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Successful Ablation of Re-Entrant and Focal Ventricular Tachycardia in a Patient with Heparin-Induced Thrombocytopenia and Pericardial Adhesions

Introduction

Catheter ablation of ventricular tachycardia (VT) in patients with non-ischemic cardiomyopathy (NICM) can be challenging. Presence of heparin-induced thrombocytopenia (HIT) and pericardial adhesions add to the complexity of endocardial and epicardial ablation. We present a case of a patient with VT, HIT, and inferior pericardial adhesions that was successfully ablated epicardially despite adhesions in the inferior pericardial space.

Case Description

A 45-year-old female, with a history of NICM and an ejection fraction of 25%, had combined endocardial and epicardial ablation for VT two months before presenting to our hospital with VT storm. Her previous procedure was complicated by HIT. On presentation, the patient was on sotalol, amiodarone, and mexiletine. However, she continued to have runs of slow VT requiring frequent anti-tachycardia pacing. Her clinical VT was right bundle branch block (RBBB) with right inferior axis morphology with QS in lead I and aVL. VT cycle length was 480 msec (Figure 1A). Given the history of HIT and VT morphology, it was decided to proceed with epicardial mapping before endocardial to avoid heparin use. Initially, inferior epicardial approach using the technique by Sosa et al1 was attempted but unsuccessful, and the wire could not be advanced into the pericardial space. Contrast injection through an 18G needle showed the presence of inferior pericardial adhesions (Figures 2A and 4B), likely from previous epicardial access and ablation. We then abandoned the inferior approach, and anterior pericardial access was attempted successfully; no adhesions were encountered in the anterior pericardial space (Figures 2A and 4B). A long, flexible sheath (35-cm Super Arrow-Flex sheath, Teleflex) was advanced over the guidewire into the pericardial space without any difficulty. Programmed stimulation was then performed from the right ventricle, and the patient’s clinical VT was easily inducible. Activation mapping showed a broad area of early activation in the inferolateral basal left ventricle. Entrainment was then performed to identify the critical isthmus (Figure 1B). After ensuring a safe distance of the ablation catheter to the major epicardial coronary arteries and phrenic nerve, ablation was performed at the site of concealed entrainment with long stimulus to QRS interval, resulting in immediate termination of VT (Figures 3A-2D). Repeat extrastimulus testing resulted in induction of VT2 (Figure 4A). VT2 was RBBB with right superior axis in morphology. Mapping of this VT was then done and the activation pattern was centrifugal, suggesting focal or microreentrant VT. Pace mapping showed a 98% match at the earliest site (Figure 4B) and ablation was performed here with immediate termination of VT2 (Figures 4C and 3D). Repeat ventricular extrastimulus testing showed no inducible VT. The patient had an uneventful hospitalization course and was planned for an advanced heart failure therapy. After 9-month follow-up, there was no recurrent episode of sustained VT.

Discussion

NICM patients with refractory VT remain a challenging patient population. Pre-procedural planning and anticipation of challenges can help improve the success rate and minimize complications during VT ablation. HIT, pericardial adhesions, and multiple VT morphologies are some of the difficulties we encountered in our case. HIT can increase the risk of thromboembolism during endocardial mapping as heparin is avoided. Baetz et al reported successful VT ablation with bivalirudin use in a patient2; however, given lack of data and experience, its routine use is not established. Twelve-lead ECG, if available, can help guide the initial mapping strategy. QRS characteristics that suggest epicardial origin include maximum deflection index >0.59, pseudo-delta wave >75 msec, and presence of Q waves in lateral leads are more reliable in patients with non-ischemic cardiomyopathy than ischemic cardiomyopathy.3 In a patient with HIT and suggestive ECG features of epicardial origin, it may be prudent to do only epicardial mapping and ablation. Pericardial adhesions from the previous ablation can happen if the inflammatory reaction is intense, even with the use of intrapericardial steroids.4,5 They are usually identified at the time of attempted repeat access as contrast pooling and difficulty in advancing the wire in the pericardial space. The presence of such adhesions can make repeat ablation challenging. In this situation, instead of persisting with repeated attempts and risking RV injury, it may be prudent to try entering the pericardial sac from an alternate surface of the pericardium.6 If there are dense adhesions inferiorly, anterior access may be successful, as was in our case. There have been case reports of adhesiolysis using the mapping catheter; however, most of these adhesions are vascular, and disruption can cause significant pericardial bleeding. Also, focal/microreentrant VT can co-occur with reentrant VT in patients with structural heart disease. Careful activation mapping and entrainment response can help delineate the mechanism. Thus, this case highlights several important aspects of VT ablation in this challenging population. 

Learning Points

  • Anterior epicardial access can be successful when inferior approach has failed due to pericardial adhesions, or vice versa;
  • In patients with HIT and ECG features suggestive of epicardial origin, only epicardial mapping and ablation should be initially attempted;
  • Concomitant focal/microrentrant and macroreentrant VT can occur in NICM patients.

Disclosures: The authors have no conflicts of interest to report regarding the content herein. Additionally, the authors disclose that this research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors.

References

  1. 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(6):531-536. 
  2. Baetz BE, Gerstenfeld EP, Kolansky DM, Spinler SA. Bivalirudin use during radiofrequency catheter ablation procedures in two patients with a history of heparin-induced thrombocytopenia. Pharmacotherapy. 2010;30(9):952.
  3. Valles E, Bazan V, Marchlinski FE. ECG criteria to identify epicardial ventricular tachycardia in nonischemic cardiomyopathy. Circ Arrhythm Electrophysiol. 2010;3(1):63-71.
  4. Buch E, Boyle NG, Shivkumar K, Bradfield JS. Incidence and significance of adhesions encountered during epicardial mapping and ablation of ventricular tachycardia in patients with no history of prior cardiac surgery or pericarditis. Heart Rhythm. 2017 Sep 14.
  5. d'Avila A, Neuzil P, Thiagalingam A, Gutierrez P, Aleong R, Ruskin JN, Reddy VY. Experimental efficacy of pericardial instillation of anti-inflammatory agents during percutaneous epicardial catheter ablation to prevent postprocedure pericarditis. J Cardiovasc Electrophysiol. 2007;18(11):1178-1183.
  6. Keramati AR, DeMazumder D, Misra S, Chrispin J, Assis FR, Raghuram C, Dey S, Calkins H, Tandri H. Anterior pericardial access to facilitate electrophysiology study and catheter ablation of ventricular arrhythmias: A single tertiary center experience. J Cardiovasc Electrophysiol. 2017;28(10):1189-1195.

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