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Procedural and clinical outcomes after catheter ablation of unstable ventricular tachycardia supported by a percutaneous left ventricular assist device Arash Aryana, MD,*† P. Gearoid O’Neill, MD,*† David Gregory, MPA,‡ Dennis Scotti, PhD, MBA,‡§ Sean Bailey, EPT,† Scott Brunton, BS,† Michael Chang, MD,*† André d’Avila, MD, PhD║ From the *Regional Cardiology Associates, Sacramento, California, †Mercy Heart & Vascular Institute, Sacramento, California, ‡Presscott Associates, a division of ParenteBeard, New York, New York, §Fairleigh Dickinson University, Teaneck, New Jersey, and ║Helmsley Cardiac Arrhythmia Service, Mount Sinai School of Medicine, New York, New York. BACKGROUND Hemodynamic support using percutaneous left ventricular assist devices (pLVADs) during catheter mapping and ablation of unstable ventricular tachycardia (VT) can provide effective end-organ perfusion. However, its effect on procedural and clinical outcomes remains unclear. OBJECTIVE To retrospectively evaluate the procedural and clinical outcomes after the catheter ablation of unstable VT with/without pLVAD support. METHODS Sixty-eight consecutive unstable, scar-mediated endocardial and/or epicardial VT ablation procedures performed in 63 patients were evaluated. During VT mapping/ablation, hemodynamic support was provided by intravenous inotropes with a pLVAD (n ¼ 34) or without a pLVAD (control; n ¼ 34). RESULTS Baseline patient characteristics were similar. VT was sustained longer with a pLVAD (27.4 ⫾ 18.7 minutes) than without a pLVAD (5.3 ⫾ 3.6 minutes) (P o .001). A higher number of VTs were terminated during ablation with a pLVAD (1.2 ⫾ 0.9 per procedure) than without a pLVAD (0.4 ⫾ 0.6 per procedure) (P o .001). Total radiofrequency ablation time was shorter with a pLVAD (53 ⫾ 30 minutes) than without a pLVAD (68 ⫾ 33 minutes) (P ¼ .022), but with similar procedural success rates (71% for both pLVAD and control groups; P ¼ 1.000). Although during 19 ⫾ 12 months of follow-up VT recurrence did not differ between pLVAD (26%) and control (41%)
Dr Aryana and Dr d’Avila have received speaker honoraria and Mr Gregory, Dr Scotti, and Dr d’Avila have received consulting fees from ABIOMED, Inc, the manufacturer of the percutaneous left ventricular assist device. Dr Aryana, Dr d’Avila, and Mr Bailey have received consulting fees and Dr Aryana, Dr d’Avila, and Dr O’Neill have received speaker honoraria from St Jude Medical, Inc, the manufacturer of an electroanatomic mapping system used in this study. Dr d’Avila has received consulting fees and speaker honoraria from Biosense Webster Inc, the manufacturer of the other electroanatomic mapping system used in this series. Address reprint requests and correspondence: Dr Arash Aryana, Regional Cardiology Associates and the Mercy Heart & Vascular Institute, 3941 J St, Suite #350, Sacramento, CA 95819. E-mail address: [email protected].
1547-5271/$-see front matter B 2014 Heart Rhythm Society. All rights reserved.
groups (P ¼ .305), the composite end point of 30-day rehospitalization, redo-VT ablation, recurrent implantable cardioverter-defibrillator therapies, and 3-month mortality was lower with a pLVAD (12%) than without a pLVAD (35%) (P ¼ .043). Q6 CONCLUSION In this nonrandomized retrospective study, catheter ablation of unstable VT supported by a pLVAD was associated with shorter ablation times and reduced hospital length of stay. While pLVAD support did not affect VT recurrence, it was associated with a lower composite end point of 30-day rehospitalization, redo-VT ablation, recurrent implantable cardioverter-defibrillator therapies, and 3-month mortality. KEYWORDS Catheter ablation; Hospital length of stay; Ischemic cardiomyopathy; Non–ischemic cardiomyopathy; Percutaneous left ventricular assist device; Ventricular tachycardia ABBREVIATIONS EMI ¼ electromagnetic interference; IABP ¼ intra-aortic balloon pump; ICD ¼ implantable cardioverterdefibrillator; ICM ¼ ischemic cardiomyopathy; LOS ¼ length of stay; non-ICM ¼ non–ischemic cardiomyopathy; pLVAD ¼ percutaneous left ventricular assist device; SctO2 ¼ cerebral tissue oxygen saturation; VT ¼ ventricular tachycardia (Heart Rhythm 2014;0:-1–9) rights reserved.
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2014 Heart Rhythm Society. All
Introduction Scar-mediated ventricular tachycardias (VTs) are often hemodynamically unstable,1 limiting detailed entrainment and activation mapping to guide catheter ablation.2 Instead, substrate-based modification is commonly used, which involves targeting the arrhythmogenic substrates in sinus rhythm.3–5 Yet in some patients, particularly in those with non–ischemic cardiomyopathy (non-ICM), mapping of lowvoltage areas does not always exhibit fractionated and/or late potentials, such that a clear substrate cannot be identified.6 http://dx.doi.org/10.1016/j.hrthm.2014.04.018
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Under these circumstances, mapping during tachycardia seems more attractive but can often only be performed given sufficient hemodynamic support. In addition, in those with significant left ventricular (LV) dysfunction, prolonged episodes of sustained VT can sometimes lead to exacerbation of heart and/or renal failure even in the setting of a hemodynamically tolerated arrhythmia, affecting patient morbidity and clinical outcomes.7 Hence, it is conceivable that such patients may benefit from hemodynamic support during catheter mapping and ablation of VT. While vasoactive drugs and intra-aortic balloon pumps (IABPs) are most commonly used for hemodynamic stabilization, frequently in the setting of unstable VT they provide insufficient support. Specifically, low systolic blood pressure and tachycardia can significantly impair IABP performance.8 In contrast, percutaneous left ventricular assist devices (pLVADs) are less susceptible to such variables and generally capable of providing greater hemodynamic stability and end-organ perfusion in the setting of unstable VT.9 Theoretically, LV unloading by pLVADs may also minimize periprocedural heart failure. However, it remains unclear whether pLVAD support during VT mapping/ablation can significantly affect the short- and long-term clinical outcomes. Here, we report a retrospective, nonrandomized analysis of the procedural and clinical outcomes after catheter ablation of unstable, scar-mediated VT with/without hemodynamic support provided by an impeller-driven axial flow pump (pLVAD) as compared with a standard-of-care control group.
Methods Study population We retrospectively evaluated a total of 68 consecutive catheter ablation procedures performed for the treatment of scar-mediated hemodynamically unstable VT (defined as a mean arterial blood pressure of r50 mm Hg and/or requiring internal/external defibrillation) in 63 patients with structural heart disease by using an endocardial/epicardial approach. The procedures were performed by 2 operators at a single center (Mercy General Hospital, Sacramento, CA) with/without a pLVAD, whenever available. Data were obtained from reviewing medical/hospital records.
Data analysis Five groups/subgroups of patients were analyzed: (1) the entire cohort (n ¼ 68); (2) cases performed with and without pLVADs (control); (3) patients with ischemic cardiomyopathy (ICM; n ¼ 36) and non-ICM (n ¼ 32); (4) patients with ICM in the pLVAD group (ICM-pLVAD group; n ¼ 18), patients with ICM in the control group (ICM-control group; n ¼ 18), patients with non-ICM in the pLVAD group (nonICM-pLVAD group; n ¼ 16), and patients with non-ICM in the control group (non-ICM-control group; n ¼ 16); and (5) cases performed with IABPs (n ¼ 12) vs control. The primary end point was defined as VT recurrence during follow-up. The secondary composite end point consisted of
Heart Rhythm, Vol 0, No 0, Month 2014 30-day rehospitalization, redo-VT ablation, recurrent implantable cardioverter-defibrillator (ICD) therapies (both shocks and antitachycardia pacing), and 3-month mortality. These end points were not predefined but were ascribed after data collection. All patients had a preexisting ICD or a cardiac resynchronization therapy-defibrillator at the time of ablation. VT recurrence and ICD therapies were examined throughout follow-up through serial ICD/cardiac resynchronization therapy-defibrillator interrogations.
