Why Temporary Pacing in Acute Inferior Myocardial Infarction or No-Reflow Becomes a Trigger - Not a Remedy - For Ventricular Fibrillation

Sep 30, 2026

Temporary pacing during acute inferior myocardial infarction or no-reflow can precipitate ventricular fibrillation instead of preventing it. The article details four mechanistic pathways: lowered VF threshold with ischemia, undersensing from fragmented electrograms, “R-on-T” asynchronous pacing onto the T wave due to long RR intervals, and catheter micro-trauma producing mechanically induced extrasystoles. A bedside decision framework and prevention bundle are proposed.

LanguageEnglish

CategoryHealthcare

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Pages3

Reading Time8 min

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ABSTRACT

Ischaemia Creates the “Vulnerable Myocardium”

Ischaemia Simultaneously Blinds the Pacemaker

Asynchronous Spikes Land on the T Wave (“R-On-T”)

Mechanical Catheter Trauma

Before Insertion, Ask Three Questions

Prevention: Make the Myocardium Less Vulnerable and the Pacemaker Smarter

Annals of Noninvasive Electrocardiology Why Temporary Pacing in Acute Inferior Myocardial Infarction or No-Reflow Becomes a Trigger—Not a Remedy—For Ventricular Fibrillation: Undersensing,“R-On-T”, Catheter Trauma and the Ischaemic Substrate Zhong-Qun Zhan | Hai-Jun Xu Department of Cardiology, Shenzhen Guangming District People's Hospital, Shenzhen, P. R. China Correspondence: Zhong-Qun Zhan ([zzqun21@126.com](zzqun21@126.com)) Received: 11 December 2025 | Revised: 11 December 2025 | Accepted: 23 December 2025 Keywords: acute inferior myocardial infarction | no-reflow phenomenon | temporary pacing | ventricular fibrillation ABSTRACT Temporary pacing during acute inferior MI or no-reflow can trigger ventricular fibrillation rather than prevent it. Four mechanisms are highlighted: (1) acute ischemia lowers VF threshold and creates repolarization heterogeneity; (2) fragmented electrograms cause undersensing and asynchronous spikes; (3) bradycardia-related long RR cycles position spikes on the T-wave (“R-on-T”); and (4) catheter micro-displacement induces mechanical extrasystoles. We propose a bedside decision framework—three questions before pacing—and a prevention bundle focused on urgent ischemia reversal, continuous electrogram surveillance, and early electrode removal. Bradycardia in this setting is often transient, but the electrophysiological vulnerability is not. Treating ischemia first and avoiding unnecessary pacing are paramount to prevent iatrogenic arrhythmia. We read with interest the case report by Wu et al. (Wu et al. 2024) describing how acute right-coronary no-reflow after percutaneous coronary intervention produced transient pacemaker undersensing that initiated ventricular fibrillation (VF) . Their example epitomizes a reproducible sequence that is still underappreciated at the bedside. We wish to highlight four intertwined mechanisms that convert a life-saving wire into a lethal one in the very setting where it is most commonly used—acute inferior/right-ventricular ischaemia or slow–/no-reflow. 1 | Ischaemia Creates the “Vulnerable Myocardium” Within minutes of RCA occlusion or contrast-induced noreflow, the ventricular fibrillation threshold in humans falls by 25%–35%(Lehmann et al. 1983) . In isolated canine sub-endocardium, action-potential amplitude decreases by ~50% within 3–5 min of ischaemia (Downaret al. 1977) . No-reflow adds micro-vascular obstruction and heterogeneous repolarisation—ideal milieu for re-entry (Kaur et al. 2022) . 2 | Ischaemia Simultaneously Blinds the Pacemaker Fragmented, low-amplitude local electrograms—common when the electrode lies within or adjacent to an ischaemic zone—have been documented to cause intermittent undersensing, forcing the generator to default to asynchronous spikes (Wu et al. 2024; McLeod and Jokhi 2004) . This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. © 2026 The Author(s). Annals of Noninvasive Electrocardiology published by Wiley Periodicals LLC. Annals of Noninvasive Electrocardiology, 2026; 31:e70149 1 of 3 [https://doi.org/10.1111/anec.70149](https://doi.org/10.1111/anec.70149) 3 | Asynchronous Spikes Land on the T Wave (“R-On-T”) Because inferior MI or no-reflow often coexists with sinus bradycardia and prolonged RR intervals, the next pacing stimulus—whether from a fixed-rate asynchronous mode or a poorly synchronized demand mode—may fall on the descending limb of the preceding T-wave, that is, the ventricular vulnerable period. This “long-cycle–short-cycle” sequence, first described by Langendorf et [al. in](al. in) 1955 for spontaneous ectopic beats (Langendorf et al. 1955), was later documented in the setting of temporary ventricular pacing during acute MI (McLeod and Jokhi 2004) . 4 | Mechanical Catheter Trauma Micro-displacement of the floating cathet

FAQs

Why can temporary pacing during acute inferior MI or no-reflow trigger ventricular fibrillation?

Because acute ischemia lowers the VF threshold and creates repolarization heterogeneity, while pacing can be mistimed and mechanically provoked. The combined effects can convert a life-saving pacing intervention into an arrhythmia trigger.

What are the four mechanisms highlighted in the article?

The article highlights: (1) ischemia-related lowering of VF threshold and repolarization heterogeneity, (2) fragmented electrograms causing undersensing and asynchronous spikes, (3) “R-on-T” timing of spikes onto the T wave during long RR intervals, and (4) catheter micro-displacement causing mechanically induced extrasystoles.

What bedside steps does the article recommend before inserting temporary pacing?

Ask three questions: whether bradycardia is hemodynamically significant, whether ischemia reversal can restore adequate rate, and whether pharmacological rate acceleration can suffice in stable patients without high-grade AV block. If any answer is “yes,” defer pacing and reassess regularly while directing therapy to ischemia.

Sep 30, 2026

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