Two Years Living with the EHRA/HRS Consensus Document of VT Ablation: Need for an Update?

Transcription

1 Two Years Living with the EHRA/HRS Consensus Document of VT Ablation: Need for an Update? David Wilber MD Loyola University of Chicago Disclosures: Biosense / Webster: Consultant, Investigator; Boston Scientific: Consultant, Investigator,; CardioInsight: consultant, investigator, Medtronic: Consultant, Investigator; St Jude: Investigator; Siemens: Consultant, Investigator

2 OVERVIEW Idiopathic VT PVC ablation spectrum of sites of origin for idiopathic VA Role of imaging and ancillary mapping techniques Scar Related VT Evolving role of substrate ablation Mortality associated with VT and ICD shocks, role of early intervention New insights on nonischemic myopathy substrates and mechanisms

3 PVC-MEDIATED MYOPATHY Subtle hemodynamic abnormalities in pts with frequent PVCs and normal LV function Increased LVEDD Diastolic dysfunction Increased BNP Normalization of LV function in pts with frequent PVCs and reduced ejection fraction of unknown etiology in small series following pharmacologic suppression (Duffee et al, MCP 1998) or catheter ablation (Takemoto et al, JACC 2005; Yarlaggadda et al, Circulation 2005; Bogun et al, Heart Rhythm 2007; Taieb et al, JICE 2007). PVC frequency in reported cases typically > 10,000/24 hr; can occur with any site of origin

4 PVC-MEDIATED MYOPATHY Mechanism unknown Not tachycardia mediated myopathy (normal heart rates) Single PVCs associated with complex transient alternation in intracellular calcium and membrane ionic currents, heart rate dynamics, and myocardial and peripheral autonomic stimulation and inhibition; cumulative effects with frequent ectopy unknown Dysynchronous myocardial activation Prevalence, individual risk, and time course of development poorly understood Differentiation from primary cardiomyopathy problematic (? role for MRI) Similar phenomenon may occur in patients with scar related ventricular ectopy, further impairing LV function

5 PVC BURDEN AND LV FUNCTION 174 pts referred for ablation of PVCs 57 pts (33%) had LVEF < 50% Mean PVC burden LV dysfunction 33+13% Normal function, dilated LV 22+11% Normal function, normal LV 13+12% 146 pts (84%) had reduction of PVCs >80% 46/57 (81%) pts with LVD, normalization of function (n=45) or improvement > 15% (n=1) Baman, Bogun, Heart Rhythm 2010; 7:

6 LONG-TERM FOLLOW-UP OF FREQUENT PVCS 281 pts with frequent PVCs (>1000/24 hr) and no other heart disease 42 pts (15%) had LVD at baseline and underwent ablation Remaining 239 pts followed for 4-8 yrs (mean 5.6 yrs), baseline EF 64+7% Overall PVC frequency stable over time; changes in LV function noted after 4 years, primarily in pts with high baseline frequency (> 20,000/ 24 hr) 5% of study cohort developed > 6% decline in EF by end of study (20% of pts with > 20,000/24 hr Niwano et al, Heart 2009

7 SPECTRUM OF IDIOPATHIC VA (n=314) RV TACHYCARDIAS (54%) RVOT Pulmonary Artery PeriHis Tricuspid Annulus Other RV EPICARDIAL VT (10%) Anterior Interventricular vein Great cardiac vein Middle cardiac vein LV TACHYCARDIAS (34%) Fascicular Aortic Sinus of Valsalva LVOT endocardium / intramural Mitral Annulus Papillary muscle Other LV BUNDLE BRANCH REENRY (2%) LUMC 8/10

8 THE LEFT VENTRICULAR OSTIUM

9 ICE IMAGING OF OUTFLOW TRACT LCC

10 SOV VT: 3-D ICE IMAGING OF AORTA

11 RVOT septum LVOT septum RSOV LSOV AIV-GCV junction -30 ms -30 ms -52 ms -35 ms -10 ms PA SUPERIOR

12 VT adjacent to LFT 25 pts underwent ablation of focal peri-left fibrous trigone (LFT) tachycardia in the following distribution: Distal Great Cardiac Vein 4 pts Endocardial Peri-LFT 16 pts Intramural Peri-LFT 5 pts (3/5 via GCV) Intramural foci had similar EPI / ENDO activation times (within 20 ms) and had larger total RF applications to effect ablation Green et al, HRS Scientific Sessions 2010 The electrocardiogram did not easily discriminate site of successful ablation.