Procedural details All procedures were performed under general anesthesia. During VT mapping/ablation, all patients received inotropic support with intravenous dobutamine or dopamine (2–20 μg/ (kg min)) and repeated boluses of phenylephrine (100 μg) with/without a pLVAD. Although not considered standard practice, we prefer the use of inotropic agents to provide hemodynamic support under general anesthesia during VT mapping. In addition to the conventional markers of hemodynamic stability, cerebral oximetry (ie, cerebral tissue oxygen saturation [SctO2]) was monitored (Figure 1) using a cerebral oximeter (INVOS, Covidien, Mansfield, MA), as described previously.10 SctO2 has been shown to represent a sensitive indicator of cerebral hypoxia and end-organ perfusion.11 SctO2 was measured at baseline and throughout the procedure on 100% fraction of inspired oxygen. During VT, a lower limit of 20%–25% of the preanesthesia induction value was allowed.11
Cardiac assist devices A 12/13-F pLVAD (Impella 2.5/Impella CP, ABIOMED, Inc, Danvers, MA) was inserted after systemic anticoagulation (target activated clotting time Z250 seconds). The pLVAD was positioned inside the LV in a retrograde transaortic fashion via a 13/14-F introducer sheath through the femoral artery. A maximum performance level of 9 (50,000 rpm, up to 2.5 L/min [Impella 2.5] or 3.8 L/min [Impella CP]) was maintained throughout the procedure unless electromagnetic interference (EMI) necessitated temporary adjustments. As previously described by Miller et al,10 this may occur with the use of a magnetic-based mapping system. The severity of EMI depends on the Impella performance level and the mapping catheter distance from the motor.10 To overcome this, the pLVAD performance was reduced to P2 (usually required only when mapping within the outflow tract endocardially or at the base of the heart epicardially10). The Impella CP seems to be associated with a smaller degree of EMI, possibly owing to improved insulation of the motor. All venous/arterial sheaths and pLVADs were inserted electively at the onset of the procedure and weaned/removed before discharge from the electrophysiology laboratory by the cardiac electrophysiologist operator. For closure of the pLVAD arteriotomy site, the preclose technique (using 2 Perclose ProGlide devices, Abbott Laboratories, Abbott Park, IL) was used.12
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100
Induction of unstable VT (without pLVAD)
90
Induction of unstable VT (with pLVAD)
80 SctO2 (%)
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pLVAD Support During VT Ablation
70 60 50 40 30 0
5
10
15
20
25
30
35
40
Time (min)
Figure 1 Noninvasive SctO2 monitoring. Continuous SctO2 recording during VT mapping in a patient with ICM and left ventricular ejection fraction of 30%. As seen, in the absence of pLVAD support, SctO2 rapidly decreases to o50% within 5 minutes after the induction of unstable VT (cycle length 343 ms). Yet, when the same VT is later induced with pLVAD support, SctO2 is sufficiently maintained for Z15 minutes with a decrease of only o20% in the SctO2 from baseline. ICM ¼ ischemic cardiomyopathy; pLVAD ¼ percutaneous left ventricular assist device; SctO2 ¼ cerebral tissue oxygen saturation; VT ¼ ventricular tachycardia.
Electrophysiology study and ablation Diagnostic electrophysiology catheters were positioned using the conventional approach, including a phased-array intracardiac echocardiography catheter (ViewFlex PLUS, St Jude Medical, Inc, St Paul, MN). Electroanatomic mapping was performed using either a hybrid magnetic/impedancebased system (CARTO 3, Biosense Webster Inc, Diamond Bar, CA) in 61 procedures or an impedance-based system (EnSite NavX, St Jude Medical, Inc) in 7 cases. A 3.5-mmtip open-irrigated ablation catheter (NaviStar/Celsius ThermoCool, Biosense Webster, Inc) was used during all procedures. To minimize high-frequency noise that can sometimes be recorded when the mapping/recording catheter is adjacent to the pLVAD motor, endocardial LV mapping was preferentially performed via a transseptal approach using an 8.5-F steerable introducer (Agilis, St Jude Medical, Inc) in pLVAD cases. RV mapping/ablation was performed via an 8.5-F Mullins-style sheath (Fast-Cath Transseptal Guiding Introducer, St Jude Medical, Inc). The target activated clotting time was 300–350 seconds during endocardial mapping/ablation. Epicardial puncture, mapping/ ablation were performed via a percutaneous subxyphoid approach.13 Epicardial mapping/ablation was performed via an 8.5-F steerable epicardial introducer (Agilis NxT, St Jude Medical, Inc) in all patients. Electrophysiology testing and radiofrequency catheter ablation were performed using the standard approach. Whenever possible, entrainment/activation mapping was attempted. During all pLVAD cases, detailed entrainment mapping and at least partial activation mapping were performed. In contrast to control cases during which extensive entrainment/activation mapping could not always be completed, in several pLVAD cases complete VT activation maps were created (Figure 2). Pace mapping and substrate-based modification were performed in both groups to varying degrees. The number of VTs induced during each
procedure was recorded as well as the number of VTs terminated during ablation. Procedural success was defined as noninducibility of any sustained monomorphic VT with programmed electrical stimulation using triple extrastimuli.
Laboratory analysis In all patients, routine laboratory tests including serum creatinine, blood urea nitrogen, and glomerular filtration rate were recorded at baseline and at hospital discharge. The maximum change (Δ) in serum creatinine, blood urea nitrogen, and glomerular filtration rate after ablation were also recorded. Arterial lactate levels immediately after the procedure were measured in all cases as well as a brain natriuretic peptide within 24 hours of ablation in 42 of 62 cases. A baseline value was not always available for comparison.
Statistical analysis Statistical analysis was performed to examine the differences between groups in baseline characteristics, procedural parameters, and end point variables. Intergroup differences for normally distributed continuous variables were tested using the Student t test. When significant departures from normality were detected, differential comparisons were performed using the Mann-Whitney U test. Whenever necessary, log transformations were performed to address data distribution anomalies identified by standard SPSS diagnostic tests. Differences between categorical variables were assessed using the Pearson’s chi-squared test or Fisher exact test, as appropriate. Statistical calculations were performed using SPSS Version 20 (IBM SPSS Statistics, Chicago, IL). All statistical analyses were 2-tailed, and a P value of o.05 was considered statistically significant.
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Heart Rhythm, Vol 0, No 0, Month 2014
Figure 2 Activation and entrainment mapping during unstable VT with pLVAD support. An electroanatomic activation map (A) and a voltage map (B) of the LV constructed during unstable VT (cycle length: 355 ms) with pLVAD support in a patient with ICM and a large anterior-apical LV scar. The entire VT cycle length was mapped. The white arrow shows the direction of VT propagation. The small insets in panel A represent the sequence of intracardiac electrograms as they traverse through electrical diastole. The red arrow points to the site of VT entrainment (C). At this site, entrainment yielded a postpacing interval (PPI) equal to the tachycardia cycle length. D: The 12-lead electrocardiographic morphology during overdrive pacing of the VT demonstrating concealed fusion. E: Radiofrequency applications delivered to this site terminated the VT. However, a second tachycardia with a slightly different morphology and a longer cycle length (395 ms) was subsequently inducible. Additional radiofrequency applications in the same region ultimately rendered both VTs non-reinducible. CT ¼ cycle length; ICM ¼ ischemic cardiomyopathy; LV ¼ left ventricular; pLVAD ¼ percutaneous left ventricular assist device; VT ¼ ventricular tachycardia.
Results Baseline patient characteristics were similar (Table 1), and there were no differences between ICM-pLVAD and ICMcontrol groups and between non-ICM-pLVAD and nonICM-control groups. Similarly, procedural and clinical characteristics did not differ between the groups and there were no differences in pre- and postablation laboratory values (Table 2). However, unstable VT was sustained longer with a pLVAD than without a pLVAD in all the groups/subgroups (Table 3). VT was sustained for Z20 minutes in 44% of the pLVAD group vs 3% of the control
group. In addition, a greater number of VTs were terminated during radiofrequency ablation with a pLVAD than without a pLVAD in all the groups/subgroups. Total radiofrequency ablation time was shorter in pLVAD group vs control group and in ICM-pLVAD group vs ICM-control group, but did not differ among ICM-pLVAD, non-ICM-pLVAD, and nonICM-control groups. There were no differences in procedural success rate among the pLVAD and control groups/subgroups (Figure 3A). However, procedural success was higher in patients with ICM (89%) than in patients with non-ICM (53%) (P ¼ .001).
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Table 1
pLVAD Support During VT Ablation
5
Baseline patient characteristics
Characteristic Clinical Age (y) Sex: male Hypertension Diabetes mellitus Chronic kidney disease Cardiac disease substrate Ischemic Coronary artery bypass graft Percutaneous coronary intervention Nonischemic Dilated Arrhythmogenic RV dysplasia Sarcoid Chagasic Hypertrophic cardiomyopathy Congenital heart disease LV ejection fraction (%) Heart failure NYHA class I-II III-IV VT/electrical storm Cardiac arrhythmia device ICD CRT-D Antiarrhythmic therapy Amiodarone Mexiletine Sotalol
All patients (N ¼ 68)
pLVAD group (n ¼ 34)
Control group (n ¼ 34)
P
66 ⫾ 12 60 (88) 46 (68) 28 (41) 39 (57)
64 ⫾ 12 28 (82) 23 (68) 16 (47) 21 (62)
67 ⫾ 12 32 (94) 23 (68) 12 (35) 18 (53)
.112 .259 1.000 .460 .624
36 (53) 19 (28) 22 (32) 32 (47) 23 (34) 3 (4) 3 (4) 1 (1) 1 (1) 1 (1) 32 ⫾ 10
18 (53) 10 (29) 11 (32) 16 (47) 13 (38) 0 (0) 2 (6) 1 (3) 0 (0) 0 (0) 30 ⫾ 11
18 (53) 9 (26) 11 (32) 16 (47) 10 (29) 3 (9) 1 (3) 0 (0) 1 (3) 1 (3) 34 ⫾ 9
1.000 1.000 1.000 1.000 .609 .239 1.000 1.000 1.000 1.000 .178
32 (47) 36 (53) 23 (34)
13 (38) 21 (62) 12 (35)
19 (56) 15 (44) 11 (32)
.224 .224 1.000
47 (69) 21 (31)
22 (65) 12 (35)
25 (74) 9 (26)
.600 .600
63 (93) 8 (12) 8 (12)
32 (94) 5 (15) 3 (9)
31 (91) 3 (9) 5 (15)
1.000 .709 .709
Values are presented as mean ⫾ SD or as n (%). CRT-D ¼ cardiac resynchronization therapy-defibrillator; ICD ¼ implantable cardioverter-defibrillator; LV ¼ left ventricular; NYHA ¼ New York Heart Association; pLVAD ¼ percutaneous left ventricular assist device; RV ¼ right ventricular; VT ¼ ventricular tachycardia.
