Epicardial ventricular arrhythmia ablation: a clinical consensus statement of the European Heart Rhythm Association of the European Society of Cardiology and the Heart Rhythm Society, the Asian Pacific Heart Rhythm Society, the Latin American Heart Rhythm Society, and the Canadian Heart Rhythm Society

Abstract

Epicardial access during electrophysiology procedures offers valuable insights and therapeutic options for managing ventricular arrhythmias (VAs). The current clinical consensus statement on epicardial VA ablation aims to provide clinicians with a comprehensive understanding of this complex clinical scenario. It offers structured advice and a systematic approach to patient management. Specific sections are devoted to anatomical considerations, criteria for epicardial access and mapping evaluation, methods of epicardial access, management of complications, training, and institutional requirements for epicardial VA ablation. This consensus is a joint effort of collaborating cardiac electrophysiology societies, including the European Heart Rhythm Association, the Heart Rhythm Society, the Asia Pacific Heart Rhythm Society, the Latin American Heart Rhythm Society, and the Canadian Heart Rhythm Society.

Keywords: Cardiomyopathies; Catheter ablation; Clinical consensus statement; Electrophysiology procedures; Epicardial access; Ventricular arrhythmias; Ventricular fibrillation; Ventricular tachycardia.

Figure 1

Anatomy of the human pericardium (anterior view)—fibrous pericardium (A) and serous pericardium with epicardium (B). Image adapted with permission from the Image Courtesy of the UCLA Cardiac Arrhythmia Center, Amara-Yad Project Collection.

Figure 2

Pericardial reflections and hilar orifices around the great cardiac vessels (posterior view). Image adapted with permission from the Image Courtesy of the UCLA Cardiac Arrhythmia Center, Amara-Yad Project Collection.

Figure 3

Upper panel: Anterior and posterosuperior view of the pericardium showing the superior or arterial hilum (red string) and the posterior or venous hilum (blue string), with the distribution of the main pericardial sinuses and recesses. Lower panel: Coronal and paramedian section of the thorax depicting the anatomical relations of the pericardium within the thorax. Left lower panel: 1. clavicle; 2. left brachiocephalic vein; 3. upper lobe of the right lung; 4. aortic arch; 5. superior vena cava; 6. right atrium; 7. coronary sinus; 8. liver; 9. second rib; 10. upper lobe of left lung; 11. pulmonary trunk; 12. ascending aorta and left coronary artery; 13. aortic valve; 14. pericardium; 15. left ventricle; 16. the lower lobe of the left lung; 17. diaphragm; 18. colon. Right lower panel: 1. aortic arch; 2. left atrium; 3. oesophagus; 4. right atrium; 5. liver. Image adapted with permission from the UCLA Cardiac Arrhythmia Centre, Amara-Yad Project Collection, and Wolters Kluwer.

Figure 4

Basics for ventricular arrhythmia-ECG morphological criteria in patients with non-ischaemic cardiomyopathy. Depolarization and ECG morphology in posterior and inferior monomorphic ventricular arrhythmias in patients with non-ischaemic cardiomyopathies with endocardial (A) and epicardial (B) exit sites. Adapted with permission from Vallès et al.

Figure 5

Four-step algorithm based on inferior Q-waves in inferior and lead I, pseudodelta, and maximum deflection index to identify left ventricular epicardial ventricular tachycardia (VT) in patients with non-ischaemic cardiomyopathy based on VT-QRS morphology. This algorithm applies to ‘basal-superior/posterior’ VTs in non-ischaemic cardiomyopathy. Adapted with permission from Vallès et al.

Figure 6

Major arteries located near the epicardial puncture site. Please note the vicinity of the left superior epigastric, left musculophrenic, and left internal thoracic (mammary) arteries to the puncture site. Image adapted with permission from the Image Courtesy of the UCLA Cardiac Arrhythmia Center, Amara-Yad Project Collection.

Figure 7

Left: Anatomic location of Larrey's space. Right: anterior (A, shallow < 45) vs. posterior (B, steep > 45) approach for subxiphoid puncture using Tuohy Needle. Be aware that using the posterior approach results in diaphragmatic puncture, potentially leading to intra-abdominal injuries. Image adapted with permission from the Image Courtesy of the UCLA Cardiac Arrhythmia Center, Amara-Yad Project Collection.

Figure 8

(A) Inferior subxiphoid puncture in right anterior oblique projection. (B) Anterior subxiphoid puncture in left lateral projection. Blue arrows show the entrance of the needle into the epicardial space. The green arrow indicates CO₂ insufflation (upper arrow - B).