13 SUPERIOR VT ORIGINATING ADJACENT TO LFT PA AO LV RAO LAO PA AO PA AO PA PA AO LV LV

14 IDIOPATHIC PVCs FROM PAPILLARY MUSCLES Anterolateral 200 ms Posterior

15 IMAGING THE PAPILLARY MUSCLES

16 ABLATION OF PVCS FROM ANTEROLATERAL PM A-L PM LPO

17 EPI ENDO ABLATION AT THE BASE OF THE ALPM

18 IDIOPATHIC EPICARDIAL LVVT - perivascular sites of origin - catecholamine enhanced, adenosine sensitive - may account for 5-10% of idiopathic VT Anterior GCV Posterior CS AIV MCV Daniels et al, Circulation 2006

19 DETECTION OF EPICARDIAL ILVT ON SURFACE ECG MDI > % sensitivity, 93% specificity for epicardial origin (N=240, 2009)

20 Baseline VT Induction RB-SA 380 ms RB-SA 430 ms RB-SA 430 ms LB-SA 500 ms

21 Other induced VTs RB-SA CL 350? RB-RIA CL 310

22 CHALLENGES Frequent spontaneous shifts in VT morphology spontaneous or catheter induced terminations (during mapping or entrainment attempts) As procedure progressed, low dose isoproterenol needed to sustain VT

23 Sinus Rhythm Mapping LVV = 390 cc Scar Area = 165 cm2 RAO LAO INFERIOR

24 Widespread Diastolic Potentials

25 Pacemapping in sinus VT4: LBBB VT3:RBBB

26 RF DEPLOYMENT Total 28 min RF application

27 Outcome Programmed stimulation with 3VES to refractioriness from the RV septum and LV apex on isoproterenol resulted in only 3-5 beats of polymorphic VT No further VT in subsequent month on low dose amiodarone 200 mg alone

28 DE-MRI for Substrate Identification Wijnmaalen et al, Eur Heart J 2011; 32:

29 Is activation mapping with hemodynamic support preferable to substrate mapping for unstable VT? Preliminary data confirm feasibility and reasonable safety Cost, case complexity are issues No data as yet to suggest superior outcomes; need for randomized studies

30 ISSUES WITH CURRENT APPROACHES TO MANAGEMENT OF ICD SHOCKS Device programming may decrease number of overall appropriate shocks, but much less often eliminates them completely; inappropriate shocks remain problematic Shocks, particularly when frequent, decrease QOL Limitations of AAD Associated with significant risk of adverse events requiring discontinuation; may be associated with increased noncardiac mortality when used at higher doses. Slow VT rate and may increase DFT and pacing thresholds Little information on efficacy in setting of prior drug failure Little or no role in setting of incessant slow VT or electrical storm

31 AAD SUPPRESSION OF ICD SHOCKS 412 pts, secondary prevention ICD within 21 days Amiodarone discontinued 18% Sotalol discontinued 23% 302 pts, secondary prevention ICD within 3 mo Sotalol discontinued 23% Connolly et al. JAMA 2006; Pacifico et al. NEJM 1999; 340:

32 ADVERSE OUTCOME AFTER ICD THERAPY 20% isolated VT/VF 4% electrical storm HR for death (storm) First 3 mo: 18 (8-40) > 3 mo: 3.5 ( HR for death (isolated) 2.5 (1.5-4) Predictors of storm (MVA) Isolated VT/VF: 9 (4-21) Predictors of HF events ICD shock 1.9 ( ) Moss, Circulation 2004; 110: Sesselberg, Heart Rhythm 2007;4: Goldenberg, Circulation 2006: 113:

33 ICD SHOCKS AND MORTALITY 269/811 pts received at least 1 ICD shock (128 appropriate only, 87 inappropriate only, 54 both) 18% mortality in first year post shock, majority from HF 30% of deaths within 24 hours of shock Exclude deaths within 24 hrs Poole et al, NEJM 2008; 359:

34 ICD THERAPY TYPE AND MORTALITY 2135 pts in 4 studies evaluating ATP (PainFREE I and II, EMPIRIC, PREPARE) Mean EF 32%, CAD 71%, BB 68%, Class I or II 82%, primary prevention 67% 24% of pts received therapy (50% ATP only); 3934 VA episodes 20% increased risk of death / shocked episode VT frequency increased risk of death ATP treated VT or fast VT: 3% / episode Shocked fast VT: 31% / episode Shocked VF: 15% / episode Sweeney et al, Heart Rhythm 2010; 7:

35 ELECTRICAL STORM 10-40% of secondary prevention ICD patients, 3-5% of primary prevention, often on a background of chronic AAD therapy Cardiac mortality 30-50% at 2-3 yrs (Bansch JACC 2000, Exner Circulation 2001, Verma JCVE 2004, Gatzoulis Europace 2005) Ablation may have favorable impact on outcome 95 pts with ES CAD 76%, NIDCM 10% hypotension, shock 50 pts Acute outcome 68 (72%) no inducible VT 17 (18%) no clinical VT 10 (11%) clinical VTs induced Overall cardiac death 12% at mean 22 mo follow-up Carbucicchio et al, Circulation 2008; 117:

36 OUTCOME OF POSTMI VT ABLATION VT frequency reduced by 75% in 2/3 of pts The Multicenter Thermocool VT Ablation Trial One year mortality 18% Stevenson, Wilber, Natale et al, Circulation 2008, 118:

