When Interventions Collide: Challenges in Ventricular Tachycardia Ablation After PARACHUTE Device Placement

Background

Ablation for ventricular tachycardia (VT) provides an effective and increasingly utilized management strategy for recurrent or medically refractory ventricular tachycardia in advanced heart failure populations. Recently, additional investigational percutaneous therapies have been developed for patients with refractory heart failure and ischemic cardiomyopathy. One such therapy, the PARACHUTE device (CardioKinetix), involves deployment of a partitioning membrane into the left ventricular cavity to isolate the aneurysmal portion of the left ventricle (LV) from the circulation. The potential therapeutic benefit relies on LV volume reduction and improved LV remodeling by decreasing ventricular tension transmitted to the aneurysmal segment.¹ The device has completed efficacy and feasibility trials, and is currently undergoing a randomized clinical trial.

Case Description

A 64-year-old male with coronary artery disease and prior coronary artery bypass grafting many years ago complicated by ischemic cardiomyopathy with a large LV anteroapical aneurysm and ejection fraction of 15% presented to our institution with NYHA Class III congestive heart failure. A cardiac resynchronization therapy defibrillator was implanted previously. He underwent PARACHUTE implantation in 2014 because of refractory heart failure. After PARACHUTE implantation, he experienced marked improvement of heart failure symptoms to stable NYHA class II heart failure on medical therapy. He later developed recurrent monomorphic ventricular tachycardia with multiple appropriate ICD shocks over several days, which continued despite trials of amiodarone and sotalol. He was referred to our laboratory for ablation of ventricular tachycardia.

We performed an electrophysiology study for VT induction and ablation using an endocardial approach. Quadripolar catheters were advanced into the right ventricle and His positions. An intracardiac echo catheter was advanced into the RV to construct chamber geometry in Carto (Biosense Webster, Inc., a Johnson & Johnson company) and visualize the PARACHUTE (Figure 1). Anticoagulation was achieved with IV heparin to target an activated clotting time of 300-350 seconds. We performed LV mapping using a transseptal approach initially. Transseptal puncture was performed using a SL1 sheath and BRK1 needle under ICE guidance, and the SL1 sheath was exchanged for a steerable long curve Agilis introducer (St. Jude Medical). A ThermoCool SF ablation catheter (Biosense Webster, Inc., a Johnson & Johnson company) was advanced and used to create an LV voltage map. Ventricular programmed stimulation was performed from the right and left ventricle.

Two primary VT morphologies that shared a similar cycle length of 490-500 msec were induced (Figure 2). The initial VT exhibited an inferior axis with predominately negative leads I and aVL and positive precordial concordance. This VT terminated during mapping. A second VT exhibited a superior axis and a predominately negative QRS in the precordial leads. This VT was more stable, did not cause hemodynamic compromise, and was successfully mapped. We localized an area of mid-diastolic activation during VT at the most apical anterior portion of the LV not covered by the PARACHUTE (Figure 3). Ablation here resulted in slowing and termination of the VT (Figure 4). This VT morphology was no longer inducible. Further attempts at induction resulted in faster unstable VT (not clinically observed or recorded from ICD electrograms) requiring cardioversion. Additional ablation was performed using a substrate modification approach targeting areas of late potentials along the anterior scar and border zones using both a transseptal and retrograde approach. Extensive ablation was performed along the anterior and anterolateral LV scar. There was a significant segment of the LV apex that could not be mapped due to partitioning from the PARACHUTE. The two primary VT morphologies were no longer inducible at the end of the study.

Discussion

Ablation for ventricular tachycardia in a patient with a PARACHUTE has been previously reported.² However, experience is limited, as the device is still investigational and not in widespread use. Placement of an endocardial LV partition presents several challenges for management of VT in ischemic heart disease. First and foremost, the device physically excludes a portion of the LV endocardium from access with an ablation catheter. This anatomical partitioning is, in fact, the intended purpose of the device. LV aneurysms have long been known to be particularly arrhythmogenic and have been targets for both surgical and catheter ablative management of VT.³ It is thus very likely that patients with a PARACHUTE device will have an ideal substrate for monomorphic VT, and, in some cases, part or all of the substrate may be difficult or impossible to map and ablate because it is covered by the partition device. Additional ablation strategies should be considered when ECG morphology and VT mapping indicate a VT site is in the area protected by the PARACHUTE. An epicardial approach may prove effective; however, prior CABG, as in this case, may limit the ease of this approach. Although epicardial mapping and ablation in prior CABG patients has been described using a surgical window, we did not pursue this as an initial management strategy in this case.

While the PARACHUTE excludes a portion of the LV aneurysm, there is likely to be additional scar and border-zone outside the PARACHUTE, which can provide potentially successful targets for ablation. We found such a site just outside the area excluded by the PARACHUTE and achieved successful termination of a clinical VT with ablation in this area. Additionally, we also induced a more basal and superior VT, which appeared to exit far from the PARACHUTE with this exit site supported by close pacemapping match. It is reasonable to perform extensive substrate modification in such instances to target all other potential sources of VT not covered by the PARACHUTE.

Another important consideration should be anticoagulation and timing of ablation after PARACHUTE deployment. As our patient was a year out from device implantation, the PARACHUTE was felt to have been fully endothelialized, and conventional peri-procedural anticoagulation was utilized.

Additionally, given the known likelihood of VT in patients with ventricular aneurysms, it may be reasonable to consider EPS for VT inducibility and potential ablation, prior to proceeding with PARACHUTE placement, should the device show benefit and gain widespread use.

Disclosures: The authors have no conflicts of interest to report regarding the content herein.  

References

1. Mazzaferri EL Jr, Gradinac S, Sagic D, et al. Percutaneous left ventricular partitioning in patients with chronic heart failure and a prior anterior myocardial infarction: results of the PercutAneous Ventricular RestorAtion in Chronic Heart failUre PaTiEnts Trial. Am Heart J. 2012;163:812-820.
2. Lauschke, J, Schneider, R, Bansch, D. Ventricular tachycardia ablation in a patient with a parachute device – a decent word of warning. Europace. 2014;16:207.
3. Josephson ME, Horowitz LN, Farshidi A, Spear JF, Moore EN. Recurrent sustained ventricular tachycardia. 2. Endocardial mapping. Circulation. 1978;57:440-447.