Epicardial Ventricular Tachycardia Ablation: Patient Selection, Access, and Ablation Techniques and Strategies to Manage Complications
Authors, Journal, Affiliations, Type, DOI
- Authors: Mohamad Raad, Gregory E. Supple
- Journal: JACC: Clinical Electrophysiology 2024;10(1):142–164
- Affiliation: Electrophysiology Section, Division of Cardiovascular Medicine, Perelman School of Medicine, University of Pennsylvania
- Type: State-of-the-art narrative review
- DOI: 10.1016/j.jacep.2023.09.007
Overview
This review is a practical guide to epicardial VT ablation, covering which cardiomyopathies and ECG/imaging patterns should prompt consideration of an epicardial approach, how to obtain pericardial access safely, how epicardial mapping differs from endocardial mapping, and how to prevent and manage the procedure's characteristic complications. It emphasises that epicardial ablation is usually a second step after endocardial mapping and ablation, but that certain substrates — non-ischaemic basal perivalvular scar, ARVC, Chagas disease, Brugada syndrome and sarcoidosis — justify preprocedural planning for epicardial access. The technical sections describe the subxiphoid Tuohy-needle and needle-in-needle techniques, CO2 insufflation via the coronary sinus, surgical pericardial windows, high-density multipolar mapping, contact-force targets, irrigated RF and cryoablation. A complication table quantifies haemopericardium, phrenic nerve injury, pericarditis and abdominal organ injury, with prevention and management strategies.
Keywords
Epicardial ablation; ventricular tachycardia; pericardial access; epicardial scar; complications
Key Takeaways
Which cardiomyopathies need epicardial ablation
| Condition | Epicardial involvement and approach |
|---|---|
| Ischaemic cardiomyopathy | 19–39% of patients referred for epicardial ablation; epicardial substrate required in 13–29%; scar is usually subendocardial but can extend transmurally |
| Non-ischaemic cardiomyopathy | Epicardial ablation required in 32–63%; basal perivalvular, midmyocardial and epicardial substrate is common |
| ARVC | Fibrofatty replacement progresses from epicardium inward; epicardial substrate exceeds endocardial; basal peritricuspid and RVOT/infundibular regions, extending to RV anterior and inferior free walls; RV apex less often involved |
| Chagas cardiomyopathy | Epicardial scar area approximately twice the endocardial area; combined endo-epicardial ablation improves freedom from VT |
| Brugada syndrome | Epicardial RVOT substrate; ablation eliminates the type 1 pattern and reduces arrhythmia more than endocardial-only ablation |
| Long QT syndrome | Epicardial RV fragmented, low-voltage, prolonged electrograms reported in high-risk patients; ablation suppressed arrhythmia and reduced QTc over 12 months |
| Cardiac sarcoidosis | Epicardial mapping/ablation beneficial in 18–25% |
| Viral myocarditis | Drug-refractory VT may require epicardial ablation in about 30% |
ECG criteria for an epicardial origin
Morphological criteria. An endocardial exit produces an initial R wave in the lead overlying the region; an epicardial exit produces a Q wave because activation travels away from that lead.
- Q wave in lead I → superior left lateral LV or anterior RV epicardium.
- Q waves in II, III and aVF → inferior LV or inferior RV epicardium.
- QS in V2 → anterior epicardial exit near the anterior interventricular sulcus.
- Absence of inferior Q waves has a high negative predictive value for inferior epicardial origin.
Interval criteria. Slow initial conduction through myocardium before the conduction system is engaged widens the initial QRS.
| Criterion | Definition | Reported performance |
|---|---|---|
| Precordial pseudo-delta wave (PdW) | Earliest ventricular activation to earliest fast deflection in any precordial lead | ≥34 ms: Sn 83%, Sp 95% (Berruezo); Sn 73%, Sp 63% (Valles) |
| V2 intrinsicoid deflection time (IDT) | Earliest activation to peak R in V2 | ≥85 ms: Sn 87%, Sp 90% (Berruezo); Sn 83%, Sp 70% (Valles) |
| Shortest precordial RS interval (SRS) | Earliest activation to nadir of first S wave in any precordial lead | ≥121 ms: Sn 76%, Sp 85% (Berruezo); Sn 74%, Sp 57% (Valles) |
| Myocardial deflection index (MDI) | Shortest QRS onset-to-earliest maximum precordial deflection / total QRS duration | ≥0.55: Sn 100%, Sp 99% (Daniels); Sn 30%, Sp 95% (Valles) |
| Q wave in lead I | — | Sn 91%, Sp 96% for basal superior/lateral LV (Valles) |
- Valles' four-step algorithm for basal superior/lateral LV epicardial origin — absence of inferior Q waves, PdW ≥75 ms, MDI ≥0.59, Q wave in lead I — achieved sensitivity 96% and specificity 93%.
