Best Practices for Mapping and Ablation of Ventricular Tachycardia

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EP LAB DIGEST. 2025;25(5):8-11.

Carmel Ashur, MD; Wendy Tzou, MD, FACC, FHRS; and Lohit Garg, MD, FACC
Cardiac Electrophysiology Section, Division of Cardiology, University of Colorado Anschutz Medical Campus, Aurora, Colorado

Ventricular tachycardia (VT) is a major cause of morbidity and mortality, particularly in patients with structural heart disease. Catheter ablation has become a key component in managing recurrent VT, offering arrhythmia control and reduction in implantable cardioverter-defibrillator (ICD) shocks.^1-7 However, the complexity and heterogeneity of VT substrates present challenges in achieving durable outcomes with high rates of recurrence, especially for nonischemic cardiomyopathy. This paper reviews the best practices for VT ablation, integrating advancements in mapping technologies, ablation strategies, and periprocedural management to optimize patient care.

Preprocedural Planning

Risk Assessment and Multidisciplinary Team Involvement
Patients undergoing VT ablation often have underlying structural heart disease and are at an elevated risk for hemodynamic decompensation. The PAINESD score can be used to identify patients at risk of acute hemodynamic compromise and high 30-day mortality (Figure 1).⁸ For intermediate (score 9-14) to high-risk (≥15) patients, early involvement of a multidisciplinary team is essential, including specialists in heart failure, cardiothoracic surgery, and anesthesia. Complex procedures are best performed in high-volume centers by experienced operators. 

Preprocedural Studies and Imaging
A 12-lead electrocardiogram (ECG) of clinical VT when available can help guide procedural planning, along with transthoracic echocardiography (TTE) to identify structural abnormalities. Cardiac magnetic resonance imaging (CMR) is particularly useful for defining areas of potential arrhythmogenic substrate.^9,10 In patients with nonischemic cardiomyopathy (NICM), CMR can reveal mid-myocardial and epicardial scar and can help anticipate need for epicardial mapping.¹¹ 

Preprocedural Medication Management
If feasible, antiarrhythmic drugs, except amiodarone, should be discontinued at least 5 half-lives before the procedure to facilitate VT induction and evaluation of clinical endpoints.¹² In situations where antiarrhythmic medications cannot be safely held, patients can be admitted prior to ablation for washout of oral medications with initiation of short-acting intravenous (IV) antiarrhythmics such as lidocaine. Warfarin is typically discontinued to achieve an INR <1.5, while direct oral anticoagulants (DOACs) are typically held for 24 to 48 hours, or 72 hours if epicardial access is anticipated.

Intraprocedural Management

Anesthesia and Hemodynamic Support
General anesthesia (GA) is preferred for these often long and complex procedures, specifically if epicardial access is required.¹³ Monitored Anesthesia Care (MAC) is favored for patients with idiopathic ventricular arrhythmias, where the procedure is expected to be shorter and the mechanism (automaticity or triggered activity) is catecholamine sensitive.¹⁴

When needed, dobutamine is the preferred inotropic agent, particularly in patients with left ventricular (LV) dysfunction. When vasopressors are indicated, combined vasopressor/inotropes (epinephrine, norepinephrine) are preferred over pure vasoconstrictors (phenylephrine, vasopressin). In patients with a very low ejection fraction or high PAINESD score, continuous monitoring with arterial line and right heart catheterization may help with inotrope and vasopressor titration, as well as to assess need for mechanical circulatory support (MCS). Regularly scheduled assessment of fluid balance is critical, with a low threshold for administration of loop diuretics to avoid postprocedural decompensation. 

Vascular and Epicardial Access
Ultrasound-guided vascular access is the preferred vascular access strategy.¹⁵ Epicardial access is typically obtained via a percutaneous subxiphoid approach under fluoroscopy guidance, with injection of contrast and/or use of a guidewire to demonstrate access in the pericardial space before placement of epicardial sheath.¹⁶ 

In patients with prior cardiac surgery, history of pericarditis, or prior epicardial ablation, adhesions may make epicardial access and maneuverability of catheters difficult. Pericardial CO2 insufflation¹⁷ via intentional coronary vein perforation can facilitate safer epicardial access¹⁸ and allow for better visualization of adhesions.¹⁹ Alternatively, surgical access with a subxiphoid window or limited lateral thoracotomy can be used.²⁰ 

Anticoagulation Use
Epicardial access should be obtained prior to starting systemic anticoagulation or after anticoagulation has been adequately reversed.²¹ Intraprocedural IV heparin with a target ACT of >300 should be used during endocardial LV mapping and ablation,²² and may be considered with right ventricular (RV) mapping/ablation in patients at high risk for thromboembolism.¹²

VT Mapping and Ablation Workflow (Figure 2)

Electrophysiologic Testing
Next, programmed electrical stimulation (PES) is performed either by pacing from a catheter in the RV or via noninvasive programmed stimulation (NIPS) in patients with an ICD. This helps provide confirmation of clinical VT, creation of a morphology template to match VTs during the case, and definition of a clinical endpoint (ie, noninducibility). While other workflows exist, our practice is to perform VT induction prior to mapping in order to avoid potentially altering the clinical VT morphology or rendering a patient noninducible.²³ When a 12-lead ECG of the clinical VT is not available, it can record intracardiac electrograms from the patient’s device during VT induction and match with stored VT episodes.²⁴ PES can be avoided if there is concern that VT will not be hemodynamically tolerated or is felt to be unsafe, such as in the setting of severe LV dysfunction.