Table 2
Procedural and laboratory characteristics
Characteristic Mapping LV endocardial Epicardial, percutaneous RV endocardial No. of induced VTs VT cycle length (ms) Time Procedure (min) Fluoroscopy (min) Serum laboratory Preablation Creatinine (mg/dL) BUN (mg/dL) GFR (mL/min) Postablation Creatinine—maximum change (mg/dL) Creatinine at discharge (mg/dL) BUN—maximum change (mg/dL) BUN at discharge (mg/dL) GFR—maximum change (mL/min) GFR at discharge (mL/min) Lactate (mmol/L) Brain natriuretic peptide (pg/mL)*
All patients (N ¼ 68)
pLVAD group (n ¼ 34)
Control group (n ¼ 34)
P
67 (99) 25 (37) 11 (16) 3.1 ⫾ 1.4 367 ⫾ 69
34 (100) 13 (38) 3 (9) 3.4 ⫾ 1.9 359 ⫾ 70
33 (97) 12 (35) 8 (24) 2.8 ⫾ 0.8 374 ⫾ 69
1.000 1.000 .186 .083 .344
338 ⫾ 67 28 ⫾ 11
345 ⫾ 81 29 ⫾ 12
331 ⫾ 49 27 ⫾ 9
.466 .906
1.5 ⫾ 1.2 26 ⫾ 14 62 ⫾ 27
1.6 ⫾ 1.6 27 ⫾ 13 61 ⫾ 30
1.3 ⫾ 0.5 24 ⫾ 15 62 ⫾ 23
.882 .102 .633
0.3 ⫾ 1.5 ⫾ 6⫾ 28 ⫾ 6 ⫾ 62 ⫾ 1.5 ⫾ 420 ⫾
0.2 ⫾ 1.6 ⫾ 5⫾ 29 ⫾ 5 ⫾ 62 ⫾ 1.5 ⫾ 398 ⫾
0.3 ⫾ 1.4 ⫾ 7⫾ 27 ⫾ 7 ⫾ 63 ⫾ 1.6 ⫾ 469 ⫾
.101 .582 .349 .382 .223 .670 .738 .276
0.5 1.2 11 16 12 30 0.5 313
0.3 1.5 11 16 11 33 0.5 317
0.7 0.7 11 17 12 26 0.5 308
Values are presented as mean ⫾ SD or as n (%). BUN ¼ blood urea nitrogen; GFR ¼ glomerular filtration rate; LV ¼ left ventricular; pLVAD ¼ percutaneous left ventricular assist device; RV ¼ right ventricular; VT ¼ ventricular tachycardia. * Data are available in only 42 of 68 (62%) patients.
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Table 3
Heart Rhythm, Vol 0, No 0, Month 2014 Procedural and clinical outcomes: pLVAD group vs control group
Outcome Procedural Maximum time in unstable VT (min) All patients (N ¼ 68) Patients with ICM (n ¼ 36) Patients with non-ICM (n ¼ 32) No. of VT terminations duringablation per procedure All patients (N ¼ 68) Patients with ICM (n ¼ 36) Patients with non-ICM (n ¼ 32) Total radiofrequency ablation time (min) All patients (N ¼ 68) Patients with ICM (n ¼ 36) Patients with non-ICM (n ¼ 32) Clinical Hospital LOS (d) All patients (N ¼ 68) Patients with ICM (n ¼ 36) Patients with non-ICM (n ¼ 32) 30-day rehospitalization All patients (N ¼ 68) Patients with ICM (n ¼ 36) Patients with non-ICM (n ¼ 32) Redo-VT ablation All patients (N ¼ 68) Patients with ICM (n ¼ 36) Patients with non-ICM (n ¼ 32) Recurrent ICD therapies All patients (N ¼ 68) Patients with ICM (n ¼ 36) Patients with non-ICM (n ¼ 32) 3-mo mortality All patients (N ¼ 68) Patients with ICM (n ¼ 36) Patients with non-ICM (n ¼ 32)
pLVAD group (n ¼ 34)
Control group (n ¼ 34)
P
27.4 ⫾ 18.7 28.8 ⫾ 24.8 26.4 ⫾ 13.3
5.3 ⫾ 3.6 5.5 ⫾ 3.5 5.1 ⫾ 3.9
o.001* .012* o.001*
1.2 ⫾ 0.9 1.3 ⫾ 1.2 1.1 ⫾ 0.6
0.4 ⫾ 0.6 0.4 ⫾ 0.6 0.3 ⫾ 0.5
o.001* .025* .005*
53 ⫾ 30 56 ⫾ 32 50 ⫾ 28
68 ⫾ 33 82 ⫾ 35 51 ⫾ 19
.022* .004* .914
4.1 ⫾ 3.0 3.6 ⫾ 2.4 4.7 ⫾ 3.6
5.4 ⫾ 3.1 6.5 ⫾ 3.7 4.1 ⫾ 1.6
.013* .004* .682
2 (6) 2 (11) 0 (0)
3 (9) 1 (6) 2 (13)
1.000 1.000 .484
1 (3) 0 (0) 1 (6)
6 (18) 2 (11) 4 (25)
.105 .486 .333
1 (3) 0 (0) 1 (6)
7 (21) 2 (11) 5 (31)
.054 .486 .172
0 (0) 0 (0) 0 (0)
2 (6) 2 (11) 0 (0)
.493 .486 1.000
Values are presented as mean ⫾ SD or as n (%). ICD ¼ implantable cardioverter-defibrillator; ICM ¼ ischemic cardiomyopathy; LOS ¼ length of stay; non-ICM ¼ non–ischemic cardiomyopathy; pLVAD ¼ percutaneous left ventricular assist device; VT ¼ ventricular tachycardia. * Significant P value.
Clinical outcomes Two (6%) major complications occurred in the pLVAD group and none in the control group (P ¼ .493). One patient in the pLVAD group developed a femoral arterial laceration related to the insertion of the 13-F introducer, requiring surgical repair. Another patient in the pLVAD group developed cardiac tamponade during epicardial mapping owing to transection of the distal posterior descending coronary artery by the epicardial introducer. The pLVAD was not considered a cause of this complication. This patient was treated with emergent pericardiocentesis and eventually required surgical repair of the lacerated artery. The hospital length of stay (LOS) was shorter in pLVAD group vs control group and in ICM-pLVAD group vs ICMcontrol group, but did not differ between non-ICM-pLVAD and non-ICM-control groups (Table 3). In addition, the pLVAD was associated with 3 fewer intensive care unit days after the procedure. Thirty-day mortality was zero. During a follow-up period of 19 ⫾ 12 months, the primary end point
of VT recurrence did not differ among the groups/subgroups (Figure 3B). However, VT recurrence was overall lower in patients with ICM (19%) than in patients with non-ICM (50%) (P ¼ .011). There was a trend toward fewer recurrent ICD therapies with a pLVAD than without a pLVAD (Table 3), with no discernible differences in 30-day rehospitalization, redo-VT ablation, and 3-month mortality among the pLVAD and control groups/subgroups. Yet, the secondary composite end point of 30-day rehospitalization, redoVT ablation, recurrent ICD therapies, and 3-month mortality was significantly lower in pLVAD group vs control group (Figure 3C), with a similar trend observed when comparing the non-ICM-pLVAD group with the non-ICMcontrol group.
Discussion The majority of VTs in patients with structural heart disease are hemodynamically unstable, precluding detailed
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pLVAD Support During VT Ablation
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Principal findings
Figure 3 Procedural and clinical outcomes. A: The procedural success rates did not differ among the pLVAD and control groups/subgroups. B: The primary end point of VT recurrence did not differ among the pLVAD and control groups/subgroups. C: The secondary composite end point of 30-day rehospitalization, redo-VT ablation, recurrent ICD therapies, and 3-month mortality was lower with the pLVAD in all patients, with a similar trend observed in those with non-ICM. *Significant P value. ICD ¼ implantable cardioverter-defibrillator; ICM ¼ ischemic cardiomyopathy; non-ICM ¼ non–ischemic cardiomyopathy; pLVAD ¼ percutaneous left ventricular assist device; VT ¼ ventricular tachycardia.
entrainment/activation mapping during catheter ablation.1,2 Moreover, even in those with well-tolerated VT, the success of the procedure can be mitigated by acute heart failure owing to prolonged episodes of sustained VT and intravascular expansion, resulting in increased morbidity and mortality.14 Thus, there has been a growing interest in the use of cardiac assist devices during mapping/ablation of unstable VT.9,10,15–18 In this study, we investigated the effect of pLVAD support during catheter ablation of unstable scarmediated VT on procedural and clinical outcomes.
