Separate Electrograms and Morphologically Distinct QRS Complexes During Ventricular Tachycardia: Critical Versus Noncritical Isthmus

DOI: 10.19102/icrm.2026.17081

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. The electrogram morphology and its timing within the ventricular tachycardia (VT) cycle enable electrophysiologists to infer the location of the scar and its relationship to the VT circuit. This becomes particularly important in the presence of double-entrance or double-exit configurations, where distinguishing the critical isthmus from a noncritical bystander is essential.

KEYWORDS. Dual exit, multiple exit, 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 December 29, 2025. Final version accepted March 4, 2026.
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

The patient was a 77-year-old woman known for ischemic cardiomyopathy with a left ventricular ejection fraction of 25%, a history of sustained monomorphic VT, and an implantable cardioverter-defibrillator. EGMs recorded along the diastolic pathway using the PentaRay™ catheter (J&J MedTech, New Brunswick, NJ, USA) intermittently demonstrated mid-diastolic potentials (MDPs) that preceded each morphologically distinct QRS complex (red arrows in Figure 1). To better understand the mechanism of the tachycardia, a detailed analysis of the intracardiac electrograms was performed.

Discussion

Multiple VT morphologies were observed in a majority (40%–80%) of post-myocardial infarction patients who underwent catheter ablation.^1,2 Miller et al. described possible mechanisms that could explain variable QRS morphologies on a surface electrocardiogram, including different expressions of the same VT circuit due to preferential exit points along a shared isthmus, distinct circuits closely placed, and widely unconnected arrhythmogenic sites.² Bimorphic VT is one of the most commonly known prototypes of electrical alternans and is characterized by a rapid, wide-complex electrocardiogram pattern with alternating QRS morphology and axis.^3,4 Bogun et al. reported that a shared isthmus with different exit points may account for up to 40% of bimorphic VTs in ischemic cardiomyopathy.⁵ Therefore, the multiple exit sites from re-entrant circuits would be associated with these changing QRS morphologies⁶; however, three more options should also be considered: whether more than one arrhythmia is occurring, whether fusion with sinus beats is occurring, or whether tachycardia originates within or in the proximity of the His–Purkinje conduction system.^6–9 In the current tracing, it is considered noteworthy that, every time the MDP appears, there is a consistent and immediate change in the QRS complex morphology. This observed pattern could theoretically represent either (1) a functional block within one pathway, resulting in activation through an alternative exit, or (2) a specific activation sequence within the scar substrate. Identification of the mechanisms for these changes is important when considering the feasibility of ablation as therapy.^1,10

The observed differences in timing and cycle length may arise from different exit sites of the isthmus (location “2” in Figure 1) rather than from a common isthmus (location “7” in Figure 1). The observed differences in timing and cycle length are more likely attributable to distinct exit sites of the isthmus (location “2” in Figure 1) rather than a single common isthmus (location “7” in Figure 1). Had the catheter been located within the common isthmus, the EGMs would be expected to be continuous rather than intermittent. The bimodal changes in QRS morphology support the presence of dual exits, while the shorter cycle length and distinct QRS morphology are more compatible with recordings from the catheter positioned in region 2. Therefore, these EGMs are most likely related to location “2” in Figure 1, which represents the only non-critical isthmus of the short VT circuit (Figure 2), and are not associated with tachycardia termination. Even with ablation, they would be expected to reflect cycle length prolongation and a transition from bimorphic to monomorphic VT rather than true termination. Simply, the EGM morphology and location within the VT cycle allow electrophysiologists to understand the scar location and relation to the VT circuit.^11,12

References

1. Costeas C, Peters NS, Waldecker B, Ciaccio EJ, Wit AL, Coromilas J. Mechanisms causing sustained ventricular tachycardia with multiple QRS morphologies: results of mapping studies in the infarcted canine heart. Circulation. 1997;96(10):3721–3731. [CrossRef] [PubMed]
2. Miller JM, Kienzle MG, Harken AH, Josephson ME. Morphologically distinct sustained ventricular tachycardias in coronary artery disease: significance and surgical results. J Am Coll Cardiol. 1984;4(6):1073–1079. [CrossRef] [PubMed]
3. Baher AA, Uy M, Xie F, Garfinkel A, Qu Z, Weiss JN. Bidirectional ventricular tachycardia: ping pong in the His-Purkinje system. Heart Rhythm. 2011;8(4):599–605. [CrossRef] [PubMed]
4. Durrani SA, Sung R, Scheinman M. Bidirectional ventricular tachycardia due to a mixture of focal fascicular firing and reentry. Card Electrophysiol Clin. 2016;8(4):753–764. [CrossRef] [PubMed]
5. Bogun F, Li YG, Groenefeld G, et al. Prevalence of a shared isthmus in postinfarction patients with pleiomorphic, hemodynamically tolerated ventricular tachycardias. J Cardiovasc Electrophysiol. 2002;13(3):237–241. [CrossRef] [PubMed]
6. 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]
7. Asirvatham SJ, Friedman PA, Cha YM. Case 13. In: Mayo Clinic Electrophysiology Manual. Rochester, MN: Mayo Clinic Scientific Press; 2014:423.
8. Mahla H, Shenthar J, Kumar KR, Manjunath CN. Ventricular tachycardia with regular capture beats. BMJ Case Rep. 2014;2014:bcr2014204121. [CrossRef] [PubMed]
9. 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]
10. Schmitt H, Cabo C, Costeas C, Coromilas J, Wit AL. Mechanisms for spontaneous changes in QRS morphology sometimes resembling torsades de pointes during reentrant ventricular tachycardia in a canine infarct model. J Cardiovasc Electrophysiol. 2001;12(6):686–694. [CrossRef] [PubMed]
11. Harmouch W, Al-Shammari AS, Sabayon MD, Narayanan A, Al Taii H. Electrogram dynamics at the site of ventricular tachycardia termination during radiofrequency ablation. J Innov Card Rhythm Manag. 2025;16(7):6346–6353. [CrossRef] [PubMed]
12. Martin R, Hocini M, Haïsaguerre M, Jaïs P, Sacher F. Ventricular tachycardia isthmus characteristics: insights from high-density mapping. Arrhythm Electrophysiol Rev. 2019;8(1):54–59. [CrossRef] [PubMed]