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Case Study

Challenges in Ablating Left Ventricular Summit Arrhythmias

July 2024
© 2024 HMP Global. All Rights Reserved.

Any views and opinions expressed are those of the author(s) and/or participants and do not necessarily reflect the views, policy, or position of EP Lab Digest or HMP Global, their employees, and affiliates.

EP LAB DIGEST. 2024;24(7):18-19.

Mapping and ablating left ventricular (LV) summit premature ventricular complexes (PVCs) or ventricular tachycardia (VT) can be very challenging due to the proximity to critical cardiac structures such as the bifurcation of the left main coronary artery and aortic valve. This procedure requires precise catheter navigation during mapping and ablation to achieve a successful outcome and avoid drastic complications.

This report describes our experience in the cardiac electrophysiology (EP) laboratory targeting this type of cardiac arrhythmia.

Case Presentation

A 58-year-old male with a history of ischemic heart disease and a percutaneous intervention to the left anterior descending artery, presenting with frequent PVCs, was admitted with palpitations and dyspnea on exertion. Frequent PVCs were noted on 12-lead electrocardiogram (ECG) (Figure 1A), suggesting an LV summit origin, despite being on metoprolol succinate 25 mg daily. The patient was referred to cardiac EP for PVC management. After discussing treatment options, the patient opted to undergo an EP study and catheter ablation.

After obtaining consent, the patient presented to the EP laboratory in a fasting state. An ECG showed the patient had sinus rhythm with PVCs in bigeminy. The patient was prepped and draped in a sterile manner. The right common femoral vein was accessed twice under ultrasound guidance, and 12 French (F) and 8F sheaths were placed in that vein. The right common femoral artery was also accessed under ultrasound guidance, and a 9F sheath was placed in that artery.

The LV summit area was mapped using a 2F EPstar catheter (Boston Scientific). The coronary sinus (CS) was initially cannulated using an SL1 catheter and radiofrequency (RF) ablation catheter. The SL1 was placed inside the CS. The ablation catheter was removed, and a JR4 6 Fr coronary guide was advanced inside the SL1 over a 260-cm soft-tip glidewire and used to cannulate the anterior interventricular vein. The glidewire was removed and the EPstar catheter was advanced to map the LV summit area. The site of origin was bracketed by moving the EPstar catheter proximally and distally in the great cardiac vein-anterior interventricular vein (GCV-AIV) area. The earliest point of activation was 90 ms ahead of the QRS origin.

 Al Taii - Fig 1 - July 2024
Figure 1.(A) Twelve-lead ECG showing PVCs, with morphology suggesting the LV summit area. (B) Patient was in bigeminy before RF ablation (A) early after RF ablation, PVC is completely resolved (B). (C and D) Mapping the GCV and AIV using the EPstar catheter (Boston Scientific). (E) ICE image showing RF ablation catheter in contact with endocardial side of the LV summit area, showing RF lesion formation.


Next, the endocardial side of the LV summit area was approached by choosing the closest anatomical point, utilizing both fluoroscopy and intracardiac echocardiography (ICE). The endocardial surface was mapped using an irrigated-tip RF catheter.
After carefully examining the catheter location and stability, an RF power of 35-40 watts was delivered for 1-3 minutes. Suppression was achieved during the first RF lesion (Figure 1B). Five more additional RF lesions were applied in that area. No further RF lesions were required to be delivered from any other areas. After 45 minutes of monitoring, no PVCs were noted. The patient was admitted overnight for observation and 24-hour telemetry monitoring showed no recurrence of PVCs.

Discussion

Ablating arrhythmias originating from the LV summit presents unique challenges. Understanding cardiac anatomy is critical to successfully treating LV summit ventricular arrhythmias. High-density electroanatomical mapping is instrumental to accurately localizing the origin of the arrhythmic site and its relation to the left main coronary, left anterior descending, and left circumflex arteries, and avoiding serious complications during ablation. Different ablation strategies have been described, such as the combined epicardial and endocardial approach by ablating distally in the GCV-AIV junction after obtaining a coronary angiogram to examine coronary artery anatomy and distance to the ablation catheter tip. This helps deliver deeper lesions to reach arrhythmogenic foci. Cryoablation can be used if the arrhythmogenic foci is close to the coronary arteries; however, these catheters might not be as flexible as RF catheters, which can be challenging to deliver from the catheter tip to the distal GCV. Bipolar and ethanol ablation are other strategies that have been successfully adopted in different centers for treating this type of arrhythmia.

In our experience, we have been successful in eliminating LV summit arrhythmias by carefully mapping the GCV, AIV, and septal vein areas. Once the earliest spot in the LV summit is bracketed (Figures 1C and 1D), we approach the closest endocardial point to the earliest electrogram (EGM) noted on the EPstar mapping catheter and carefully examine the sharpness of EGM in that area, even though the activation timing is not the earliest in that spot. Another aspect to successfully eliminating these arrhythmias is catheter stability during RF delivery; this can be achieved via closely monitoring catheter stability with ICE. Furthermore, ICE can help assess lesion size and ensure adequate depth during RF delivery (Figure 1E).

Summary 

This case demonstrates a simplified approach to successfully mapping and treating LV summit arrhythmias. Continued research and advanced technology in electroanatomical mapping and ICE are essential to refine ablation techniques and improve care in complex arrhythmias. 

Haider AL Taii, MD1; Ramez Morcos MD2Arun Narayanan MD1; Muhie Dean Sabayon, MD1

1Department of Internal Medicine, Division of Cardiovascular Medicine, University of Texas Medical Branch, Galveston, Texas; 2Geisinger Heart Institute, Wilkes Barre, Pennsylvania

Disclosure: The authors have completed and returned the ICMJE Form for Disclosure of Potential Conflicts of Interest, and report no conflicts of interest regarding the content herein. 


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