Improved hemodynamic support provided by the pLVAD in this cohort permitted significantly longer intervals during which unstable VT was sustained, which in turn allowed more detailed entrainment/activation mapping, ultimately yielding a greater number of VT terminations. However, this did not affect the procedural success or VT recurrence during follow-up. In addition, the use of the pLVAD was not associated with an increase in periprocedural adverse events. Nor did its use prohibit successful VT mapping/ablation due to EMI with the magnetic-based mapping system during any of the cases. These observations are generally consistent with prior reports.9,17,18 Yet, several findings from this study are noteworthy. First, total ablation time was shorter with a pLVAD than without a pLVAD. This may be explained through fundamental differences between the 2 ablation strategies. That is, the principal approach adopted in the pLVAD arm involved detailed VT mapping to guide ablation. Although the predominant approach used in the control arm consisted of limited entrainment/activation mapping but more extensive substrate-based modification that ultimately led to longer ablation times. Not surprisingly, this difference in ablation time was noted only in the patients with ICM who unlike patients with non-ICM exhibited a clear and definable substrate that could be targeted for extensive ablation. Second, not only was hospital LOS shorter with the pLVAD, but it was also associated with fewer intensive care unit days as compared with control. One explanation may be that improved end-organ perfusion by the pLVAD led to reduced periprocedural heart and/or renal failure exacerbation. While this could not be corroborated through laboratory assessments, it should be emphasized that postprocedural brain natriuretic peptide levels were measured in only 62% without a baseline value always available for comparison. Another explanation may actually relate to the differences observed in total ablation time. That is, prolonged open-irrigated radiofrequency ablation in the control arm may have been associated with greater intravascular volume expansion, thereby increasing the likelihood of heart failure exacerbation in an already vulnerable patient cohort. Subsequent management of this complication could in turn have led to longer hospital LOS. In fact, it is notable that the patterns observed in total ablation time and LOS greatly mirrored one another. That is, the ICM-control group was subjected to significantly longer total ablation times and consequently required longer hospital LOS, whereas total ablation times were similar for non-ICM-control and non-ICM-pLVAD groups as was the hospital LOS. Third, as consistent with other published reports,19,20 we observed a significantly higher VT recurrence rate in patients with non-ICM. While there were no clear benefits with regard to VT recurrence associated with the use of the pLVAD, the secondary composite end point was lower in pLVAD group than in control group, which was driven primarily by differences in recurrent ICD therapies and
695 696 697 698 699 700 701 702 703 704 705 706 707 708 709 710 711 712 713 714 715 716 717 718 719 720 721 722 723 724 725 726 727 728 729 730 731 732 733 734 735 736 737 738 739 740 741 742 743 744 745 746 747 748 749 750 751
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Table 4
Procedural and clinical characteristics and outcomes: IABP group vs control group
Characteristic/outcome Procedural No. of induced VTs VT cycle length (ms) Maximum time in unstable VT (min) No. of VT terminations during ablation per procedure Procedural success Clinical Hospital LOS (d) 30-d rehospitalization Redo-VT ablation Recurrent ICD therapies 3-mo mortality VT recurrence Secondary composite end point
IABP group (n ¼ 12)
Control group (n ¼ 34)
P
3.0 ⫾ 0.6 361 ⫾ 46 7.3 ⫾ 8.5 0.3 ⫾ 0.5 8 (67)
2.8 374 5.3 0.4 24
⫾ 0.8 ⫾ 69 ⫾ 3.6 ⫾ 0.6 (71)
.309 .635 .669 .856 .817
5.3 ⫾ 2.5 1 (8) 2 (17) 1 (8) 1 (8) 4 (33) 4 (33)
5.4 ⫾ 3.1 3 (9) 6 (18) 7 (21) 2 (6) 12 (35) 14 (41)
.738 1.000 1.000 .660 1.000 1.000 .739
Values are presented as mean ⫾ SD or as n (%). IABP ¼ intra-aortic balloon pump; ICD ¼ implantable cardioverter-defibrillator; LOS ¼ length of stay; VT ¼ ventricular tachycardia.
redo-VT ablation in patients with non-ICM. This seems plausible, as substrate-based modification in the absence of detailed arrhythmia mapping has been shown to provide an effective approach to catheter ablation of unstable, scar-mediated VT.1–5 Therefore, it is not surprising that the approach of the pLVAD vs control yielded similar clinical outcomes in patients with ICM who commonly exhibit a clear and identifiable scar for modification. In contrast, in patients with non-ICM in whom a discrete substrate cannot always be detected, the outcomes were likely enhanced further by the use of the pLVAD. Lastly, the authors believe that the above findings associated with the use of the pLVAD do not seem to apply to the use of the IABP. The authors also compared a similar but smaller cohort of 12 patients who underwent catheter ablation of unstable, scar-mediated VT with hemodynamic support provided by the IABP. As indicated by Table 4, both procedural and clinical outcomes associated with the use of the IABP seem to strongly mimic the use of control as opposed to the pLVAD.
Study limitations First, this study represents a single-center, retrospective, nonrandomized analysis of consecutive patients undergoing VT ablation. Second, we were unable to quantify specific differences in certain procedural characteristics such as the extent of entrainment/activation vs substrate-based mapping between the groups. Third, a potential difference in the primary end point of VT recurrence in the non-ICM patient group could have been missed because of the underpowered comparison of relatively small samples evaluated in this study. Larger and prospective randomized trials are necessary to better evaluate the role of the pLVAD in catheter ablation of unstable VT, particularly in patients with nonICM. In addition, a cost analysis is essential to shed light on the cost-effectiveness of the pLVAD in VT ablation. Lastly, there is great variability among operators with regard to VT mapping/ablation techniques and pre- and postablation
management of patients, which may further limit the generalization of the observed findings.
Conclusion In this nonrandomized retrospective study, the use of pLVAD support during catheter mapping and ablation of hemodynamically unstable VT permitted significantly longer intervals of sustained tachycardia and a greater number of VT terminations during radiofrequency ablation. It was associated with shorter hospital LOS and lower secondary composite end point of 30-day rehospitalization, redo-VT ablation, recurrent ICD therapies, and 3-month mortality. However, the use of the pLVAD did not significantly affect procedural success or VT recurrence after ablation.
Acknowledgments We thank Christina Cool, MPH, for her assistance with statistical analysis of the data.
References 1. Tanner H, Hindricks G, Volkmer M, Furniss S, Kühlkamp V, Lacroix D, DE Chillou C, Almendral J, Caponi D, Kuck KH, Kottkamp H. Catheter ablation of recurrent scar-related ventricular tachycardia using electroanatomical mapping and irrigated ablation technology: results of the prospective multicenter Euro-VTstudy. J Cardiovasc Electrophysiol 2010;21:47–53. 2. Zeppenfeld K, Stevenson WG. Ablation of ventricular tachycardia inpatients with structural heart disease. Pacing Clin Electrophysiol 2008;31:358–374. 3. Stevenson WG, Wilber DJ, Natale A, et al. Irrigated radiofrequency catheter ablation guided by electroanatomic mapping for recurrent ventricular tachycardia after myocardial infarction: the multicenter thermocool ventricular tachycardia ablation trial. Circulation 2008;118:2773–2782. 4. Marchlinski FE, Callans DJ, Gottlieb CD, Zado E. Linear ablation lesions for control of unmappable ventricular tachycardia in patients with ischemic and nonischemic cardiomyopathy. Circulation 2000;101:1288–1296. 5. Soejima K, Suzuki M, Maisel WH, Brunckhorst CB, Delacretaz E, Blier L, Tung S, Khan H, Stevenson WG. Catheter ablation in patients with multiple and unstable ventricular tachycardias after myocardial infarction: short ablation lines guided by reentry circuit isthmuses and sinus rhythm mapping. Circulation 2001;104: 664–669. 6. Della Bella P, Maccabelli G. Temporary percutaneous left ventricular support for ablation of untolerated ventricular tachycardias: is it worth the trouble? Circ Arrhythm Electrophysiol 2012;5:1056–1058.
