Atlas Contents

Epicardial ablation of arrhythmias

Epicardial mapping and ablation extend electrophysiological exploration from the endocardial cavities to the outer myocardial surface. This is particularly relevant when an arrhythmic substrate is subepicardial or intramural, when endocardial energy cannot reach it, or when anatomical obstacles prevent an effective endocardial approach. The epicardial surface, however, is not a smooth and uniformly accessible shell. It is shaped by the pericardium, coronary vessels, epicardial fat, phrenic nerves, appendages, and the changing relations between the heart, diaphragm, lungs, and mediastinum. [1-4]

1  Anatomical basis of the epicardial approach

The visceral layer of the serous pericardium adheres to the heart and forms the epicardium. It reflects onto the parietal layer around the arterial and venous roots, creating the transverse and oblique sinuses and multiple recesses. The potential pericardial cavity normally contains only a small amount of fluid. Once entered, it permits a catheter to move over much of the ventricular surface, but reflections around the great arteries and caval and pulmonary veins limit passage towards the superior and posterior atria. The fibrous pericardium is fused inferiorly to the central tendon of the diaphragm and attached anteriorly by variable sternopericardial ligaments. [3,4]

Percutaneous access is usually obtained through the subxiphoid region. The anatomical corridor passes near the xiphoid process, costal margin, diaphragm, pleural reflections, liver, and anterior or inferior ventricular surfaces. Respiratory phase, body habitus, cardiomegaly, and xiphoid morphology alter these relationships. The right ventricle occupies most of the anterior surface and has a relatively thin wall; it is therefore especially vulnerable during entry. A guidewire that freely outlines the cardiac silhouette in several projections supports intrapericardial placement, whereas a restricted or intracavitary course requires reassessment.

2  Distribution of epicardial arrhythmic substrates

The likelihood of an epicardial substrate depends on the underlying disease. Epicardial or subepicardial scar is frequent in arrhythmogenic right ventricular cardiomyopathy and may extend over the right ventricular free wall, often exceeding the endocardial abnormality. Non-ischaemic dilated cardiomyopathy can produce basal lateral or inferolateral left ventricular scar, while Chagas cardiomyopathy commonly involves the inferolateral and apical regions. Sarcoidosis, myocarditis, and repaired congenital heart disease may create patchy or transmural substrates. In ischaemic cardiomyopathy, scar is usually predominantly subendocardial but can be transmural and accessible from the epicardium. [2,5]

Surface activation or voltage abnormalities do not necessarily identify the full depth of disease. Epicardial fat attenuates electrogram amplitude, and distant or poorly oriented wave fronts can mimic scar. Conversely, viable epicardial myocardium may overlie intramural fibrosis. Electroanatomical findings should therefore be interpreted alongside cardiac magnetic resonance, computed tomography, unipolar endocardial mapping, and the known disease pattern.

3  Epicardial surfaces and catheter movement

After inferior access, a catheter commonly reaches the diaphragmatic surfaces of both ventricles and can then be directed around the acute or obtuse margins. The right ventricular free wall, inferior interventricular groove, left ventricular inferior and lateral walls, and apical region are relatively accessible when no adhesions are present. The anterior interventricular groove is occupied by the anterior interventricular coronary artery and great cardiac vein. Inferiorly, the corresponding groove contains the inferior interventricular artery and middle cardiac vein. At the crux, the coronary sinus, atrioventricular nodal artery, and adjacent inferior paraseptal tissues create a densely populated region.

The ventricular summit is a challenging superior epicardial region bounded by the bifurcation of the left coronary artery and related to the anterior interventricular and circumflex arteries, great cardiac vein, and anterior interventricular vein. Part of the summit is accessible through venous or adjacent endocardial sites, but the portion closest to the proximal coronary arteries is often unsuitable for direct energy delivery. The basal inferolateral left ventricle is crossed by marginal branches of the circumflex artery and accompanied by coronary veins. Anatomy must be defined for the individual target rather than inferred from a generic segmental model.

4  Epicardial fat and pericardial adhesions

Epicardial adipose tissue is concentrated in the atrioventricular and interventricular grooves and can be substantial over the right ventricle. Fat separates a catheter from myocardium, alters electrogram amplitude, reduces effective lesion formation, and may conceal coronary arteries. A broad low-voltage region in a fat-rich groove is not equivalent to myocardial scar. Cross-sectional imaging can identify fat thickness and coronary course before the procedure.

