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Review
. 2025 Aug 6;15(15):1973.
doi: 10.3390/diagnostics15151973.

The Role of Imaging in Ventricular Tachycardia Ablation

Affiliations
Review

The Role of Imaging in Ventricular Tachycardia Ablation

Pasquale Notarstefano et al. Diagnostics (Basel). .

Abstract

Ventricular tachycardia (VT) remains a major cause of morbidity and mortality in patients with structural heart disease. While catheter ablation has become a cornerstone in VT management, recurrence rates remain substantial due to limitations in electroanatomic mapping (EAM), particularly in cases of deep or heterogeneous arrhythmogenic substrates. Cardiac imaging, especially when multimodal and integrated with mapping systems, has emerged as a critical adjunct to enhance procedural efficacy, safety, and individualized strategy. This comprehensive review explores the evolving role of various imaging modalities, including echocardiography, cardiac magnetic resonance (CMR), computed tomography (CT), positron emission tomography (PET), and intracardiac echocardiography (ICE), in the preprocedural and intraprocedural phases of VT ablation. We highlight their respective strengths in substrate identification, anatomical delineation, and real-time guidance. While limitations persist, including costs, availability, artifacts in device carriers, and lack of standardization, future advances are likely to redefine procedural workflows.

Keywords: Imaging; cardiac magnetic resonance; catheter ablation; computed tomography; intracardiac echocardiography; ventricular tachycardia.

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Conflict of interest statement

A.L.C. is employed by the company Johnson & Johnson Medial SpA. The remaining authors declare no conflicts of interest.

Figures

Figure 1
Figure 1
A 35-year-old female with mitral valve prolapse presented an elevated ventricular arrhythmic burden and underwent cardiological evaluation. (A) A resting ECG showing the presence of PVCs with right bundle branch block-like morphology (qR in lead V1) and superior axis; (B) TEE showed the presence of bileaflet mitral valve prolapse with mitral annular disjunction (yellow arrow); (C) reduced strain values in the lateral wall shown in speckle tracking echocardiography; (D) and (E): CMR demonstrated significant midwall LGE in inferolateral segments (red arrow) and in the postero-medial papillary muscle (orange arrow); (F) after ineffective anti arrhythmic treatments, the patient underwent PVC ablation at the posterior–medial papillary muscle. Adequate contact between the ablation catheter and the papillary muscle was assured through ICE. PVC, premature ventricular complex; TEE, transesophageal echocardiography; CMR, cardiac magnetic resonance; LGE, late gadolinium enhancement; ICE, intracardiac echocardiography.
Figure 2
Figure 2
A 55-year-old male with non-ischemic cardiomyopathy was evaluated for catheter ablation of symptomatic PVCs and NSVT (A); (B,C) CMR demonstrated the presence of patchy LGE in the interventricular septum and inferolateral wall; (D,E) intense 18-FDG uptake was detected by a PET scan in the interventricular septum and inferolateral wall and in the apical right pulmonary lobe; (F) inflammatory infiltrates and non-caseating granulomas were identified through histology after pulmonary lymphonode biopsy, compatible with pulmonary sarcoidosis. After steroid therapy, the patient experienced significant symptomatic improvement and reduction in arrhythmic burden; therefore, catheter ablation was postponed. PVCs, premature ventricular complexes; NSVT, non-sustained ventricular tachycardia; CMR, cardiac magnetic resonance; LGE, late gadolinium enhancement; 18-FDG PET, 18-fluorodeoxyglucose positron emission tomography.
Figure 3
Figure 3
Examples of applications of ICE in VT ablation: (A) 3D reconstruction of the left ventricle obtained with the ICE probe positioned in the right ventricle, showing a subendocardial scar area on the lateral wall (red arrows); (B) intraprocedural detection of pericardial effusion; (C) identification of a large aortic plaque at the sino-tubular junction, which prompted the operator to avoid the transaortic approach and proceed exclusively via the transseptal route. ICE, intracardiac echocardiography; VT, ventricular tachycardia.
Figure 4
Figure 4
MDCT imagery from an ischemic patient post-processed with a dedicated software (ADAS 3D). A Three-dimensional reconstruction of the aorta (pink) and left ventricle with lipomatous metaplasia (transparent black) and wall thickness analysis. LV wall thickness is shown as a color map (from blue > 6 mm to red < 1 mm). LV, left ventricle; MDCT, multidetector CT.
Figure 5
Figure 5
A patient with previous myocardial infarction experienced multiple ICD shocks due to recurrent episodes of VT. (A,B) The comparison of preprocedural CMR with (A) and without (B) WB sequences. The inferolateral scar was much more clearly delineated on the WB sequence than on the conventional one and was successfully imported into the EAM system using ADAS 3D software. (C) A posterior view of the bipolar voltage map with standard thresholds for dense scar (<0.5 mV) and border zone (<1.5 mV). (D) The corresponding projection of the color-coded LGE-CMR-derived PSI map (red = dense scar, blue = normal tissue, cream/orange = border zone). Putative conducting corridors were identified, annotated with yellow (10% layer) and blue (20% layer) lines, and superimposed onto the voltage map. (E,F) Following substrate ablation targeting LAVAs identified by EAM, VT was still inducible. The critical isthmus, exhibiting a diastolic potential ((F), red circle), was located in a region previously identified as an HTC on the PSI map ((D), yellow circle). (G) The application of radiofrequency energy resulted in prompt termination of the VT. ICD, implanted cardioverter defibrillator; VT, ventricular tachycardia; WB, wideband; CMR, cardiac magnetic resonance; EAM, electroanatomic mapping; LGE, late gadolinium enhancement; PSI, pixel signal intensity; LAVA, local abnormal ventricular activity; HTC, heterogeneous tissue channel.
Figure 6
Figure 6
CMR-guided VT ablation in a patient with previous inferolateral MI and recurrent episodes of VT. (A) A color-coded LGE-CMR-derived PSI map. Blue: normal myocardium; red: dense scar; green lines: putative HTCs. (B) The dots indicate lesions set at the entrance and within the HCT. At the end of the procedure, VT was no longer inducible. After 36 months of follow-up, no arrhythmia recurrences occurred. CMR, cardiac magnetic resonance; MI, myocardial infarction; VT, ventricular tachycardia; LGE, late gadolinium enhancement; PSI, pixel signal intensity; HTC, heterogeneous tissue channel.

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