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7. Knight BP, Jacobson JT. Assessing patients for catheter ablation during hospitalization for acute heart failure. Heart Fail Rev 2011;16:467–476. 8. Papaioannou TG, Stefanadis C. Basic principles of the intra-aortic balloon pump and mechanisms affecting its performance. ASAIO J 2005;51:296–300. 9. Miller MA, Dukkipati SR, Mittnacht AJ, Chinitz JS, Belliveau L, Koruth JS, Gomes JA, d’Avila A, Reddy VY. Activation and entrainment mapping of hemodynamically unstable ventricular tachycardia using a percutaneous left ventricular assist device. J Am Coll Cardiol 2011;58:1363–1371. 10. Miller MA, Dukkipati SR, Koruth JS, d’Avila A, Reddy VY. How to perform ventricular tachycardia ablation with a percutaneous left ventricular assist device. Heart Rhythm 2012;9:1168–1176. 11. Fischer GW. Recent advances in application of cerebral oximetry in adult cardiovascular surgery. Semin Cardiothorac Vasc Anesth 2008;12:60–69. 12. Lee WA, Brown MP, Nelson PR, Huber TS. Total percutaneous access for endovascular aortic aneurysm repair (“Preclose” technique). J Vasc Surg 2007;45:1095–1101. 13. Sosa E, Scanavacca M, d’Avila A, Pilleggi F. A new technique to perform epicardial mapping in the electrophysiology laboratory. J Cardiovasc Electrophysiol 1996;7:531–536. 14. Aliot EM, Stevenson WG, Almendral-Garrote JM, et al. EHRA/HRS expert consensus on catheter ablation of ventricular arrhythmias: developed in a partnership with the European Heart Rhythm Association (EHRA), a Registered Branch of the European Society of Cardiology (ESC), and the Heart Rhythm
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Society (HRS); in collaboration with the American College of Cardiology (ACC) and the American Heart Association (AHA). Heart Rhythm 2009;6:886–933. Abuissa H, Roshan J, Lim B, Asirvatham SJ. Use of the Impella microaxial blood pump for ablation of hemodynamically unstable ventricular tachycardia. J Cardiovasc Electrophysiol 2010;21:458–461. Ostadal P, Mlcek M, Holy F, et al. Direct comparison of percutaneous circulatory support systems in specific hemodynamic conditions in a porcine model. Circ Arrhythm Electrophysiol 2012;5:1202–1206. Miller MA, Dukkipati SR, Chinitz JS, Koruth JS, Mittnacht AJ, Napolitano C, d’Avila A, Reddy VY. Percutaneous hemodynamic support with Impella 2.5 during scar-related ventricular tachycardia ablation (PERMIT 1). Circ Arrhythm Electrophysiol 2013;6:151–159. Bunch TJ, Darby A, May HT, Ragosta M, Lim DS, Taylor AM, DiMarco JP, Ailawadi G, Revenaugh JR, Weiss JP, Mahapatra S. Efficacy and safety of ventricular tachycardia ablation with mechanical circulatory support compared with substrate-based ablation techniques. Europace 2012;14:709–714. Tokuda M, Tedrow UB, Kojodjojo P, Inada K, Koplan BA, Michaud GF, John RM, Epstein LM, Stevenson WG. Catheter ablation of ventricular tachycardia in nonischemic heart disease. Circ Arrhythm Electrophysiol 2012;5:992–1000. Dinov B, Fiedler L, Schönbauer R, Bollmann A, Rolf S, Piorkowski C, Hindricks G, Arya A. Outcomes in catheter ablation of ventricular tachycardia in dilated non-ischemic cardiomyopathy in comparison to ischemic cardiomyopathy: results from the Prospective Heart Centre of Leipzig VT (HELP-VT) Study. Circulation 2014;129:728–736.
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Procedural and clinical outcomes after catheter ablation of unstable ventricular tachycardia supported by a percutaneous left ventricular assist device Arash Aryana, MD,*† P. Gearoid O’Neill, MD,*† David Gregory, MPA,‡ Dennis Scotti, PhD, MBA,‡§ Sean Bailey, EPT,† Scott Brunton, BS,† Michael Chang, MD,*† André d’Avila, MD, PhD║ From the *Regional Cardiology Associates, Sacramento, California, †Mercy Heart & Vascular Institute, Sacramento, California, ‡Presscott Associates, a division of ParenteBeard, New York, New York, §Fairleigh Dickinson University, Teaneck, New Jersey, and ║Helmsley Cardiac Arrhythmia Service, Mount Sinai School of Medicine, New York, New York. BACKGROUND Hemodynamic support using percutaneous left ventricular assist devices (pLVADs) during catheter mapping and ablation of unstable ventricular tachycardia (VT) can provide effective end-organ perfusion. However, its effect on procedural and clinical outcomes remains unclear. OBJECTIVE To retrospectively evaluate the procedural and clinical outcomes after the catheter ablation of unstable VT with/without pLVAD support. METHODS Sixty-eight consecutive unstable, scar-mediated endocardial and/or epicardial VT ablation procedures performed in 63 patients were evaluated. During VT mapping/ablation, hemodynamic support was provided by intravenous inotropes with a pLVAD (n ¼ 34) or without a pLVAD (control; n ¼ 34). RESULTS Baseline patient characteristics were similar. VT was sustained longer with a pLVAD (27.4 ⫾ 18.7 minutes) than without a pLVAD (5.3 ⫾ 3.6 minutes) (P o .001). A higher number of VTs were terminated during ablation with a pLVAD (1.2 ⫾ 0.9 per procedure) than without a pLVAD (0.4 ⫾ 0.6 per procedure) (P o .001). Total radiofrequency ablation time was shorter with a pLVAD (53 ⫾ 30 minutes) than without a pLVAD (68 ⫾ 33 minutes) (P ¼ .022), but with similar procedural success rates (71% for both pLVAD and control groups; P ¼ 1.000). Although during 19 ⫾ 12 months of follow-up VT recurrence did not differ between pLVAD (26%) and control (41%)
Dr Aryana and Dr d’Avila have received speaker honoraria and Mr Gregory, Dr Scotti, and Dr d’Avila have received consulting fees from ABIOMED, Inc, the manufacturer of the percutaneous left ventricular assist device. Dr Aryana, Dr d’Avila, and Mr Bailey have received consulting fees and Dr Aryana, Dr d’Avila, and Dr O’Neill have received speaker honoraria from St Jude Medical, Inc, the manufacturer of an electroanatomic mapping system used in this study. Dr d’Avila has received consulting fees and speaker honoraria from Biosense Webster Inc, the manufacturer of the other electroanatomic mapping system used in this series. Address reprint requests and correspondence: Dr Arash Aryana, Regional Cardiology Associates and the Mercy Heart & Vascular Institute, 3941 J St, Suite #350, Sacramento, CA 95819. E-mail address: [email protected].
1547-5271/$-see front matter B 2014 Heart Rhythm Society. All rights reserved.
groups (P ¼ .305), the composite end point of 30-day rehospitalization, redo-VT ablation, recurrent implantable cardioverter-defibrillator therapies, and 3-month mortality was lower with a pLVAD (12%) than without a pLVAD (35%) (P ¼ .043). Q6 CONCLUSION In this nonrandomized retrospective study, catheter ablation of unstable VT supported by a pLVAD was associated with shorter ablation times and reduced hospital length of stay. While pLVAD support did not affect VT recurrence, it was associated with a lower composite end point of 30-day rehospitalization, redo-VT ablation, recurrent implantable cardioverter-defibrillator therapies, and 3-month mortality. KEYWORDS Catheter ablation; Hospital length of stay; Ischemic cardiomyopathy; Non–ischemic cardiomyopathy; Percutaneous left ventricular assist device; Ventricular tachycardia ABBREVIATIONS EMI ¼ electromagnetic interference; IABP ¼ intra-aortic balloon pump; ICD ¼ implantable cardioverterdefibrillator; ICM ¼ ischemic cardiomyopathy; LOS ¼ length of stay; non-ICM ¼ non–ischemic cardiomyopathy; pLVAD ¼ percutaneous left ventricular assist device; SctO2 ¼ cerebral tissue oxygen saturation; VT ¼ ventricular tachycardia (Heart Rhythm 2014;0:-1–9) rights reserved.
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2014 Heart Rhythm Society. All
Introduction Scar-mediated ventricular tachycardias (VTs) are often hemodynamically unstable,1 limiting detailed entrainment and activation mapping to guide catheter ablation.2 Instead, substrate-based modification is commonly used, which involves targeting the arrhythmogenic substrates in sinus rhythm.3–5 Yet in some patients, particularly in those with non–ischemic cardiomyopathy (non-ICM), mapping of lowvoltage areas does not always exhibit fractionated and/or late potentials, such that a clear substrate cannot be identified.6 http://dx.doi.org/10.1016/j.hrthm.2014.04.018
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Under these circumstances, mapping during tachycardia seems more attractive but can often only be performed given sufficient hemodynamic support. In addition, in those with significant left ventricular (LV) dysfunction, prolonged episodes of sustained VT can sometimes lead to exacerbation of heart and/or renal failure even in the setting of a hemodynamically tolerated arrhythmia, affecting patient morbidity and clinical outcomes.7 Hence, it is conceivable that such patients may benefit from hemodynamic support during catheter mapping and ablation of VT. While vasoactive drugs and intra-aortic balloon pumps (IABPs) are most commonly used for hemodynamic stabilization, frequently in the setting of unstable VT they provide insufficient support. Specifically, low systolic blood pressure and tachycardia can significantly impair IABP performance.8 In contrast, percutaneous left ventricular assist devices (pLVADs) are less susceptible to such variables and generally capable of providing greater hemodynamic stability and end-organ perfusion in the setting of unstable VT.9 Theoretically, LV unloading by pLVADs may also minimize periprocedural heart failure. However, it remains unclear whether pLVAD support during VT mapping/ablation can significantly affect the short- and long-term clinical outcomes. Here, we report a retrospective, nonrandomized analysis of the procedural and clinical outcomes after catheter ablation of unstable, scar-mediated VT with/without hemodynamic support provided by an impeller-driven axial flow pump (pLVAD) as compared with a standard-of-care control group.
