Key result
Narrower CT anatomic isthmus 3 width linked to ~2.3-fold higher odds of slow conduction per 5 mm decrease.
Why the study?
Ventricular tachycardia propagated through slow conducting anatomic isthmus 3 is a significant cause of morbidity in repaired tetralogy of Fallot, and there is an unmet need for non-invasive identification of this substrate.
Does pre-procedural cardiac CT-derived anatomic isthmus 3 (AI 3) width predict the presence of slowly conducting AI 3 (SCAI 3) and inducible SCAI 3-dependent ventricular tachycardia during electrophysiology study in adults with repaired tetralogy of Fallot?
Cohort (n=27)
Cardiac CTs were analyzed by two cardiologists blinded to each other's measurements and EPS outcomes
No
Does pre-procedural cardiac CT-derived anatomic isthmus 3 (AI 3) width predict the presence of slowly conducting AI 3 (SCAI 3) and inducible SCAI 3-dependent ventricular tachycardia during electrophysiology study in adults with repaired tetralogy of Fallot?
Pre-procedural cardiac CT measurement of anatomic isthmus 3 width provides a reproducible, non-invasive marker with an 80% negative predictive value (above 21.5 mm) to help guide invasive arrhythmia risk stratification prior to pulmonary valve replacement in adults with repaired tetralogy of Fallot.
May aid noninvasive SCAI 3 identification in repaired tetralogy of Fallot; hypothesis-generating and requires prospective validation.
Background Anatomic isthmus 3 (AI 3) is defined as the myocardium between the pulmonary valve annulus and the ventricular septal defect patch that persists after tetralogy of Fallot (ToF) repair. Ventricular tachycardia (VT) propagated through slow conducting AI 3 (SCAI 3) represents a significant cause of morbidity in ToF. There is an unmet need for non-invasive identification of SCAI 3 in patients with ToF. Objectives To assess whether the anatomic features of AI 3 as derived from cardiac computed tomography (CT) can predict slow conduction velocity during EP study. Methods This retrospective single-center study included patients with ToF who underwent an electrophysiologic study and had AI 3 width measured from the pre-procedure cardiac CT. All patients underwent programmed ventricular stimulation, and electroanatomic. Logistic regression was performed to assess the relationship between AI 3 width and the presence of SCAI 3. Results Of 27 consecutive patients with ToF, twelve patients were found to have SCAI 3, and ten patients were found to have SCAI 3 mediated VT. The AI 3 was significantly narrower in patients with SCAI 3 compared to those with normal AI 3 conduction (18.4 ± 6.6 mm vs. 29.2 ± 9.0 mm; p = 0.001). An AI 3 width above 21.5 mm carried a negative predictive value of 80.0%. Conclusion In adults with repaired ToF referred for electrophysiology study, a narrower CT-derived AI 3 width was associated with SCAI 3 identification. AI 3 width measured on a CT obtained before PV replacement could help guide invasive risk stratification.
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Kosmopoulos et al. (2026) conducted a cohort in Repaired tetralogy of Fallot (rToF) (n=27). CT-derived anatomic isthmus 3 (AI 3) width (per 5 mm decrease) vs. Wider / normal conducting AI 3 was evaluated on Presence of slowly conducting anatomic isthmus 3 (SCAI 3, conduction velocity <0.5 m/s) during invasive electrophysiology mapping (OR 2.31 per 5 mm decrease in AI 3 width, 95% CI 1.21-4.40, p=0.011). Narrower CT-derived anatomic isthmus 3 width was associated with 2.31-fold higher odds of slow conduction per 5 mm decrease (95% CI 1.21-4.40; p=0.011) in repaired tetralogy of Fallot.
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