Tachycardia Termination Without Global Propagation: Is the Pacing Site In or Out?

DOI: 10.19102/icrm.2025.16123

OZCAN OZEKE, MD,¹ DURSUN ARAS, MD,² and SERKAN TOPALOGLU, MD¹

¹Department of Cardiology, University of Health Sciences, Ankara Bilkent City Hospital, Ankara, Turkey

²Department of Cardiology, İstanbul Medipol University, Istanbul, Turkey

Download PDF

Follow Us >> Tweet

ABSTRACT. Ventricular tachycardia termination by pacing with non-global capture is a specific criterion for identifying a critical component of the re-entrant circuit, regardless of whether concealed entrainment can be demonstrated at that site. It is usually observed almost by chance, but it can also be intentionally demonstrated by introducing a single extrastimulus during tachycardia.

KEYWORDS. Non-global capture, tachycardia termination without global propagation, ventricular tachycardia.

The authors report no conflicts of interest for the published content. No funding information was provided. ORCID ID, O.O., 0000-0002-4770-8159.
Manuscript received July 24, 2025. Final version accepted September 11, 2025.
Address correspondence to: Ozcan Ozeke, MD, Sağlık Bilimleri Üniversitesi, Ankara Bilkent Şehir Hastanesi, Kardiyoloji Klinigi, Bilkent, Ankara 06800, Turkey. Email: ozcanozeke@gmail.com.

Case presentation

A 72-year-old man was referred for catheter ablation of incessant ventricular tachycardia (VT). He had experienced a myocardial infarction 12 years earlier and had previously undergone coronary bypass and mitral valve replacement surgery. An electrocardiogram revealed sustained monomorphic VT characterized by a QRS morphology with a right bundle branch block pattern and a superior axis; the tachycardia cycle length was 430 ms (Figure 1). The clinical VT was spontaneously induced and was hemodynamically tolerated and mapped (Video 1). During the tachycardia, a series of single ventricular extrastimuli was delivered from the putative diastolic potential region. Based on the response to ventricular entrainment attempts (Figure 2), we questioned whether the pacing site was in or out of the re-entrant circuit.

Discussion

In the setting of structural heart disease, VT is typically associated with a re-entrant mechanism.^1–4 Successful catheter ablation of VT depends on identifying the critical tissues that sustain the arrhythmia.⁵ Four mapping techniques consistently play a role in successful VT ablation: activation mapping, entrainment mapping, pace mapping, and substrate mapping. Entrainment mapping, or continuous resetting of a re-entrant tachycardia, provides a powerful tool for distinguishing between focal and re-entrant VT, as well as identifying critical circuit components such as the entrance, critical isthmus (CI), and exit sites.^1,6–12 The detection of the ideal site for ablation within a central CI is a mid-diastolic potential during VT that exhibits concealed fusion with a post-pacing interval equal to the tachycardia cycle length.¹³ Thus, entrainment mapping helps to identify the CI, but it is not always feasible and, in some cases, terminates VT,¹⁴ as occurred in the current tracing. Indeed, local capture of the CI without global ventricular capture (non-global capture [NGC]) can terminate VT by resulting in a bidirectional block (orthodromic or non-orthodromic capture) within the CI.^15–18 However, termination might also occur due to a rate-dependent block in the slow-conduction zone during pacing,^4,19,20 and catheter contact at a critical endocardial site can interrupt postinfarction VT.²¹ The stimulus–QRS (S–QRS) interval was significantly shorter at sites where mechanical trauma affected the re-entrant circuit compared with sites having concealed entrainment.²¹ Therefore, if an arrhythmia terminates during overdrive pacing but several stimuli that should capture do not, then the termination might have been spontaneous or caused by mechanical trauma; such events do not carry the same implications as termination by NGC. Furthermore, all these pacing attempts rely on consistent capture of tissue with each stimulus. While “capture” refers to whether the pacing stimulus depolarizes the local myocardium, “global capture” means that the entire QRS complex (ie, the full ventricular myocardium) is activated by the pacing stimulus and the morphology differs from the VT QRS. On the contrary, NGC (also termed “concealed entrainment”) means that only a part of the VT circuit or surrounding myocardium is depolarized without altering the overall QRS morphology during VT, supporting CI involvement.^15,18 VT termination by pacing with NGC is a specific criterion for identifying a critical component of the re-entrant circuit, regardless of whether concealed entrainment can be demonstrated at that site.^15,16 It is usually observed almost by chance, but it can also be intentionally demonstrated by introducing a single extrastimulus during tachycardia.