Methods Study population We retrospectively evaluated a total of 68 consecutive catheter ablation procedures performed for the treatment of scar-mediated hemodynamically unstable VT (defined as a mean arterial blood pressure of r50 mm Hg and/or requiring internal/external defibrillation) in 63 patients with structural heart disease by using an endocardial/epicardial approach. The procedures were performed by 2 operators at a single center (Mercy General Hospital, Sacramento, CA) with/without a pLVAD, whenever available. Data were obtained from reviewing medical/hospital records.
Data analysis Five groups/subgroups of patients were analyzed: (1) the entire cohort (n ¼ 68); (2) cases performed with and without pLVADs (control); (3) patients with ischemic cardiomyopathy (ICM; n ¼ 36) and non-ICM (n ¼ 32); (4) patients with ICM in the pLVAD group (ICM-pLVAD group; n ¼ 18), patients with ICM in the control group (ICM-control group; n ¼ 18), patients with non-ICM in the pLVAD group (nonICM-pLVAD group; n ¼ 16), and patients with non-ICM in the control group (non-ICM-control group; n ¼ 16); and (5) cases performed with IABPs (n ¼ 12) vs control. The primary end point was defined as VT recurrence during follow-up. The secondary composite end point consisted of
Heart Rhythm, Vol 0, No 0, Month 2014 30-day rehospitalization, redo-VT ablation, recurrent implantable cardioverter-defibrillator (ICD) therapies (both shocks and antitachycardia pacing), and 3-month mortality. These end points were not predefined but were ascribed after data collection. All patients had a preexisting ICD or a cardiac resynchronization therapy-defibrillator at the time of ablation. VT recurrence and ICD therapies were examined throughout follow-up through serial ICD/cardiac resynchronization therapy-defibrillator interrogations.
Procedural details All procedures were performed under general anesthesia. During VT mapping/ablation, all patients received inotropic support with intravenous dobutamine or dopamine (2–20 μg/ (kg min)) and repeated boluses of phenylephrine (100 μg) with/without a pLVAD. Although not considered standard practice, we prefer the use of inotropic agents to provide hemodynamic support under general anesthesia during VT mapping. In addition to the conventional markers of hemodynamic stability, cerebral oximetry (ie, cerebral tissue oxygen saturation [SctO2]) was monitored (Figure 1) using a cerebral oximeter (INVOS, Covidien, Mansfield, MA), as described previously.10 SctO2 has been shown to represent a sensitive indicator of cerebral hypoxia and end-organ perfusion.11 SctO2 was measured at baseline and throughout the procedure on 100% fraction of inspired oxygen. During VT, a lower limit of 20%–25% of the preanesthesia induction value was allowed.11
Cardiac assist devices A 12/13-F pLVAD (Impella 2.5/Impella CP, ABIOMED, Inc, Danvers, MA) was inserted after systemic anticoagulation (target activated clotting time Z250 seconds). The pLVAD was positioned inside the LV in a retrograde transaortic fashion via a 13/14-F introducer sheath through the femoral artery. A maximum performance level of 9 (50,000 rpm, up to 2.5 L/min [Impella 2.5] or 3.8 L/min [Impella CP]) was maintained throughout the procedure unless electromagnetic interference (EMI) necessitated temporary adjustments. As previously described by Miller et al,10 this may occur with the use of a magnetic-based mapping system. The severity of EMI depends on the Impella performance level and the mapping catheter distance from the motor.10 To overcome this, the pLVAD performance was reduced to P2 (usually required only when mapping within the outflow tract endocardially or at the base of the heart epicardially10). The Impella CP seems to be associated with a smaller degree of EMI, possibly owing to improved insulation of the motor. All venous/arterial sheaths and pLVADs were inserted electively at the onset of the procedure and weaned/removed before discharge from the electrophysiology laboratory by the cardiac electrophysiologist operator. For closure of the pLVAD arteriotomy site, the preclose technique (using 2 Perclose ProGlide devices, Abbott Laboratories, Abbott Park, IL) was used.12
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100
Induction of unstable VT (without pLVAD)
90
Induction of unstable VT (with pLVAD)
80 SctO2 (%)
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pLVAD Support During VT Ablation
70 60 50 40 30 0
5
10
15
20
25
30
35
40
Time (min)
Figure 1 Noninvasive SctO2 monitoring. Continuous SctO2 recording during VT mapping in a patient with ICM and left ventricular ejection fraction of 30%. As seen, in the absence of pLVAD support, SctO2 rapidly decreases to o50% within 5 minutes after the induction of unstable VT (cycle length 343 ms). Yet, when the same VT is later induced with pLVAD support, SctO2 is sufficiently maintained for Z15 minutes with a decrease of only o20% in the SctO2 from baseline. ICM ¼ ischemic cardiomyopathy; pLVAD ¼ percutaneous left ventricular assist device; SctO2 ¼ cerebral tissue oxygen saturation; VT ¼ ventricular tachycardia.
Electrophysiology study and ablation Diagnostic electrophysiology catheters were positioned using the conventional approach, including a phased-array intracardiac echocardiography catheter (ViewFlex PLUS, St Jude Medical, Inc, St Paul, MN). Electroanatomic mapping was performed using either a hybrid magnetic/impedancebased system (CARTO 3, Biosense Webster Inc, Diamond Bar, CA) in 61 procedures or an impedance-based system (EnSite NavX, St Jude Medical, Inc) in 7 cases. A 3.5-mmtip open-irrigated ablation catheter (NaviStar/Celsius ThermoCool, Biosense Webster, Inc) was used during all procedures. To minimize high-frequency noise that can sometimes be recorded when the mapping/recording catheter is adjacent to the pLVAD motor, endocardial LV mapping was preferentially performed via a transseptal approach using an 8.5-F steerable introducer (Agilis, St Jude Medical, Inc) in pLVAD cases. RV mapping/ablation was performed via an 8.5-F Mullins-style sheath (Fast-Cath Transseptal Guiding Introducer, St Jude Medical, Inc). The target activated clotting time was 300–350 seconds during endocardial mapping/ablation. Epicardial puncture, mapping/ ablation were performed via a percutaneous subxyphoid approach.13 Epicardial mapping/ablation was performed via an 8.5-F steerable epicardial introducer (Agilis NxT, St Jude Medical, Inc) in all patients. Electrophysiology testing and radiofrequency catheter ablation were performed using the standard approach. Whenever possible, entrainment/activation mapping was attempted. During all pLVAD cases, detailed entrainment mapping and at least partial activation mapping were performed. In contrast to control cases during which extensive entrainment/activation mapping could not always be completed, in several pLVAD cases complete VT activation maps were created (Figure 2). Pace mapping and substrate-based modification were performed in both groups to varying degrees. The number of VTs induced during each
procedure was recorded as well as the number of VTs terminated during ablation. Procedural success was defined as noninducibility of any sustained monomorphic VT with programmed electrical stimulation using triple extrastimuli.
Laboratory analysis In all patients, routine laboratory tests including serum creatinine, blood urea nitrogen, and glomerular filtration rate were recorded at baseline and at hospital discharge. The maximum change (Δ) in serum creatinine, blood urea nitrogen, and glomerular filtration rate after ablation were also recorded. Arterial lactate levels immediately after the procedure were measured in all cases as well as a brain natriuretic peptide within 24 hours of ablation in 42 of 62 cases. A baseline value was not always available for comparison.
Statistical analysis Statistical analysis was performed to examine the differences between groups in baseline characteristics, procedural parameters, and end point variables. Intergroup differences for normally distributed continuous variables were tested using the Student t test. When significant departures from normality were detected, differential comparisons were performed using the Mann-Whitney U test. Whenever necessary, log transformations were performed to address data distribution anomalies identified by standard SPSS diagnostic tests. Differences between categorical variables were assessed using the Pearson’s chi-squared test or Fisher exact test, as appropriate. Statistical calculations were performed using SPSS Version 20 (IBM SPSS Statistics, Chicago, IL). All statistical analyses were 2-tailed, and a P value of o.05 was considered statistically significant.
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Figure 2 Activation and entrainment mapping during unstable VT with pLVAD support. An electroanatomic activation map (A) and a voltage map (B) of the LV constructed during unstable VT (cycle length: 355 ms) with pLVAD support in a patient with ICM and a large anterior-apical LV scar. The entire VT cycle length was mapped. The white arrow shows the direction of VT propagation. The small insets in panel A represent the sequence of intracardiac electrograms as they traverse through electrical diastole. The red arrow points to the site of VT entrainment (C). At this site, entrainment yielded a postpacing interval (PPI) equal to the tachycardia cycle length. D: The 12-lead electrocardiographic morphology during overdrive pacing of the VT demonstrating concealed fusion. E: Radiofrequency applications delivered to this site terminated the VT. However, a second tachycardia with a slightly different morphology and a longer cycle length (395 ms) was subsequently inducible. Additional radiofrequency applications in the same region ultimately rendered both VTs non-reinducible. CT ¼ cycle length; ICM ¼ ischemic cardiomyopathy; LV ¼ left ventricular; pLVAD ¼ percutaneous left ventricular assist device; VT ¼ ventricular tachycardia.
