Defining the role of multiple RV/LV pacing sites
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1 Defining the role of multiple RV/LV pacing sites Yves Van Belle, MD, PhD Disclosures: None
2 Multisite RV/LV pacing Multisite RV-pacing Echo/hemodynamic data Clinical evidence Multisite LV-pacing Echo/hemodynamic data Clinical evidence Leipzig experience in optimizing CRT
3 Multisite pacing van Campen et al, pts, NYHA III-IV, QRS>120ms, LVEF <35% CRT-candidates Acute hemodynamic effects of 9 pacing configurations CI determined using Doppler Highest CI compared to baseline: >+10% = responder
4 AV-delay 100ms VDD-mode Echodoppler each configuration CI calculation TVI aortic valve
5 Van Campen et al, Heart 2006
6 14 patients responded better to other pacing sites compared to RVA-CSPL Van Campen et al, Heart 2006
7 Multisite RV-pacing Res et al., Europace 2007: BRIGHT-study Randomized multicentre trial: 9 centres NL 42 CRT-candidates Blind crossover study: RVA-pacing Bifocal RV-pacing Res et al, Europace 2007
8 Res et al, Europace 2007
9 Res et al, Europace 2007
10 Multisite RV-pacing vs BiVe Acute TDI BiVe superior to BiF for acute mechanical CRT Lane et al, Heart 2008
11 Multisite RV-pacing vs BiVe Clinical studies n Improvement BiF BiV BiF BiV O Donnell et al Rocha et al Malecka et al Scarce data suggests that BiF does improve clinical outcome, but less than BiV
12 Multisite LV CRT Acute haemodynamic data 21 pts, NYHA III-IV QRS 183±36ms Invasive haemodynamics Triangle pacing Yoshida et al, EHJ 2007
13 Yoshida et al, EHJ 2007
14 Multisite LV CRT Acute haemodynamic data 12 pts, NYHA III-IV QRS ms Invasive haemodynamics Comparing dual LV stimulation with single site CRT at best response Y-connector: unipolar single site, bipolar dual site LV B A Padeletti et al, AJC 2008
15 No additional value of dual LV-pacing at optimal AV-delay Padeletti et al, AJC 2008
16 Multisite LV CRT Clinical data Echo Clinical n EF ESV NYHA QRS VO2M 6MWD Bi 27 26±7 198±86 2,2±0,6 183±45 1,1±2,5 400±75 Lenaczyk (RETRO) Leclercq (PROSP, CROSS) Tri 27 36±8 147±64 1,4±0,5 150±34 2,9±3,1 388±80 p <0,001 <0,05 NS <0,05 <0,05 NS 431±10 Bi 27±11 157±69-155± Tri 35±13 134±75-171±20-401±91 p 0,001 0,02-0,01-0,06 HD RESPONSE +/+ CLIN RESPONSE +/-
17 Trials to watch Trial Exp. Comp. n Prim. Est. SEPTAL CRT Rand. Multic. Single LV Septal RV Single LV Apex RV 263 LVESV 6 months TRIV TRIAL Rand. Multic. Single LV Dual RV Single LV Apex RV 100 Safety 6 months V3 TRIAL Rand. Multic. Dual LV Apex RV Single LV Apex RV 84 Clinical Response 12 months TRUST CRT Rand. Single Dual LV Single RV Single LV Single RV 100 Clinical Response 6m FU?