In the current tracing, VT was terminated with NGC by a single extrastimulus at this site; however, concealed entrainment could not be assessed due to the termination of the VT. In general, amplifier saturation from pacing typically obscures the local electrogram (EGM) on the pacing electrodes at the time of pacing, as seen in Figure 2 (5-6 with PentaRay^® [JNJ Medtech, New Brunswick, NJ, USA]); thus, a careful examination of adjacent electrode recordings (PentaRay^® 1-2 and 7-8, Figure 3) is important to confirm evidence of local capture. Examination of the adjacent electrode recording (red rectangles in Figure 3) confirms that the similarly timed component was captured just downstream of the stimulus, as it is no longer observed at the expected interval (red blank rectangle in Figure 3 indicates absent EGM).¹⁴

Following termination of VT, stimuli directly captured the local CI myocardium, probably including the exit site, as confirmed by the QRS morphology matching that of the VT.¹⁹ The S–QRS interval is a well-known indicator of the conduction time from the pacing site to the exit VT.²² If it is prolonged and furthermore reveals a conduction delay in the isthmus after VT termination by NGC, these support the NGC location as a critical position in the re-entrant circuit.¹⁵ In the current tracing, there was also evidence of a conduction delay (Figure 3, note the blue “plus sign”), with gradual prolongation of the S–QRS interval following tachycardia termination by NGC. Combining all these observations, ablation at this site rendered the clinical VT non-inducible.