37 Substrate Mapping & Ablation in Sinus Rhythm to Halt Ventricular Tachycardia (SMASH VT) Trial Patients with recent ICD (within 6 mo) for secondary prevention (cardiac arrest, VT, syncope with inducible VT) and history of myocardial infarction Randomization to substrate ablation (N=64) or standard medical therapy (N=64) All pts received ACEI or ARB, ASA, and beta blockers Mean age 67+10, LVEF 32+9, FC III, IV 19% No procedure related deaths, major complications 5% No AAD permitted unless pt already receiving for supraventricular arrhythmia Reddy et al, NEJM 2007; 357:

38 Substrate Mapping & Ablation in Sinus Rhythm to Halt Ventricular Tachycardia (SMASH VT) Trial P = ICD Events (shocks+atp) All Cause Mortality Reddy et al, NEJM 2007; 357:

39 We need to consider earlier scar related VT ablation because. AAD have modest efficacy, particularly if shocks occur on preexisting drug therapy, and are associated with significant risk of adverse events Even a single or limited number of shocks predict increase risk of adverse cardiac events, including HF, electrical storm, and death Current techniques are applicable to all presentations, dramatically decrease the risk of therapies, and may completely eliminate VT in > 50% of pts Initial data suggest a more favorable response to ablation, with lower risk, when applied at an earlier stage of the disease BUT we need randomized trials to convince many

40 FREQUENCY OF EPICARDIAL SITES OF VT ORIGIN Structural heart disease Chagas Disease (30-40%) NIDCM (25-50%) Hypertrophic cardiomyopathy (up to 50%) ARVD (~ 30%) Post infarction VT (10%) Other ( Idiopathic LV aneurysm, sarcoid, noncompaction) Idiopathic ventricular tachycardia (5-10%)

41 IMAGING OF NIDCM SUBSTRATE 14/29 pts with NIDCM and VA had scar (endo 7, mid 5, epi 2) Correlated with voltage maps, and sites of successful VT ablation for endo and epi scar; arrhythmias associated with predominantly intramural scar not successfully ablated Absence of scar more common in pts with PVCs only Bogun et al, JACC 2009; 53:

42 Superior View INTRAMURAL ORIGIN OF VT IN NIDCM MVA Endo Sinus Voltage Endo VT Activation EGM at earliest site MVA Epi Sinus Voltage Epi VT Activation

43 Ablation at earliest endocardial site terminated VT after 15 sec, but could be easily reinduced Ablation at earliest epicardial site terminated VT within 5 sec. No further inducible VT

44 Epicardial Ablation in ARVC 13 pts with failed endocardial ablation LVA more extensive on epicardium (< 1 mv, cm2) than endocardium (<1.5 mv, cm2) Basal RV thickness > 10 mm in 6/13 pts 27 epicardial VTs targeted Epicardial VTs opposite normal myocardium in 10 pts (77%), opposite ineffective endocardial sites 11 pts (85%, closest distance between sites 4-16 mm) 11/13 (85%) had no inducible VT at the end of the procedure During mean follow-up of mo, 77% no recurrent VT Garcia et al, Circulation 2009; 120:

45 Garcia et al, Circulation 2009; 120:

46 COMBINED EPI/ENDO APPROACH LUMC Experience 8 pts (5 prior failed endo ablation) Mean age 39 (20-62), 4 F 2 pts with mildly abnormal LV function All pts with ICDs, multiple sks despite AAD, incessant in 3 RV endo and epicardial mapping in all, LV mapping in 2 RV epicardial LVA exceeded endo LVA in 7/8 No LV LVA Ablation with 3.5 mm IT, max power 50 W 20 VTs induced 7 eliminated by endocardial ablation alone 11 required epicardial ablation (7/8 pts required epi ablation) 1 VT (CL 240) could not be localized

47 27 year old woman with ARVD and multiple VTs, prior ICD, and incompletely successful endocardial VT ablation Endo Endo Epi VT Epi RAO Sinus LAO

48 Reddy VY, d Avila A, Dukkipati S, Neuzil P, Doshi SK, Dauber K, Wilber D Long-term outcome after combined epi-endo ablation of ventricular tachycardia related to arrhythmogenic right ventricular cardiomyopathy. HRS pts (71% prior failed endo ablation) meeting ITF criteria 40 VTs induced at baseline (mean CL ms) 38/40 VTs (95%) eliminated acutely Mean follow-up mo Single procedure success rate 88% (15/17 pts)

49 EPICARDIAL ABLATION IN HOCM 10 pts with HOCM and SMVT 80% epicardial scar, 60% endocardial scar, 10% no scar 3/5 pts with ablation during SMVT had termination on endocardium (1 surgical cryo) 4 additional pts had both endocardial and epicardial substrate ablation During mean f/u mo, 7/9 pts free of recurrent VT Dukkipati S R et al. Circ A and E 2011;4:

50

51 Dickfeld T et al. Circ Arrhythm Electrophysiol 2011;4:

52 Tian J et al. Circ Arrhythm Electrophysiol 2010;3: