With the number of cardiac transplants plateaued at 2,200 each year due to limited organ availability, left ventricular assist devices (LVAD) offer short and long-term hemodynamic support in end-stage heart failure.1 The device and surgical implant technology has progressed over time from axial continuous flow pumps to, most recently, the HeartMate 3™ Left Ventricular Assist Device (Abbott), which is a pericardially implanted, fully magnetically levitated, centrifugal pump.2 Despite improving survival and quality of life in Stage D heart failure, there are considerable challenges involved in managing LVAD patients long term. From an electrophysiologist’s perspective, arrhythmias are a major concern, particularly ventricular tachycardia (VT) and fibrillation. This is especially true when arrhythmias become resistant to medical therapy. While post-LVAD ventricular arrhythmias (VA) might well be tolerated for a short period, recurrent and long-lasting arrhythmias can result in right ventricular (RV) failure (from arrhythmia itself or in a setting of multiple ICD shocks), recurrent hospitalizations, and overall reduced quality of life.3 Current evidence points to the safety and efficacy of catheter ablation of VT in LVAD patients with high burden of VA. Performing an ablation procedure on such patients requires meticulous planning and a multidisciplinary team approach including the electrophysiologist, anesthesiologist, and heart failure specialist. In the modern era, an important aspect of being an interventional electrophysiologist is to be cognizant of the progressive LVAD device technology as well as to address clinical and device-related issues unique to LVAD recipients. In this article, we present a case of medically refractory VT in a patient with a HeartMate 3 LVAD.
A 56-year-old male with permanent atrial fibrillation, atrioventricular node ablation, biventricular implantable cardioverter-defibrillator (BiV-ICD) implant, ischemic cardiomyopathy, and Stage D congestive heart failure, was hospitalized with multiple ICD shocks for monomorphic and polymorphic VT. Four months prior to presentation, the patient had destination therapy LVAD implantation (HeartMate 3). Post-operative course was significant for multiple appropriate ICD shocks for recurrent polymorphic and monomorphic VT. In the 3 weeks preceding hospitalization, the patient had symptoms of exertional dyspnea, dizziness, and palpitations secondary to VT. He failed to improve despite decreasing LVAD pump speed from 5800 RPM to 5500 RPM, antiarrhythmic therapy (metoprolol and amiodarone), and he received multiple appropriate ICD shocks. Upon admission, he received IV amiodarone and lidocaine, but still had recurrent sustained VT. Thus, the decision was made to proceed with catheter ablation of VT.
Catheter Ablation of VT: Our Approach
The patient was brought to the electrophysiology lab in a stable paced rhythm (atrial, biventricular). The procedure was performed on uninterrupted warfarin (INR of 2.1). His BiV-ICD was interrogated prior to the procedure; tachy therapies were programmed off, leaving detection on, and the device was set to pace (DDD) at 70 beats per minute during mapping. The mode was changed to DOO during ablation with arrhythmia detection off. A transseptal approach was used for left heart access using a large curl deflectable sheath (Agilis, Abbott) and BRK-1 needle (Abbott). A target ACT >350 was maintained. Intracardiac echocardiography (ICE) was used for assisting transseptal puncture as well as for defining anatomical landmarks and monitoring for complications during the procedure. A 4 French quadripolar catheter was placed in the RV apex for pacing and induction. The EnSite Precision Cardiac Mapping System (Abbott) was used for electroanatomic mapping. A high density (>3000 usable points) LV endocardial voltage map was created using the AutoMap feature of the EnSite Precision Cardiac Mapping System and standard cut-off values (dense scar if bipolar voltage <0.5 mV and normal voltage being >1.5 mV). The voltage map showed extensive anterior wall scar from base to apex, most of it very dense with extension to the lateral wall, and multiple areas of patchy scar in the posterolateral LV (from the base to the LVAD cannula suture line). Special care was taken not to enter the VAD cannula with the catheter while mapping. Large areas of late potentials as well as fractionated electrograms were seen in the posterolateral LV, especially towards the apex and around the cannula, as well as in the mid and apical anterior wall. All the fragmented and late potentials were tagged using 3D location markers. (Figures 1A and 1B)
Arrhythmia Induction and Mapping
