Antitachycardia Pacing for Fast Scar-Mediated Ventricular Tachycardia Across Non-Ischemic Cardiomyopathies: A Case Series

Abstract

Background

Fast monomorphic ventricular tachycardia (VT) in non-ischemic and inherited cardiomyopathies is frequently treated as an imminently shock-requiring rhythm. Yet ventricular rate is an imperfect surrogate for tachycardia mechanism. When VT remains regular, monomorphic, and sustained by an organized reentrant circuit with an accessible excitable gap, antitachycardia pacing (ATP) may terminate even very rapid episodes without high-energy shock delivery.

Case Series

We report five patients with distinct non-ischemic arrhythmogenic substrates in whom fast sustained monomorphic VT (≥188 beats/min; tachycardia cycle length ≤320 ms), including very fast/VF-zone events >250 beats/min, was successfully terminated by ATP. The phenotypes comprised LMNA cardiomyopathy with conduction disease and septal fibrosis; TTN truncating variant-associated dilated cardiomyopathy with VT at approximately 260 beats/min; δ-sarcoglycan-associated dilated cardiomyopathy with clustered VT/electrical storm; severe non-ischemic cardiomyopathy with left bundle branch block, CRT-D implantation, and circumferential ring-like fibrosis, followed by 27 early post-implant VT episodes all terminated by ATP; and hypertrophic cardiomyopathy with an apical left ventricular aneurysm and diffuse late gadolinium enhancement, complicated by shock-free electrical storm. Several episodes were asymptomatic or initially attributed to atrial arrhythmia, whereas device interrogation documented sustained VT requiring therapy.

Discussion

Across these heterogeneous non-ischemic substrates, the unifying electrophysiological phenotype was fast, regular, monomorphic VT that remained susceptible to termination by ATP. The series illustrates how ATP response reflects the interaction among circuit organization, scar architecture, tachycardia cycle length, pacing-vector access, detection-zone design, and ATP programming. These observations complement randomized evidence supporting ATP for fast VT and contemporary shock-minimizing ICD programming, including PainFREE Rx II, PITAGORA ICD, MADIT-RIT, ADVANCE III, and APPRAISE ATP.

Conclusion

Fast VT in non-ischemic cardiomyopathy should not be considered intrinsically shock-dependent. When the tachycardia is sustained, regular, monomorphic, and electrophysiologically organized, ATP may successfully terminate even very rapid episodes while preserving defibrillation as back-up therapy. The key clinical implication is that ventricular rate, although relevant to risk assessment and therapy, is an imperfect surrogate for ATP susceptibility and should not alone dictate device-programming strategy.

Introduction

The therapeutic value of an implantable cardioverter-defibrillator (ICD) extends beyond its ability to deliver high-energy defibrillation; it also depends on accurate arrhythmia detection, discrimination, and selection of the least morbid effective therapy. Contemporary ICD programming has therefore evolved from a predominantly shock-centered strategy toward longer detection intervals, rate and rhythm discrimination, antitachycardia pacing (ATP), and deliberate shock minimization.^1,2 This shift is clinically relevant because ICD shocks are painful, adversely affect quality of life, and are consistently associated with worse subsequent outcomes.^3,4 In SCD-HeFT, both appropriate and inappropriate shocks were associated with increased mortality, although such associations also reflect the severity of the underlying arrhythmic and myocardial substrate.⁵

ATP exploits a fundamental property of organized reentry: a paced wavefront delivered at a cycle length shorter than the tachycardia cycle length can enter an excitable gap, reset the circuit, collide with the circulating wavefront, or render a critical isthmus refractory, thereby terminating VT without shock delivery.^6,7 Accordingly, ATP susceptibility is not determined by ventricular rate alone. Cycle-length stability, electrogram organization, excitable-gap width, conduction through scar channels, proximity of the pacing vector to a critical circuit component, and the programmed pacing sequence all influence efficacy.^8–10 A very rapid monomorphic VT may therefore remain pace-terminable, whereas a slower but polymorphic or unstable ventricular tachyarrhythmia may not.

This distinction is particularly relevant in non-ischemic and inherited cardiomyopathies, in which fibrosis is often mid-myocardial, subepicardial, septal, patchy, or circumferential rather than confined to a subendocardial coronary distribution.^11,12 Such scar architectures may generate slow-conduction corridors, functional lines of block, protected channels, and heterogeneous wavefront propagation capable of sustaining monomorphic reentry. Genotype further modulates this substrate: LMNA cardiomyopathy combines conduction-system disease with disproportionate ventricular arrhythmic risk;¹³ TTN truncating variant-associated dilated cardiomyopathy may exhibit clinically important arrhythmic vulnerability;^14,15 sarcoglycan-related disease reflects disruption of the cytoskeletal-sarcolemmal complex;¹⁶ and hypertrophic cardiomyopathy with apical aneurysm provides a fibrotic border zone capable of supporting monomorphic VT.^17,18

Despite robust evidence supporting ATP for fast VT in contemporary ICD populations, substrate-specific data in non-ischemic and inherited cardiomyopathies remain limited. In particular, little is known about whether very rapid scar-mediated monomorphic VT arising from diverse genetic and non-ischemic fibrosis patterns remains sufficiently organized to permit reliable pacing termination. This gap is clinically relevant because these substrates differ substantially from the predominantly ischemic scar architectures that have informed much of the mechanistic and programming evidence for ATP.

Against this background, we describe five patients with distinct non-ischemic cardiomyopathic substrates in whom fast sustained monomorphic VT, including clustered VT and electrical storm, was successfully terminated by ATP. Rather than re-establishing ATP efficacy, this series illustrates that even very rapid, rate-defined fast-VT or VF-zone events may retain an organized, pacing-susceptible substrate.