Baseline Substrate Mapping
Following PES, high-density voltage and functional mapping is performed in normal sinus rhythm, RV pacing, and/or LV pacing.²⁵ Mapping is ideally performed with a linear multielectrode mapping catheter (eg, Optrell Mapping Catheter, Johnson & Johnson MedTech; Advisor HD Grid Mapping Catheter, Sensor Enabled, Abbott). Multispline catheters should be avoided, as they can cause significant ectopy and make mapping more challenging.²⁶ While point-by-point mapping can be performed with a bipolar catheter if needed, mapping with a high-density catheter is preferred when applying newer functional-based techniques.

Baseline voltage mapping is performed to identify border zone regions (voltage 0.5-1.5 mV).²⁷ Annotation of local abnormal ventricular activity (LAVA) and fractionated signals can help define areas that are often components required for a VT circuit.²⁸ When near-field signals are hidden within larger far-field signals, decrement evoked potential (DEEP) mapping can be used to unmask poorly coupled substrate that may be a viable target for ablation.²⁹ 

Functional and activation mapping should be performed to identify areas of slow conduction/deceleration zones (DZs). This is performed via isochronal late activation mapping (ILAM), where ventricular signals are timed to the offset of the latest component of the bipolar electrogram and then ventricular activation is divided into 8 equally distributed time intervals, or isochrones.³⁰ DZs are defined as regions where 3 isochrones are present within a 1-cm radius.³⁰ These DZs are often critical components required to sustain VT (Figure 3, Video 1). 

VT Mapping
Once baseline substrate and functional mapping are complete, attempts at VT induction are repeated. Pre-treatment with atropine can help reduce the associated vagal response with VT and allow a longer duration for mapping and entrainment.³¹ Strategic multielectrode positioning (StaMP) in different high-yield locations identified through ILAM mapping can help capture maximal spatial information over a short time period.³² There is limited evidence to support the use of MCS for the purposes of mapping poorly tolerated VT.³³

For re-entrant VT, diastolic potentials may represent critical components of the circuit. Fractionated electrograms immediately preceding surface QRS onset typical signify an exit site, where ablation could terminate VT or cause shifting to a new exit site. Mid-diastolic potentials are preferred ablation targets, as they more likely represent critical isthmus sites. VT circuits often exist in a 3-dimentional model, where gaps in activation sequence may reflect an intramural component not recorded by an electrode on the endocardial surface.³⁴

When VT is hemodynamically tolerated, activation mapping is prioritized to better visualize the VT circuit (Figure 3, Video 2). When possible, entrainment mapping can provide insight into the different components within the VT circuit.³⁵ Important pitfalls to consider include decremental conduction with faster pacing, far-field capture with higher pacing outputs, inaccurate measurement of far-field signals as near-field, easy termination/modification of VT with pacing and prolonged post-pacing interval with AAD use,³⁶ or after partial ablation due to conduction slowing. For these reasons, entrainment mapping should be considered as one component to an overarching ablation strategy, typically combined with a form of substrate modification. 

Finally, pace mapping can help localize the exit site for VT, without the need for VT induction. This is done with bipolar pacing close to the VT cycle length, with an output just above threshold and small/closely spaced electrodes in order to simulate clinical VT and avoid far-field capture.³⁷ It is important to consider that a good pace match can occur in noncritical sites adjacent to an exit and poor pace match can occur in critical sites near an entrance that propagate retrograde from the VT circuit. 

Target Endpoint
The procedural endpoint is largely based on the specific ablation strategy chosen. The most clinically relevant endpoint is VT noninducibility, which has been associated with lower VT recurrence;^1,38 however, is difficult to interpret in the setting of baseline noninducibility. Similarly, VT noninducibility under GA can be falsely reassuring; therefore, performing a NIPS under MAC 48 to 72 hours following ablation may be more clinically meaningful.³⁹ 
Noninducibility is typically combined with one of the following substrate-specified end points:⁴⁰ 

•    Elimination of DZs: loss of areas with isochronal crowding on repeat ILAM41 or complete elimination of late potentials/LAVAs.^42,43 
•    Elimination of excitability: transection of likely critical isthmus sites, as defined by entrainment or pace mapping.⁴⁴
•    Substrate homogenization: loss of pace capture within a broadly defined region of potentially arrhythmic tissue (low voltage, isolated components/late potentials, conduction channels, etc.).⁵
•    Core isolation: entrance and exit block within region containing dense scar (<0.5 mV) and critical VT circuit elements.⁴⁵

Regardless of whether the desired clinical end point was met, it is important to consider the progressive increase in hospital mortality associated with longer procedure duration, with an inflection in risk after around 6 hours. This risk is enhanced if MCS is needed during the case.⁴⁶ 

Postprocedural Management

If heparin was used, protamine is administered prior to sheath removal to shorten time to hemostasis and ambulation.⁴⁷ Treatment with reduced or full-dose DOAC should be given following LV ablation, initiated within 48 hours of the procedure, and continued for at least 30 days to reduce stroke risk.⁴⁸

If epicardial access was obtained, a pericardial drain is typically left in place, especially if bleeding or tamponade occurred. The drain can be removed once there is <50 cc of output over 24 hours and no effusion reaccumulation on TTE following a clamping trial. Prophylactic intrapericardial steroids are given during the procedure to reduce the incidence of postprocedural pericarditis.⁴⁹

Most patients require overnight monitoring post ablation. Patients with severe ventricular dysfunction, ongoing hemodynamic compromise requiring vasopressor support, retained pericardial drain, or a procedural complication should be admitted to a cardiac intensive care unit for ongoing management. 

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.