Figure 9

Virtual and fluoroscopic visualization of epicardial guidewire pathways is presented. The left panel: virtual guidewire trajectories through the anterior (red, the line without arrow) and inferior (yellow, the line with arrow) approaches on a 3D cardiac reconstruction. The arrowheads mark the location of the guidewire. The right panel: use of a long guidewire inside the pericardium (arrow heads) to demonstrate the crossing of multiple chambers encircling the heart. Image adapted with permission from the Image Courtesy of the UCLA Cardiac Arrhythmia Center, Amara-Yad Project Collection.

Figure 10

Surgical access for epicardial ablation. The surgical window approach for epicardial access involves creating a small subxiphoid incision to reach the pericardial space. (A and B) A limited incision is made just beneath the xiphoid process, and the subcutaneous tissues are dissected to reveal the pericardium. A small incision in the pericardium is performed under direct visualization to prevent injury to adjacent structures. (C and D) A flexible sheath is then advanced into the pericardial space, facilitating the insertion of mapping and ablation catheters. (E and F) 3D late potential mapping and 3D mapping integrated with fluoroscopy images.

Figure 11

Planning and ablation of epicardial ventricular tachycardia (VT) in a patient with cardiac sarcoidosis. (A) ECG: The initial step in procedural planning involves the ECG, showing the presence of a large pseudodelta wave, and the QRS axis-based algorithm indicates an inferoseptal and basal exit of the VT. The suspected segment of origin is highlighted in purple. (B) Cardiac imaging: Cardiac magnetic resonance imaging (CMR) confirms the presence of an inferoseptal scar. CMR Segmentation reveals a channel with an inferoseptal extension, potentially involved in the clinical VT. The CMR is integrated with a computed tomography scan to confirm the channel's anatomical location within the patient's specific anatomy. (C) Ablation procedure: Despite its clear epicardial origin, the VT was terminated after the first application, as the middle cardiac vein coincided with the VT isthmus trajectory. The lower panel illustrates the reconstruction of the coronary venous system and its integration with the electroanatomical map.

Figure 12

Epicardial puncture is not necessary in all patients with an epicardial substrate. Top panel: A patient with an early stage arrhythmogenic right ventricular cardiomyopathy (ARVC) is shown. The bipolar voltage map of the right ventricular endocardium (left) shows a small low-voltage area on the subtricuspid region. Unipolar voltage map of the right ventricular endocardium showing a significant area of low unipolar voltage (middle). Significant epicardial scar is observed in regions opposite those with low unipolar voltage. A large arrhythmogenic epicardial substrate area with late potential channels is shown (right). The ventricular arrhythmia (VA) was successfully ablated from the epicardium. Lower panel: A patient at a late stage of ARVC is shown. The bipolar voltage map of the right ventricle shows already a big area of low voltage on the endocardial surface (left). An extensive area of low unipolar voltage is observed (middle). The unipolar endocardial voltage map indicates the presence of epicardial involvement. The bipolar epicardial map shows a very large epicardial scar area. Bipolar vs. unipolar low-voltage area (LVA) ratios and epicardial arrhythmogenic substrate area (ASA) values are shown. The VAs were successfully ablated endocardially. The image was adapted with permission from Berruezo et al.

Figure 13

Algorithm for differentiation between scar and viable myocardium during epicardial mapping. Adapted with permission from Piers et al.

Figure 14

Clinical presentation, investigation, management, and prevention of pericarditis and pericarditis-related symptoms.^,, NSAID, non-steroidal anti-inflammatory drugs.

Figure 15

Clinical presentation, investigation, management, and prevention of tamponade and haemopericardium.^, HP, haemopericardium; T, tamponade.

Figure 16

(A) Integration of coronary angiography in 3D mapping during the ablation procedure. The large white points delineate the course of the left phrenic nerve. (B) Three-dimensional epicardial surface mesh colour-coded for fat thickness. (C) Fusion between the electroanatomical mapping and epicardial three-dimensional surface reconstruction showing coronary arteries and colour-coded fat thickness, registered using the left main coronary artery (LM) landmark. The triangle demonstrates the predicted epicardial target site in the vicinity of the left anterior descending artery (LAD), covered by >4 mm of fat. Images B and C are adapted with permission from van Huls van Taxis et al.

Figure 17

Clinical presentation, investigation, management, and prevention of phrenic nerve damage.^, BiPAP, bilevel positive airway pressure; CPAP, continuous positive airway pressure; PTA, percutaneous transcatheter angioplasty.

Figure 18

Phrenic nerve palsy after epicardial ablation for refractory ventricular tachycardia. (A and B) Anteroposterior and lateral chest X-rays before the procedure, showing the normal position of the left diaphragm dome. (C and D) Elevation of left hemidiaphragm, particularly in the posterior segment, after epicardial ablation. Note the relative elevation of the gastric bubble after the nerve palsy.