- Caveats: derivation cohorts were small (N=12–67), criteria are site-specific (LV vs RV, and region within the ventricle), cut-offs vary between studies, and criteria perform poorly in transmural infarction because infarct Q waves obscure the origin. QRS duration does not reliably distinguish epicardial from endocardial RV VT, and QRS criteria failed in an ischaemic cardiomyopathy cohort (Martinek 2012).
- Faster VT rates can superimpose T waves on the QRS onset; pacing at a rate close to the VT cycle length can help with pace mapping.
Imaging
- CMR showing prominent epicardial or subepicardial delayed enhancement supports an epicardial approach, particularly in NICM and post-viral myocarditis.
- Transthoracic echocardiography is rarely sensitive enough; intracardiac echocardiography can show subepicardial hyperechogenicity, especially in the basal lateral wall, early in the procedure.
- CT/MRI registration can map epicardial fat distribution and help distinguish fat from scar.
Pericardial anatomy and access
- The pericardial space normally contains <50 mL of fluid and is bounded by visceral and parietal serous layers plus an outer fibrous layer 1.0–2.5 mm thick.
- Epicardial fat lies beneath the visceral pericardium and is distinct from pericardial fat outside the sac. Epicardial fat insulates, dampens electrograms, raises pacing thresholds and reduces RF efficacy; it is concentrated around coronary vessels.
- Subxiphoid access (Sosa): general anaesthesia is preferred; anticoagulation should be discontinued and reversed; blood products and surgical backup should be available. Access is obtained one finger-width below and left of the xiphoid, in the triangle between the xiphoid and the lowest costal margin, through the foramen of Morgagni (space of Larrey). A 6-inch 17-gauge Tuohy needle with a curved blunt tip is used; a 0.035-inch J wire is kept extended past the tip except during advancement. Fluoroscopy uses RAO 25–35° and LAO 45–55°; the LAO view confirms a tangential entry. Entry is confirmed by loss of resistance, "dye hanging" with contrast, and free wire passage into the pericardial space.
- Anterior vs posterior approach: the anterior approach reduces intra-abdominal organ injury and is the authors' preferred strategy; the posterior approach may be preferable when anterior adhesions are severe. Access at the mid-apical RV avoids the RV marginal and posterior descending arteries.
- Needle-in-needle technique: an 18-gauge Cook needle creates the track, a 21-gauge micropuncture or Chiba needle punctures the pericardium, and an 0.018-inch wire confirms access.
- CO2 insufflation via the coronary sinus (Silberbauer): a deflectable sheath cannulates the coronary sinus, a distal posterolateral branch is punctured with a 0.014-inch high-tip-force wire, and 150–250 mL of CO2 separates the layers. Reported success is higher and complications lower than with traditional subxiphoid access; CO2 is rapidly resorbed, but pneumopericardium can raise the defibrillation threshold.
- Surgical window: indicated for severe adhesions, prior cardiac surgery or epicardial leads, or when direct visualisation of coronaries is needed. Options are a subxiphoid window or limited anterior thoracotomy (third to fifth intercostal space). A perfusionist and bypass standby should be available.
Epicardial mapping
- Clues that the circuit is epicardial or intramural: no sharp early pre-QRS signal, failure to entrain the critical isthmus, or failed ablation despite an apparent exit-site entrainment.
- Unipolar voltage <8.3 mV in the RV and <5.5 mV in the LV suggests epicardial scar even when endocardial bipolar voltage is normal.
- Normal epicardial bipolar voltage is >0.94 mV. Fat over the coronary sulcus and interventricular grooves can mimic scar; late, fractionated or split potentials are more reliable markers, and CT/MRI fat registration helps.
- Thin epicardial scar over healthy myocardium can produce normal voltage; look for fractionation, late potentials and long stimulus-to-QRS.
- High-density multipolar catheters with small bipoles are preferred because the epicardial surface is smooth and untrabeculated. Linear/uniplanar catheters oppose the surface better than basket or PentaRay-type catheters.
- Contact force: bipolar signal amplitude increases up to about 10 g; 4 g is the threshold for normal signal in the epicardium and 9 g for adequate LV epicardial contact. Median adequate CF is lower epicardially (8 g) than endocardially (13–15 g), and catheter vector orientation is toward the myocardium <50% of the time epicardially versus >90% endocardially.