VT was induced with programmed electrical stimulation (triple extrastimuli 600/350/350/350) from the RV. We used a 7 Fr, 20-pole duo-decapolar catheter with 2x2 spacing for activation mapping of VT as well as mapping of late potentials during sinus rhythm. The first induced VT had a right bundle branch block / superior axis morphology with no precordial transition and positive complexes in aVR and aVL; VT cycle length (CL) was 405 milliseconds (ms), and this was hemodynamically well tolerated (VT-1; Figures 4 and 5). With the HeartMate 3 in place, we noted significant surface ECG noise when compared to the HeartMate II devices; interestingly, the noise abated during the “pulse” delivered by the device every 2 seconds. However, no evidence of noise was seen in the intracardiac electrograms (Figure 5). The activation map showed clear evidence for continuous diastolic activity at the low posterolateral LV adjacent to the VAD cannula, and the propagation map also confirmed reentrant nature (Figure 4). The duo-decapolar catheter was replaced with an irrigated ablation catheter (8 Fr FlexAbility, F-J curve, Abbott); mid-diastolic activation during VT was seen, and ablation at this location terminated VT-1 within a few seconds (Figures 2A and 6). Further ablation was done targeting the substrate, and guided by fractionated electrograms and late potentials. Re-induction following this resulted in induction of a second VT with a left bundle branch block pattern with a CL of 440 ms, inferior axis, and V3 transition (VT-2). Activation map performed during VT-2 showed likely a microreentrant circuit within a small area of scar in the mid anteroseptal/anterior wall, where again, continuous diastolic activation was seen. Ablation at this location terminated VT-2 within seconds (Figures 2B and 7). No further sustained VTs were inducible with aggressive extrastimulus testing from the RV and LV. There were no procedure-related complications.
Amiodarone was discontinued, and the patient was discharged home in stable condition. He did not have any further VT episodes at 4-month follow-up.
This case highlights the management of ventricular arrhythmias in patients who receive continuous flow LVADs. The latest in the evolution of the continuous flow LVADs is the HeartMate 3, with several unique features aimed at reducing LVAD-related complications.2,12 While evidence supports a reduction in post-LVAD arrhythmias due to cardiac unloading, reverse remodeling, and reduction of QRS interval and QT duration, VAs are still quite common (20-50%) in these patients, with the incidence of reported VT/VF being as high as 20.2% in the first 30 days after implant and 23.4% in the late post-operative period.4-6 A history of pre-LVAD VT has been considered as the most important predictor of post-procedure VT/VF occurrence.4,5 Post-implant VA may recur in up to 45.5% patients with prior VA history versus only 4.0% with de novo arrhythmia after surgery.5 In a large series of 100 patients with predominantly ischemic cardiomyopathy and the HeartMate LVAD, Ziv et al observed that new monomorphic VT occurred more frequently than polymorphic VT/VF; they further observed that the nature of these arrhythmias was more incessant in post-surgical patients with resistance to antiarrhythmic drugs.7 Early post-operative VA (polymorphic or monomorphic) can be exacerbated and related to a number of factors including ongoing ischemia, inflammation, electrolyte imbalance, inotropic support, and QT prolongation (effect of mechanical unloading on cardiac repolarization).3,5-8,11
Although the newer LVADs are thought to reduce the overall complications related to assist devices, there is a paucity of randomized data comparing arrhythmogenesis in pulsatile versus continuous flow VADs. Additionally, the effect of VA on mortality is controversial.5-8 While they are usually well tolerated by LVAD-supported patients, sustained and prolonged arrhythmia can cause RV dysfunction, decreased cardiac output, poor quality of life, and frequent hospitalizations.6-8,12 Garan et al observed that incessant early arrhythmia and ICD shocks occur more commonly in older patients with non-ischemic cardiomyopathy, and have shown a trend towards decreased survival, prolonged hospitalization, and RV failure.3 The most important question in this regard is whether prophylactic or aggressive early intervention results in decreased mortality. Earlier data is indicative of a potential benefit based on observations made in LVAD patients with ICDs programmed to detect and treat VT/VF.3,9,13 Studies have also shown an increased likelihood of arrhythmia recurrence in patients with pre-LVAD VA, its association with decreased survival, and improved outcomes in those with implanted ICDs.4,9,13 The role of VA occurrence and ICD therapies is less well defined in continuous flow LVADs.13 Enriquez et al showed no mortality benefit in 106 consecutive patients undergoing HeartMate II LVAD implants, with 63% having active ICDs and 27% receiving appropriate therapy for VAs.14
Despite lack of definitive guidelines, various non-randomized single and multicenter cohort studies favor interventions to reduce arrhythmia burden and definitive therapy to prevent recurrence. Amiodarone is the preferred drug therapy in these patients, but as observed by Ziv et al, a significant proportion of VT/VF becomes incessant and drug resistant.7 Catheter ablation of arrhythmias has been reported as a safe and feasible option in this subgroup.15-17
The mechanisms for monomorphic VT, particularly those that occur later in the post-operative course, are thought to be due to focal or scar-related macroreentrant mechanisms.10 Scar is present prior to LVAD in many patients, while in others, it may develop post operatively.15 Prior reports implicated the role of apical inflow cannula in VT generation; however, recent series show that the majority of sustained VTs arise from preexistent scar rather than suction events or other interference related to the inflow cannula.15,16 Ablation adjacent to the cannula site can be tedious with limited success for several reasons, including extreme care to avoid catheter entrapment, lack of accuracy with 3-dimensional mapping because of magnetic interference, inaccessible epicardial substrate, and inadequate power delivery on or near the sewing ring.10,12 Cannula site VT has most often a right bundle branch morphology, superior axis, and late transition (V3-V5). The RBBB superior axis VT (VT-1) in our patient was successfully mapped despite magnetic interference, terminated with ablation, and remained non-inducible. From an operator’s perspective, it is vital to understand the limitations of available tools and improvise where needed to achieve the desired results.
The approach to catheter ablation in LVAD patients can be either substrate homogenization until VT is rendered non-inducible, or targeted to a specific mechanism when VT is inducible and tolerated.10 Some authors recommend reducing LVAD speed with permissive hypotension to decrease magnetic interference. Additionally, the use of ICE for real-time imaging, as well as incorporating features from mapping systems that allow for superimposition of implanted hardware on 3D maps, may be helpful.18
We opted for a stepwise approach in this patient: 1) We characterized the substrate with voltage map; 2) We used a duo-decapolar catheter with 2x2 spacing to create a detailed map of the late potentials as well as an activation map of VT; and 3) We identified the mechanism and continuous diastolic activity correlating with reentry with successful ablation using an irrigated tip catheter.
Salient Features of the HeartMate 3 Left Ventricular Assist System:
- Textured blood-contacting surfaces encourage a tissue-to-blood interface, which potentially reduces complications;
- Full MagLev™ (magnetically-levitated) Flow technology allows the device’s rotor to be “suspended” by magnetic forces, preventing friction and wear and tear on the rotor, and reducing blood trauma through gentle blood handling;
- Artificial Pulse technology prevents the formation of zones of recirculation and stasis.19
Challenges to Performing VT Ablation with the HeartMate 3:
- We have found a high-frequency noise on surface ECG makes morphology discrimination challenging; noise seems to disappear with higher revolutions per minute (rpms) during the “pulse” delivery by the device every 2 seconds;
- Inflow cannula may limit mapping and ablation of arrhythmia originating around insertion;
- Retrograde approach may be challenging;
- Transseptal puncture into a decompressed smaller sized left atrium may pose higher risk of perforation;
- Fluoroscopic barriers: LVAD cannula and drive line, prior implanted leads, pacing catheters, and transseptal sheath;
- Inadequate power delivery on cannula adjacent target sites;
- Epicardial access is usually not feasible.10,12
VT ablation in patients with the LVAD is safe and feasible. However, there are some potential challenges for the operator with regard to procedure planning, patient optimizing strategies, or performing the ablation. Based on available data, catheter ablation should be offered to patients with VT/VF with multiple ICD shocks that do not respond to medical therapy. ICD therapies in these patients is known to increase morbidity. More data is needed regarding the role of pre-surgical MRI-based substrate characterization, preemptive ablation during LVAD implant, particularly at the cannula insertion site, and optimal device programming in patients with continuous flow devices.
Disclosures: Dr. Batul has no conflicts of interest to report regarding the content herein. Dr. Gopinathannair reports consultancy/honoraria with Abbott, Pfizer, and ZOLL Medical Corporation; he is also on the advisory board at HealthTrust PG.