References

1. Waldo AL, Henthorn RW. Use of transient entrainment during ventricular tachycardia to localize a critical area in the reentry circuit for ablation. Pacing Clin Electrophysiol. 1989;12(1 Pt 2):231–244. [CrossRef] [PubMed]
2. Stevenson WG, Sager PT, Friedman PL. Entrainment techniques for mapping atrial and ventricular tachycardias. J Cardiovasc Electrophysiol. 1995;6(3):201–216. [CrossRef] [PubMed]
3. Stevenson WG, Sager PT, Natterson PD, Saxon LA, Middlekauff HR, Wiener I. Relation of pace mapping QRS configuration and conduction delay to ventricular tachycardia reentry circuits in human infarct scars. J Am Coll Cardiol. 1995;26(2):481–488. [CrossRef] [PubMed]
4. Stevenson WG, Nademanee K, Weiss JN, et al. Programmed electrical stimulation at potential ventricular reentry circuit sites. Comparison of observations in humans with predictions from computer simulations. Circulation. 1989;80(4):793–806. [CrossRef] [PubMed]
5. Miller JM, Szwed JM, Chakka MN. Postextrastimulus delay of ventricular tachycardia return cycle: indicator of a good ablation site. Heart Rhythm. 2006;3(7):870–871. [CrossRef] [PubMed]
6. Ozcan Cetin EH, Ozeke O, Kara M, et al. Electrophysiological mechanism of wide QRS complex tachycardia revealed by an unexpected intervention. J Cardiovasc Electrophysiol. Published online August 19, 2025. [CrossRef] [PubMed]
7. Ozcan Cetin EH, Korkmaz A, Kara M, et al. Multiple wide QRS tachycardias in the same individual with ischemic cardiomyopathy. J Cardiovasc Electrophysiol. 2023;34(1):241–245. [CrossRef] [PubMed]
8. Kara M, Korkmaz A, Ozeke O, et al. Wide QRS tachycardia with alternating QRS morphologies: what is the mechanism? Pacing Clin Electrophysiol. 2020;43(1):146–148. [CrossRef] [PubMed]
9. Tuncez A, Aslan AO, Merovci I, et al. Entrainment of ventricular tachycardia with V-shaped diastolic activation pattern: is the pacing site in or out? J Cardiovasc Electrophysiol. 2022;33(7):1609–1613. [CrossRef] [PubMed]
10. Sertdemir AL, Kara M, Bastug S, et al. An unusual electrogram sequence with a questionable potential on the His-bundle catheter during sinus rhythm: what is the mechanism? J Innov Card Rhythm Manag. 2022;13(3):4929–4932. [CrossRef] [PubMed]
11. Cetin M, Ornek E, Bastug S, et al. An incessant tachycardia with alternating QRS complexes: what is the mechanism? J Innov Card Rhythm Manag. 2022;13(2):4900–4904. [CrossRef] [PubMed]
12. Kocyigit Burunkaya D, Ozeke O, Korkmaz A, et al. The initial part of polymorphic ventricular tachycardia as a clue for the sustainability of tachycardia and ablation success: a varying degree of Purkinje-myocardial complicity? J Innov Card Rhythm Manag. 2023;14(6):5472–5480. [CrossRef] [PubMed]
13. Miller JM, Scherschel JA. Catheter ablation of ventricular tachycardia: skill versus technology. Heart Rhythm. 2009;6(8 Suppl):S86–S90. [CrossRef] [PubMed]
14. Tung R. Challenges and pitfalls of entrainment mapping of ventricular tachycardia: ten illustrative concepts. Circ Arrhythm Electrophysiol. 2017;10(4):e004560. [CrossRef] [PubMed]
15. Katsume Y, Hasegawa K, Limprasert S, et al. Termination without global propagation in re-entrant ventricular tachycardia: electrophysiologic characteristics and 3D-electroanatomical mapping analysis. JACC Clin Electrophysiol. 2024;10(12):2545–2553. [CrossRef] [PubMed]
16. Bogun F, Krishnan SC, Marine JE, et al. Catheter ablation guided by termination of postinfarction ventricular tachycardia by pacing with nonglobal capture. Heart Rhythm. 2004;1(4):422–426. [CrossRef] [PubMed]
17. Garan H, Ruskin JN. Reproducible termination of ventricular tachycardia by a single extrastimulus within the reentry circuit during the ventricular effective refractory period. Am Heart J. 1988;116(2 Pt 1):546–550. [CrossRef] [PubMed]
18. Shimada H, Nishizaki M, Yamawake N, Suzuki M, Sakurada H, Hiraoka M. A case of scar-related ventricular tachycardia demonstrating termination with nonglobal capture at the site of concealed entrainment with dual slow conduction pathways. HeartRhythm Case Rep. 2018;4(10):459–463. [CrossRef] [PubMed]
19. Bogun F, Hohnloser SH, Bender B, et al. Mechanism of ventricular tachycardia termination by pacing at left ventricular sites in patients with coronary artery disease. J Interv Card Electrophysiol. 2002;6(1):35–41. [CrossRef] [PubMed]
20. Bogun F, Kim HM, Han J, et al. Comparison of mapping criteria for hemodynamically tolerated, postinfarction ventricular tachycardia. Heart Rhythm. 2006;3(1):20–26. [CrossRef] [PubMed]
21. Bogun F, Good E, Han J, et al. Mechanical interruption of postinfarction ventricular tachycardia as a guide for catheter ablation. Heart Rhythm. 2005;2(7):687–691. [CrossRef] [PubMed]
22. de Chillou C, Sellal J-M, Magnin-Poull I. Pace mapping to localize the critical isthmus of ventricular tachycardia. Card Electrophysiol Clin. 2017;9(1):71–80. [CrossRef] [PubMed]