Previous cardiac surgery, pericarditis, or earlier epicardial ablation can replace the potential pericardial cavity with adhesions. Adhesions tether visceral and parietal layers, restrict guidewire and catheter movement, distort the expected relationship to the ventricular surface, and can isolate regional compartments. Their extent is unpredictable from the external scar alone. A surgical or hybrid approach may be required when the target cannot be reached safely through a percutaneous pericardial route. [2]

5  Coronary arteries and cardiac veins

The coronary arteries run beneath the epicardium, usually embedded in fat within the grooves before giving branches across the ventricular surfaces. Their proximity is the principal limitation to epicardial radiofrequency delivery. Coronary angiography or accurately integrated coronary imaging is required when a target is near a major artery or branch. The relationship must be assessed in projections that separate the catheter from the vessel, because apparent distance in one view may reflect superimposition. [2,5]

The coronary sinus and its tributaries are both landmarks and potential routes for mapping. The great cardiac vein and anterior interventricular vein approach the ventricular summit; lateral and posterolateral veins cross the left ventricular surface; and the middle cardiac vein occupies the inferior interventricular groove. Ablation from within a vein introduces additional constraints: thin venous walls, limited catheter cooling, nearby coronary arteries, and the possibility of venous injury. Venous anatomy should not be treated as interchangeable with free pericardial epicardial access.

6  Phrenic nerves and extracardiac structures

The right and left phrenic nerves descend on the lateral surfaces of the fibrous pericardium between the pericardium and mediastinal pleura. The right nerve usually relates to the superior caval vein and right atrium before reaching the diaphragm. The left nerve crosses the pericardium over the left atrial appendage and left ventricular region, although its precise course is variable. It can lie close to an epicardial target on the lateral or posterolateral left ventricle. High-output pacing is used to identify functional phrenic capture; displacement techniques may create separation when ablation would otherwise threaten the nerve. [6]

Other structures can be injured despite lying outside the pericardial cavity. The oesophagus is posterior to the left atrium and adjacent pericardial reflections. The lungs and pleura flank the heart, while the diaphragm separates the inferior pericardium from the liver and stomach. Energy delivery near these boundaries requires an understanding of both intracardiac and extracardiac anatomy. Pericardial bleeding can rapidly compress the cardiac chambers, particularly the right-sided chambers, and must be distinguished from irrigation fluid accumulating without active vascular injury.

7  Anatomical integration and clinical perspective

Epicardial ablation is most effective when access, mapping, and energy delivery are planned as a single anatomical problem. Preprocedural imaging can show scar distribution, ventricular wall thickness, coronary arteries, veins, epicardial fat, previous surgical material, and the relations of the diaphragm and abdominal organs. Fluoroscopy defines catheter movement, electroanatomical mapping reconstructs the surface, angiography protects coronary vessels, and pacing identifies the phrenic nerve. None of these methods alone fully describes the operative field.

Although the percutaneous epicardial route was developed for ventricular tachycardia, epicardial anatomy is also relevant to surgical and hybrid treatment of atrial arrhythmias. The posterior left atrium and pulmonary venous antra are constrained by the oblique sinus, pulmonary venous reflections, oesophagus, and adjacent neural structures. These approaches should be distinguished from percutaneous ventricular epicardial mapping because their access, targets, and risk profile differ. [2]

Key Anatomical Messages

  • The pericardial cavity is a reflected and regionally restricted space rather than a uniform sac.
  • The anterior right ventricular wall is particularly vulnerable during subxiphoid entry.
  • Epicardial fat can mimic low voltage scar and reduce lesion formation.
  • Coronary arteries must be located in relation to each intended epicardial lesion.
  • The left phrenic nerve is especially relevant on the lateral left ventricular surface.
  • Pericardial adhesions can make normally accessible regions unreachable.
  • Imaging electrograms pacing and angiography provide complementary anatomical information.

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;7:531-536. doi:10.1111/j.1540-8167.1996.tb00559.x.
  2. Arya A, Di Biase L, Bazán V, et al. Epicardial ventricular arrhythmia ablation: a clinical consensus statement of the EHRA, HRS, APHRS, LAHRS, and CHRS. Europace. 2025;27:euaf055. doi:10.1093/europace/euaf055.
  3. Cabrera JA, Sánchez-Quintana D. Cardiac anatomy: what the electrophysiologist needs to know. Heart. 2013;99:417-431. doi:10.1136/heartjnl-2011-301154.
  4. Anderson RH, Spicer DE, Hlavacek AM, Cook AC, Backer CL. Wilcox’s Surgical Anatomy of the Heart. 4th ed. Cambridge University Press; 2013.
  5. Cronin EM, Bogun FM, Maury P, et al. 2019 HRS/EHRA/APHRS/LAHRS expert consensus statement on catheter ablation of ventricular arrhythmias. Heart Rhythm. 2020;17:e2-e154. doi:10.1016/j.hrthm.2019.03.002.
  6. Sánchez-Quintana D, Cabrera JA, Climent V, Farré J, Weiglein A, Ho SY. How close are the phrenic nerves to cardiac structures? Implications for cardiac interventionalists. J Cardiovasc Electrophysiol. 2005;16:309-313. doi:10.1046/j.1540-8167.2005.40759.x.

Media

Generic selectors
Exact matches only
Search in title
Search in content
Post Type Selectors
Lorem ipsum dolor sit amet, consectetur adipiscing elit, sed do eiusmod tempor incididunt ut labore et dolore