Results Baseline patient characteristics were similar (Table 1), and there were no differences between ICM-pLVAD and ICMcontrol groups and between non-ICM-pLVAD and nonICM-control groups. Similarly, procedural and clinical characteristics did not differ between the groups and there were no differences in pre- and postablation laboratory values (Table 2). However, unstable VT was sustained longer with a pLVAD than without a pLVAD in all the groups/subgroups (Table 3). VT was sustained for Z20 minutes in 44% of the pLVAD group vs 3% of the control
group. In addition, a greater number of VTs were terminated during radiofrequency ablation with a pLVAD than without a pLVAD in all the groups/subgroups. Total radiofrequency ablation time was shorter in pLVAD group vs control group and in ICM-pLVAD group vs ICM-control group, but did not differ among ICM-pLVAD, non-ICM-pLVAD, and nonICM-control groups. There were no differences in procedural success rate among the pLVAD and control groups/subgroups (Figure 3A). However, procedural success was higher in patients with ICM (89%) than in patients with non-ICM (53%) (P ¼ .001).
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Table 1
pLVAD Support During VT Ablation
5
Baseline patient characteristics
Characteristic Clinical Age (y) Sex: male Hypertension Diabetes mellitus Chronic kidney disease Cardiac disease substrate Ischemic Coronary artery bypass graft Percutaneous coronary intervention Nonischemic Dilated Arrhythmogenic RV dysplasia Sarcoid Chagasic Hypertrophic cardiomyopathy Congenital heart disease LV ejection fraction (%) Heart failure NYHA class I-II III-IV VT/electrical storm Cardiac arrhythmia device ICD CRT-D Antiarrhythmic therapy Amiodarone Mexiletine Sotalol
All patients (N ¼ 68)
pLVAD group (n ¼ 34)
Control group (n ¼ 34)
P
66 ⫾ 12 60 (88) 46 (68) 28 (41) 39 (57)
64 ⫾ 12 28 (82) 23 (68) 16 (47) 21 (62)
67 ⫾ 12 32 (94) 23 (68) 12 (35) 18 (53)
.112 .259 1.000 .460 .624
36 (53) 19 (28) 22 (32) 32 (47) 23 (34) 3 (4) 3 (4) 1 (1) 1 (1) 1 (1) 32 ⫾ 10
18 (53) 10 (29) 11 (32) 16 (47) 13 (38) 0 (0) 2 (6) 1 (3) 0 (0) 0 (0) 30 ⫾ 11
18 (53) 9 (26) 11 (32) 16 (47) 10 (29) 3 (9) 1 (3) 0 (0) 1 (3) 1 (3) 34 ⫾ 9
1.000 1.000 1.000 1.000 .609 .239 1.000 1.000 1.000 1.000 .178
32 (47) 36 (53) 23 (34)
13 (38) 21 (62) 12 (35)
19 (56) 15 (44) 11 (32)
.224 .224 1.000
47 (69) 21 (31)
22 (65) 12 (35)
25 (74) 9 (26)
.600 .600
63 (93) 8 (12) 8 (12)
32 (94) 5 (15) 3 (9)
31 (91) 3 (9) 5 (15)
1.000 .709 .709
Values are presented as mean ⫾ SD or as n (%). CRT-D ¼ cardiac resynchronization therapy-defibrillator; ICD ¼ implantable cardioverter-defibrillator; LV ¼ left ventricular; NYHA ¼ New York Heart Association; pLVAD ¼ percutaneous left ventricular assist device; RV ¼ right ventricular; VT ¼ ventricular tachycardia.
Table 2
Procedural and laboratory characteristics
Characteristic Mapping LV endocardial Epicardial, percutaneous RV endocardial No. of induced VTs VT cycle length (ms) Time Procedure (min) Fluoroscopy (min) Serum laboratory Preablation Creatinine (mg/dL) BUN (mg/dL) GFR (mL/min) Postablation Creatinine—maximum change (mg/dL) Creatinine at discharge (mg/dL) BUN—maximum change (mg/dL) BUN at discharge (mg/dL) GFR—maximum change (mL/min) GFR at discharge (mL/min) Lactate (mmol/L) Brain natriuretic peptide (pg/mL)*
All patients (N ¼ 68)
pLVAD group (n ¼ 34)
Control group (n ¼ 34)
P
67 (99) 25 (37) 11 (16) 3.1 ⫾ 1.4 367 ⫾ 69
34 (100) 13 (38) 3 (9) 3.4 ⫾ 1.9 359 ⫾ 70
33 (97) 12 (35) 8 (24) 2.8 ⫾ 0.8 374 ⫾ 69
1.000 1.000 .186 .083 .344
338 ⫾ 67 28 ⫾ 11
345 ⫾ 81 29 ⫾ 12
331 ⫾ 49 27 ⫾ 9
.466 .906
1.5 ⫾ 1.2 26 ⫾ 14 62 ⫾ 27
1.6 ⫾ 1.6 27 ⫾ 13 61 ⫾ 30
1.3 ⫾ 0.5 24 ⫾ 15 62 ⫾ 23
.882 .102 .633
0.3 ⫾ 1.5 ⫾ 6⫾ 28 ⫾ 6 ⫾ 62 ⫾ 1.5 ⫾ 420 ⫾
0.2 ⫾ 1.6 ⫾ 5⫾ 29 ⫾ 5 ⫾ 62 ⫾ 1.5 ⫾ 398 ⫾
0.3 ⫾ 1.4 ⫾ 7⫾ 27 ⫾ 7 ⫾ 63 ⫾ 1.6 ⫾ 469 ⫾
.101 .582 .349 .382 .223 .670 .738 .276
0.5 1.2 11 16 12 30 0.5 313
0.3 1.5 11 16 11 33 0.5 317
0.7 0.7 11 17 12 26 0.5 308
Values are presented as mean ⫾ SD or as n (%). BUN ¼ blood urea nitrogen; GFR ¼ glomerular filtration rate; LV ¼ left ventricular; pLVAD ¼ percutaneous left ventricular assist device; RV ¼ right ventricular; VT ¼ ventricular tachycardia. * Data are available in only 42 of 68 (62%) patients.
467 468 469 470 471 472 473 474 475 476 477 478 479 480 481 482 483 484 485 486 487 488 489 490 491 492 493 494 495 496 497 498 499 500 501 502 503 504 505 506 507 508 509 510 511 512 513 514 515 516 517 518 519 520 521 522 523
6 524 525 526 527 528 529 530 531 532 533 534 535 536 537 538 539 540 541 542 543 544 545 546 547 548 549 550 551 552 553 554 555 556 557 558 559 560 561 562 563 564 565 566 567 568 569 570 571 572 573 574 575 576 577 578 579 580
Table 3
Heart Rhythm, Vol 0, No 0, Month 2014 Procedural and clinical outcomes: pLVAD group vs control group
Outcome Procedural Maximum time in unstable VT (min) All patients (N ¼ 68) Patients with ICM (n ¼ 36) Patients with non-ICM (n ¼ 32) No. of VT terminations duringablation per procedure All patients (N ¼ 68) Patients with ICM (n ¼ 36) Patients with non-ICM (n ¼ 32) Total radiofrequency ablation time (min) All patients (N ¼ 68) Patients with ICM (n ¼ 36) Patients with non-ICM (n ¼ 32) Clinical Hospital LOS (d) All patients (N ¼ 68) Patients with ICM (n ¼ 36) Patients with non-ICM (n ¼ 32) 30-day rehospitalization All patients (N ¼ 68) Patients with ICM (n ¼ 36) Patients with non-ICM (n ¼ 32) Redo-VT ablation All patients (N ¼ 68) Patients with ICM (n ¼ 36) Patients with non-ICM (n ¼ 32) Recurrent ICD therapies All patients (N ¼ 68) Patients with ICM (n ¼ 36) Patients with non-ICM (n ¼ 32) 3-mo mortality All patients (N ¼ 68) Patients with ICM (n ¼ 36) Patients with non-ICM (n ¼ 32)
pLVAD group (n ¼ 34)
Control group (n ¼ 34)
P
27.4 ⫾ 18.7 28.8 ⫾ 24.8 26.4 ⫾ 13.3
5.3 ⫾ 3.6 5.5 ⫾ 3.5 5.1 ⫾ 3.9
o.001* .012* o.001*
1.2 ⫾ 0.9 1.3 ⫾ 1.2 1.1 ⫾ 0.6
0.4 ⫾ 0.6 0.4 ⫾ 0.6 0.3 ⫾ 0.5
o.001* .025* .005*
53 ⫾ 30 56 ⫾ 32 50 ⫾ 28
68 ⫾ 33 82 ⫾ 35 51 ⫾ 19
.022* .004* .914
4.1 ⫾ 3.0 3.6 ⫾ 2.4 4.7 ⫾ 3.6
5.4 ⫾ 3.1 6.5 ⫾ 3.7 4.1 ⫾ 1.6
.013* .004* .682
2 (6) 2 (11) 0 (0)
3 (9) 1 (6) 2 (13)
1.000 1.000 .484
1 (3) 0 (0) 1 (6)
6 (18) 2 (11) 4 (25)
.105 .486 .333
1 (3) 0 (0) 1 (6)
7 (21) 2 (11) 5 (31)
.054 .486 .172
0 (0) 0 (0) 0 (0)
2 (6) 2 (11) 0 (0)
.493 .486 1.000
Values are presented as mean ⫾ SD or as n (%). ICD ¼ implantable cardioverter-defibrillator; ICM ¼ ischemic cardiomyopathy; LOS ¼ length of stay; non-ICM ¼ non–ischemic cardiomyopathy; pLVAD ¼ percutaneous left ventricular assist device; VT ¼ ventricular tachycardia. * Significant P value.