Ablation
- Irrigated RF is preferred because the pericardial space lacks convective cooling; irrigation prevents tip overheating and creates larger lesions through fat. Fluid accumulates in the pericardial space and can impair filling or cause tamponade, so intermittent aspiration through the sheath side port is used; continuous suction is avoided because it limits catheter movement.
- Contact force improves lesion formation but excess force is associated with steam pops, coronary injury and phrenic nerve injury.
- Cryoablation is an alternative when the target is near a coronary artery or the phrenic nerve; animal data show epicardial lesions similar in size to endocardial lesions, but cryo can cause neointimal proliferation in adjacent epicardial vessels.
- Midmyocardial substrate is approached from the endocardium with low starting power (~25 W), gradual titration to a 10–15-unit impedance drop, and 2–3-minute applications.
Complications
| Complication | Frequency | Main causes | Management |
|---|---|---|---|
| Early haemopericardium (within 10 min) | 5–14% | RV puncture, epicardial vessel injury, adhesion disruption | Coronary angiography before access, mid-ventricular access, echocardiography, RV contrast injection; drain, window or thoracotomy depending on severity |
| Haemopericardium during the procedure | 0–1% | Slow bleeding from multiple punctures, steam pops | Usually self-limiting; drain if needed |
| Late haemopericardium (end of procedure) | ~1% | Access-tract vessel injury, double RV puncture | Advance a long wire before sheath removal to detect double RV puncture; re-advance sheath to tamponade; surgical repair |
| Delayed haemopericardium (post-procedure) | ~1% | Anticoagulation resumption, pericarditis/Dressler | Pericarditis workup and treatment; drainage; brief anticoagulation hold |
| Phrenic nerve injury | 0–1% | Ablation over the nerve | Identify by pacing; displace nerve with CO2/air/saline or a balloon; cryoablation; usually self-limiting, diaphragmatic plication for severe cases |
| Pericarditis | Up to 30% | Parietal layer irritation; extent of ablation | NSAIDs and colchicine; intrapericardial triamcinolone 2–3 mg/kg; early drain removal |
| Haemoperitoneum/intra-abdominal injury | 0–1% | Diaphragm, liver or bowel puncture | Anterior approach, inspiration during puncture, imaging; supportive care, reverse anticoagulation, surgery for severe cases |
- Hypotension during epicardial ablation should prompt evaluation for tamponade, coronary injury, anaesthetic complication and intra-abdominal bleeding.
- Procedures should be performed where surgical backup, rapid anticoagulation reversal and blood transfusion are available.
Limitations of the document
- Narrative review from a single high-volume centre. Technical preferences and complication estimates reflect the authors' practice and may not generalise to lower-volume operators.
- ECG criteria are weak and heterogeneous. Derivation studies were small, cut-offs differ, and performance falls in ischaemic cardiomyopathy and transmural scar; the review does not provide a prospectively validated algorithm.
- Complication frequencies come from heterogeneous registries with different definitions, access techniques and follow-up, so the ranges are broad and likely underpowered for rare events.
- No outcome meta-analysis. The review does not pool freedom-from-VT or mortality data across epicardial cohorts, and comparative effectiveness versus endocardial-only ablation is not established.
- Pre-PFA era. The ablation section focuses on RF and cryo; epicardial pulsed field ablation is not covered, and its risk profile near coronaries and the phrenic nerve remains to be defined.
- Limited paediatric/congenital guidance. Adhesions after congenital surgery are discussed briefly, but complex congenital anatomy is not addressed in detail.
Key Concepts Mentioned
- concepts/Epicardial-VT-Ablation — the subject of the review
- concepts/VT-Ablation — general mapping and ablation principles
- concepts/VT-Ablation-Nonischemic-Cardiomyopathy — the main epicardial substrate
- concepts/Late-Gadolinium-Enhancement — imaging of epicardial scar
- concepts/Ventricular-PFA — an emerging energy source not covered here
- entities/ARVC — the classic epicardial cardiomyopathy
- entities/Brugada-Syndrome — epicardial RVOT substrate
- concepts/Electrical-Storm — a common indication for epicardial rescue ablation
Key Entities Mentioned
- University of Pennsylvania / Perelman School of Medicine
- Biosense Webster (CARTO, Decanav, PentaRay, SmartTouch, SoundStar)
- Abbott (EnSite, Agilis, Livewire, Advisor HD-Grid)
- Boston Scientific (Rhythmia, Orion)
- Circa Scientific (PeriCross)
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