- Nakhara S, Chien C, Gelow J, et al. Ventricular arrhythmias after left ventricular assist device. Circ Arrhythm Electrophysiol. 2013;6:648-654.
- Mehra MR, Naka Y, Uriel N, et al; MOMENTUM 3 Investigators. A fully magnetically levitated circulatory pump for advanced heart failure. N Engl J Med. 2017;376:440-450.
- Garan AR, Levin AP, Topkara V, et al. Early post-operative ventricular arrhythmias in patients with continuous-flow left ventricular assist devices. J Heart Lung Transplant. 2015;34:1611-1616.
- Makki N, Mesubi O, Steyers C, Olshansky B, Abraham WT. Meta-analysis of the relation of ventricular arrhythmias to all-cause mortality after implantation of a left ventricular assist device. Am J Cardiol. 2015;116:1385-1390.
- Garan AR, Yuzefpolskaya M, Colombo PC, et al. Ventricular arrhythmia and implantable cardioverter-defibrillator therapy in patients with continuous-flow left ventricular assist devices: need for primary prevention? J Am Coll Cardiol. 2013;61:2542-2550.
- Effimova E, Fischer J, Bertagnolli L, et al. Predictors of ventricular arrhythmia after left ventricular assist device implantation: A large single-center observational study. Heart Rhythm. 2017;14:1812-1819.
- Ziv O, Dizon J, Thosani A, Naka Y, Magnano AR, Garan H. Effects of left ventricular assist device therapy on ventricular arrhythmias. J Am Coll Cardiol. 2005;45:1428-1434.
- Raash H, Jensen BC, Chang PP, et al. Epidemiology, management, and outcomes of sustained ventricular arrhythmias after continuous-flow left ventricular assist device implantation. Am Heart J. 2012;164:373-378.
- Cantillon DJ, Tarakji KG, Kumbhani DJ, Smedira NG, Starling RC, Wilkoff BL. Improved survival among ventricular assist device recipients with concomitant implantable cardioverter-defibrillator. Heart Rhythm. 2010;7:466-471.
- Sacher F, Reichlin T, Zado ES, et al. Characteristics of ventricular tachycardia ablation in patients with continuous flow left ventricular assist devices. Circ Arrhythm Electrophysiol. 2015;8:592-597.
- Harding JD, Piacentino V 3rd, Rothman S, Chambers S, Jessup M, Margulies KB. Prolonged repolarization after ventricular assist device support is associated with arrhythmias in humans with congestive heart failure. J Card Fail. 2005;11(3):227-232.
- Hottigoudar RU, Deam G, Slaughter MS, et al. Ventricular tachycardia ablation in patients with HeartMate II left ventricular assist devices: rhythm matters in the bionic age. J Innov Cardiac Rhythm Manag. 2011;2:537-547.
- Vakil K, Kazmirczak F, Sathnur N, et al. Implantable cardioverter-defibrillator use in patients with left ventricular assist devices: A systematic review and meta-analysis. JACC Heart Fail. 2016;4:772-779.
- Enriquez AD, Calenda B, Miller MA, Anyanwu AC, Pinney SP. The role of implantable cardioverter-defibrillators in patients with continuous flow left ventricular assist devices. Circ Arrhythm Electrophysiol. 2013;6(4):668-674.
- Snipelisky D, Reddy YN, Manocha K, et al. Effect of Ventricular Arrhythmia Ablation in Patients with Heart Mate II Left Ventricular Assist Devices: An Evaluation of Ablation Therapy. J Cardiovasc Electrophysiol. 2017;28:68-77.
- Moss JD, Flatley EE, Beaser AD, et al. Characterization of ventricular tachycardia after left ventricular assist device implantation as destination therapy. A single center experience. J Am Coll Cardiol EP. 2017. (Article in press)
- Garan AR, Iyer V, Whang W, et al. Catheter ablation for ventricular tachyarrhythmias in patients supported by continuous-flow left ventricular assist devices. ASAIO J. 2014;60:311-316.
- Higgins SL, Haghani K, Meyer D, Pless T. Minimizing magnetic interaction between an electroanatomic navigation system and left ventricular assist device. J Innov Cardiac Rhythm Manag. 2013;4:1440-1446.
- HeartMate 3™ Left Ventricular Assist System (LVAS) Fact Sheet. Abbott. Available online at http://bit.ly/2AUfRrk. Accessed December 18, 2017.