Clinical outcomes Two (6%) major complications occurred in the pLVAD group and none in the control group (P ¼ .493). One patient in the pLVAD group developed a femoral arterial laceration related to the insertion of the 13-F introducer, requiring surgical repair. Another patient in the pLVAD group developed cardiac tamponade during epicardial mapping owing to transection of the distal posterior descending coronary artery by the epicardial introducer. The pLVAD was not considered a cause of this complication. This patient was treated with emergent pericardiocentesis and eventually required surgical repair of the lacerated artery. The hospital length of stay (LOS) was shorter in pLVAD group vs control group and in ICM-pLVAD group vs ICMcontrol group, but did not differ between non-ICM-pLVAD and non-ICM-control groups (Table 3). In addition, the pLVAD was associated with 3 fewer intensive care unit days after the procedure. Thirty-day mortality was zero. During a follow-up period of 19 ⫾ 12 months, the primary end point
of VT recurrence did not differ among the groups/subgroups (Figure 3B). However, VT recurrence was overall lower in patients with ICM (19%) than in patients with non-ICM (50%) (P ¼ .011). There was a trend toward fewer recurrent ICD therapies with a pLVAD than without a pLVAD (Table 3), with no discernible differences in 30-day rehospitalization, redo-VT ablation, and 3-month mortality among the pLVAD and control groups/subgroups. Yet, the secondary composite end point of 30-day rehospitalization, redoVT ablation, recurrent ICD therapies, and 3-month mortality was significantly lower in pLVAD group vs control group (Figure 3C), with a similar trend observed when comparing the non-ICM-pLVAD group with the non-ICMcontrol group.
Discussion The majority of VTs in patients with structural heart disease are hemodynamically unstable, precluding detailed
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pLVAD Support During VT Ablation
7
Principal findings
Figure 3 Procedural and clinical outcomes. A: The procedural success rates did not differ among the pLVAD and control groups/subgroups. B: The primary end point of VT recurrence did not differ among the pLVAD and control groups/subgroups. C: The secondary composite end point of 30-day rehospitalization, redo-VT ablation, recurrent ICD therapies, and 3-month mortality was lower with the pLVAD in all patients, with a similar trend observed in those with non-ICM. *Significant P value. ICD ¼ implantable cardioverter-defibrillator; ICM ¼ ischemic cardiomyopathy; non-ICM ¼ non–ischemic cardiomyopathy; pLVAD ¼ percutaneous left ventricular assist device; VT ¼ ventricular tachycardia.
entrainment/activation mapping during catheter ablation.1,2 Moreover, even in those with well-tolerated VT, the success of the procedure can be mitigated by acute heart failure owing to prolonged episodes of sustained VT and intravascular expansion, resulting in increased morbidity and mortality.14 Thus, there has been a growing interest in the use of cardiac assist devices during mapping/ablation of unstable VT.9,10,15–18 In this study, we investigated the effect of pLVAD support during catheter ablation of unstable scarmediated VT on procedural and clinical outcomes.
Improved hemodynamic support provided by the pLVAD in this cohort permitted significantly longer intervals during which unstable VT was sustained, which in turn allowed more detailed entrainment/activation mapping, ultimately yielding a greater number of VT terminations. However, this did not affect the procedural success or VT recurrence during follow-up. In addition, the use of the pLVAD was not associated with an increase in periprocedural adverse events. Nor did its use prohibit successful VT mapping/ablation due to EMI with the magnetic-based mapping system during any of the cases. These observations are generally consistent with prior reports.9,17,18 Yet, several findings from this study are noteworthy. First, total ablation time was shorter with a pLVAD than without a pLVAD. This may be explained through fundamental differences between the 2 ablation strategies. That is, the principal approach adopted in the pLVAD arm involved detailed VT mapping to guide ablation. Although the predominant approach used in the control arm consisted of limited entrainment/activation mapping but more extensive substrate-based modification that ultimately led to longer ablation times. Not surprisingly, this difference in ablation time was noted only in the patients with ICM who unlike patients with non-ICM exhibited a clear and definable substrate that could be targeted for extensive ablation. Second, not only was hospital LOS shorter with the pLVAD, but it was also associated with fewer intensive care unit days as compared with control. One explanation may be that improved end-organ perfusion by the pLVAD led to reduced periprocedural heart and/or renal failure exacerbation. While this could not be corroborated through laboratory assessments, it should be emphasized that postprocedural brain natriuretic peptide levels were measured in only 62% without a baseline value always available for comparison. Another explanation may actually relate to the differences observed in total ablation time. That is, prolonged open-irrigated radiofrequency ablation in the control arm may have been associated with greater intravascular volume expansion, thereby increasing the likelihood of heart failure exacerbation in an already vulnerable patient cohort. Subsequent management of this complication could in turn have led to longer hospital LOS. In fact, it is notable that the patterns observed in total ablation time and LOS greatly mirrored one another. That is, the ICM-control group was subjected to significantly longer total ablation times and consequently required longer hospital LOS, whereas total ablation times were similar for non-ICM-control and non-ICM-pLVAD groups as was the hospital LOS. Third, as consistent with other published reports,19,20 we observed a significantly higher VT recurrence rate in patients with non-ICM. While there were no clear benefits with regard to VT recurrence associated with the use of the pLVAD, the secondary composite end point was lower in pLVAD group than in control group, which was driven primarily by differences in recurrent ICD therapies and
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Heart Rhythm, Vol 0, No 0, Month 2014
Table 4
Procedural and clinical characteristics and outcomes: IABP group vs control group
Characteristic/outcome Procedural No. of induced VTs VT cycle length (ms) Maximum time in unstable VT (min) No. of VT terminations during ablation per procedure Procedural success Clinical Hospital LOS (d) 30-d rehospitalization Redo-VT ablation Recurrent ICD therapies 3-mo mortality VT recurrence Secondary composite end point
IABP group (n ¼ 12)
Control group (n ¼ 34)
P
3.0 ⫾ 0.6 361 ⫾ 46 7.3 ⫾ 8.5 0.3 ⫾ 0.5 8 (67)
2.8 374 5.3 0.4 24
⫾ 0.8 ⫾ 69 ⫾ 3.6 ⫾ 0.6 (71)
.309 .635 .669 .856 .817
5.3 ⫾ 2.5 1 (8) 2 (17) 1 (8) 1 (8) 4 (33) 4 (33)
5.4 ⫾ 3.1 3 (9) 6 (18) 7 (21) 2 (6) 12 (35) 14 (41)
.738 1.000 1.000 .660 1.000 1.000 .739
Values are presented as mean ⫾ SD or as n (%). IABP ¼ intra-aortic balloon pump; ICD ¼ implantable cardioverter-defibrillator; LOS ¼ length of stay; VT ¼ ventricular tachycardia.
redo-VT ablation in patients with non-ICM. This seems plausible, as substrate-based modification in the absence of detailed arrhythmia mapping has been shown to provide an effective approach to catheter ablation of unstable, scar-mediated VT.1–5 Therefore, it is not surprising that the approach of the pLVAD vs control yielded similar clinical outcomes in patients with ICM who commonly exhibit a clear and identifiable scar for modification. In contrast, in patients with non-ICM in whom a discrete substrate cannot always be detected, the outcomes were likely enhanced further by the use of the pLVAD. Lastly, the authors believe that the above findings associated with the use of the pLVAD do not seem to apply to the use of the IABP. The authors also compared a similar but smaller cohort of 12 patients who underwent catheter ablation of unstable, scar-mediated VT with hemodynamic support provided by the IABP. As indicated by Table 4, both procedural and clinical outcomes associated with the use of the IABP seem to strongly mimic the use of control as opposed to the pLVAD.
Study limitations First, this study represents a single-center, retrospective, nonrandomized analysis of consecutive patients undergoing VT ablation. Second, we were unable to quantify specific differences in certain procedural characteristics such as the extent of entrainment/activation vs substrate-based mapping between the groups. Third, a potential difference in the primary end point of VT recurrence in the non-ICM patient group could have been missed because of the underpowered comparison of relatively small samples evaluated in this study. Larger and prospective randomized trials are necessary to better evaluate the role of the pLVAD in catheter ablation of unstable VT, particularly in patients with nonICM. In addition, a cost analysis is essential to shed light on the cost-effectiveness of the pLVAD in VT ablation. Lastly, there is great variability among operators with regard to VT mapping/ablation techniques and pre- and postablation
management of patients, which may further limit the generalization of the observed findings.
Conclusion In this nonrandomized retrospective study, the use of pLVAD support during catheter mapping and ablation of hemodynamically unstable VT permitted significantly longer intervals of sustained tachycardia and a greater number of VT terminations during radiofrequency ablation. It was associated with shorter hospital LOS and lower secondary composite end point of 30-day rehospitalization, redo-VT ablation, recurrent ICD therapies, and 3-month mortality. However, the use of the pLVAD did not significantly affect procedural success or VT recurrence after ablation.
Acknowledgments We thank Christina Cool, MPH, for her assistance with statistical analysis of the data.
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