compared to similarly optimized drug therapy supported by ventricular backup pacing. • Study design: • - Single blind, multicenter, parallel group, randomized trial comparing DDDR (70 bpm lower rate) vs. VVI (40 bpm lower rate) pacing modes Wilkoff B, et al. JAMA. 2002; 288: 3115-3123.

  44. 506 randomized DAVID Trial Protocol 760 assessed for eligibility 250 excluded 149 Did not meet Rx criteria 55 refused 46 Other 510 eligible 4 Not randomized 2 Required pacing 1 Inadequate defibrillation threshold 1 Decided not to implant VVI-40 (n=256) DDDR-70 (n= 250) • 1 had pacing mode set to DDD • 1 LTF • 10 Discontinued intervention • 5 Bradycardia • 1 CHF and AF • 1 Brady induced Torsade • 1 Heart Tx workup • 1 AF w rapid V response • 1 multiple shocks due to double counting • 3 had pacing mode set to VVI • 2 LTF • 5 Discontinued intervention • 1 Angina • 1 CHF and Lead Failure • 1 CHF Hospitalization • 1 Exacerbation of VT • 1 Lead Migration Wilkoff B, et al. JAMA. 2002; 288: 3115-3123.

  45. VVI-40 DDDR-70 HR (p-value, adj.) CHF Hospitalization or Death 16.1% 26.7% 1.61 (p = 0.03) CHF Hospitalization 13.3% 22.6% 1.54 (p=0.07) Death 6.5% 10.1% 1.61 (p=0.15) DAVID Trial Results Wilkoff B, et al. JAMA. 2002; 288: 3115-3123.

  46. DAVID Wilkoff B, et al. JAMA. 2002; 288: 3115-3123.

  47. DAVID Conclusions • Bradycardia pacing operation in dual-chamber ICDs should be optimized for individual patients. • -RV pacing in patients with LV dysfunction and no bradycardia indication for pacing can be harmful. • -Programming of dual chamber devices to backup ventricular pacing is justified in this patient population. Wilkoff B, et al. JAMA. 2002; 288: 3115-3123.

  48. Left Ventricular-Based Cardiac Stimulation Post AV Nodal Ablation Evaluation(The PAVE Study) • The PAVE study was a prospective, patient-blinded, randomized, multicenter clinical trial comparing chronic biventricular to right ventricular pacing in patients with chronic atrial fibrillation undergoing AV node ablation.

  49. PAVE Study (J Cardiovasc Electrophysiol, Vol. 16, pp. 1160-1165, November 2005)

  50. PAVE Study • Ablation of the AV node was permitted up to 4 weeks post-implantation • Pacemaker was reprogrammed to a VVIR mode with a lower rate of 80 ppm for the next 4 weeks so to mitigate the risk of polymorphic ventricular tachycardia. All patients received rate-esponsive pacing, with the sensor optimized 4 weeks after implantation.

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