18 Management in the Herzzentrum Leipzig 3D-Analyse of the LV-Leadposition 3D-Analyse of the latest contractionsite in the LV 3D-Optimisation of the VV-Delays Visualisation of the Contractionpattern without CRT & various VV-Delays (RT-3D-Echocardiography + ICD-programmer) Analysis of the ventricular contractionpattern without CRT & various VV-Delays (RT-3D-Echocardiographie + Manufacturer software) Visualisation & Reconstruction of the LV- Leadposition (non-invasive Rotational angiography) Fusion of both (EPre-Navigator Prototype Philips)
19
20 Case 74 yo Patient with DCM (1/8) Anamnese: DCM with implanted CRT-ICD 07 PAF : ECV 07 diffuse coronary sclerosis Renal insufficiency Prostate-Ca : Brachytherapie 06 Klinik: progressive Dyspnoe NYHA III despite CRT & optimal medical therapy Medikation: BB, ACE-I, Diuretics, Aldosteron-AT Allopurinol, Warfarin, OAD, Insuline CVRF: AHT, IDDM Typ II, Adipositas
21 Case 74 yo Patient with DCM (2/8) ECG: SR with VAT-Stimulation, LBBB QRS=140ms 80% V-stimulation (VES) Echocardiography: EF 28%, MI I LEDD 63mm, LVESD 51mm LVEDV 165ml, LVESV 118ml no interventricular asynchrony (deltapep 11ms) intraventricular asynchronie (SPWMD 158ms)
22 Case 74 yo Patient with DCM (3/8) 3D Reconstruction of the LV & LV-Leadposition Contractionpattern with CRToff / discordant Leadposition RAO LAO LL Early Contraction Late Contraction BullsEye-Analysis of Contractionpattern with VV-Delay Optimisation RV30 before RV only bivent LV only Simultaneous LV30 before = baseline inhibited
23 Case 74 yo Patient with DCM (4/8) RV 30ms before RV only Bivent Simultaneous LV only LV 30ms before baseline inhibited EF% SDI% 13,9 13,3 11,6 16,7 12,4 13,0 Conclusions and considerations Late contraction inferior + LV-Leadposition lateral = discordant leadposition despite VV-Delay-Optimisation not sufficient Resynchronisation Connection of a 2nd LV-Lead over a Y-Connector possible Visualisation of a inferior vein Implantation 2nd LV-Lead in inferior Vene
24 Case 74 yo Patient with DCM (5/8) 1. CS-Angiography
25 Case 74 yo Patient with DCM (5/8) RAO Inferior Vene 1. CS-Angiography
26 Case 74 yo Patient with DCM (5/8) 2. Implantation
27 Case 74 yo Patient with DCM (5/8) 1.LV-Lead RA-Lead RV-Lead LAO 2.LV-Lead 2. Implantation
28 Case 74 yo Patient with DCM (5/8) 3. Reconstruction
29 Case 74 yo Patient with DCM (5/8) LAO RV-Sonde 1.LV-Sonde 2.LV-Sonde 3. Reconstruction
30 Case 74 yo Patient with DCM (5/8)
31 Case 74 yo Patient with DCM (6/8) Invasive Diastolic BP Invasive Systolic BP inhibited LV only LV30 before bivent simultaneous RV30 before RV only mmhg Lead 2 Leads
32 Case 74 yo Patient with DCM (7/8) LV 30ms before: EF% 40, AI% 5,5 4. RT-3D-TEE & Analysis of the Contractionpattern with a 2nd LV-Lead
33 Case 74 yo Patient with DCM (8/8) Response after 3 Months
34 Analysis and Optimization of Cardiac Resynchronization Therapy Non-Responders using 3-dimensional Echocardiography and non-invasive Rotational Angiography B. Nitsche 1, F. Braunschweig 2, T. Gaspar 1, M. Döring 1, C. Eitel 1, S. Richter 1 U. Wetzel 1, C. Piorkowski 1, G. Hindricks 1 14 clinical non-responders to CRT (65y, NYHA III, LVEF 30%, DCM 80%), SR, 97% pacing Non-invasive rotational angiography: 3D model RV + LV lead position (Philips EPre-Navigator). Realtime 3D TEE: SLMA : intrinsic activation. LV contraction pattern + SDI: different VV-delay programming (intrinsic activation, VV-delay -30, 0, +30 ms, RV only and LV only stimulation). 3D models merged: anatomical landmarks along the RV lead (EPre-Navigator) 8/14 patients LV lead position discordant, in 4/14 partly concordant, 2/14 concordant with SLMA 10/14 patients VV-optimization: more synchronous 3D LV contraction. 4/14 patients with discordant LV lead position or largely extended SLMA : not improved by VVoptimization: second LV lead concordant with the SLMA 3 months: patients had improved in NYHA class (I class) LVEF (relative 10%) VO 2 max (30%) 6 min-walk-test (8%) BNP (4%)
35 Conclusions Bifocal RV if Biventricular no option Optimisation of AV and VV-delays Consider second LV lead if delay optimisation fails and if proven potential for stimulating SLMA through vein anatomy Role of baseline double LV-lead implantation to be determined by ongoing trials.
36
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