Case Presentations

This case series included patients with non-ischemic or inherited cardiomyopathy in whom ICD or CRT-D interrogation documented sustained, regular, monomorphic VT treated with ATP. Because definitions of fast VT vary across ICD studies, for descriptive consistency we defined fast VT as a ventricular rate ≥188 beats/min (tachycardia cycle length ≤320 ms), consistent with previous ATP studies encompassing a broad range of fast ventricular tachyarrhythmias.^19,20 Episodes >250 beats/min were additionally identified as very fast VT/VF-zone events according to the programmed device detection zone. Stored intracardiac electrograms were reviewed to confirm ventricular origin, cycle-length regularity, and stable morphology. VT cycle length was determined from consecutive ventricular intervals immediately preceding therapy and converted to rate as appropriate. ATP was considered successful when termination occurred during or immediately following the programmed ATP sequence, without redetection or subsequent shock therapy. Across the episodes reviewed in the present series, no documented fast monomorphic VT episode failed ATP or required subsequent shock therapy.

Case 1: LMNA Cardiomyopathy with Septal Fibrosis and Fast ATP-Terminated VT

A 46-year-old woman with a laminopathy phenotype was referred for symptomatic second-degree atrioventricular block of Wenckebach type in the context of quadriceps myopathy and a family history of sudden cardiac death. Baseline evaluation showed low limb-lead voltage, mildly reduced left ventricular ejection fraction (LVEF) of approximately 45%, and mid-wall septal fibrosis on cardiac magnetic resonance. Genetic testing identified an LMNA c.1272+2T>C splice-site variant classified as pathogenic in the context of the clinical and genetic evaluation. Given the combination of conduction-system disease, familial sudden death, myocardial fibrosis, and early systolic impairment, an ICD was implanted for primary prevention. Subsequent device interrogation documented clinically silent, sustained monomorphic VT at approximately 220 beats/min, successfully terminated by ATP (Figure 1).

Figure 1.

Device programming and stored electrograms demonstrating ATP termination of fast monomorphic VT in Case 1: (A) Implantable cardioverter-defibrillator programming at the time of the episode. The device was programmed in DDD mode with a base rate of 50 beats/min. The ventricular therapy zones included a VT-1 monitor zone beginning at 155 beats/min, a VT-2 therapy zone beginning at 179 beats/min with antitachycardia pacing followed by shocks, and a VF zone beginning at 222 beats/min with ATP during capacitor charging followed by high-energy shocks if required. Antitachycardia pacing was programmed as burst pacing with 8 stimuli at 85% of the tachycardia cycle length; (B) Stored intracardiac electrograms demonstrating a regular fast ventricular tachyarrhythmia classified in the VF zone by rate. The stable morphology and cycle length are consistent with fast monomorphic VT and (C) ATP during charging terminates the episode, restoring sinus/DDD rhythm and avoiding shock delivery.

Abbreviations: ATP, antitachycardia pacing; ICD, implantable cardioverter-defibrillator; VF, ventricular fibrillation; VT, ventricular tachycardia.

The phenotype is characteristic of LMNA cardiomyopathy, in which conduction disease, myocardial fibrosis, skeletal myopathy, and ventricular arrhythmias may precede advanced ventricular dilatation or severe systolic dysfunction. Arrhythmic risk can therefore be disproportionate to LVEF. In a multicenter European cohort of LMNA mutation carriers, malignant ventricular arrhythmias were associated with non-missense variants, non-sustained VT, LVEF <45%, and male sex, with events confined to patients carrying at least two of these risk factors.²¹

ATP termination provides additional, albeit indirect, mechanistic information. The stored rhythm was regular and monomorphic, supporting an organized reentrant mechanism rather than disorganized ventricular activation. Septal mid-wall fibrosis can create anisotropic conduction, localized delay, and protected channels; a circuit with these properties may retain an accessible excitable gap even at approximately 220 beats/min. Thus, the response to ATP is mechanistically compatible with scar-mediated reentry, although definitive circuit localization would require invasive electrophysiological mapping.

Case 2: TTN Truncating Variant-Associated Dilated Cardiomyopathy with Very Fast VT

A 41-year-old woman with dilated cardiomyopathy attributed to a TTN truncating variant had undergone ICD implantation for primary prevention. Device interrogation subsequently demonstrated sustained monomorphic VT at approximately 260 beats/min. The episode was asymptomatic and was terminated by ATP without shock delivery (Figure 2).

Figure 2.

ATP termination of very fast monomorphic VT in Case 2. Stored ICD electrograms from the ventricular near-field and shock-channel electrograms demonstrate detection of a regular fast ventricular tachyarrhythmia with cycle lengths in the VF zone. Despite rate-based VF-zone classification, the stable electrogram morphology and cycle-length organization are consistent with very fast monomorphic VT. Burst ATP is delivered, followed by prompt termination of the episode and return to sensed/paced ventricular rhythm without shock delivery.

Abbreviations: ATP, antitachycardia pacing; ICD, implantable cardioverter-defibrillator; VF, ventricular fibrillation; VT, ventricular tachycardia.

TTN truncating variants are the most common genetic cause of dilated cardiomyopathy and have also been associated with clinically important ventricular arrhythmic risk. Among patients with non-ischemic dilated cardiomyopathy carrying ICD or CRT-D systems, TTN truncating variants have been linked to a higher incidence of appropriate device therapy for VT or ventricular fibrillation.¹⁴ This case therefore illustrates the arrhythmic, rather than exclusively pump-failure, expression of TTN-related cardiomyopathy.

The ventricular rate—approximately 260 beats/min—is particularly informative. Tachycardias at this rate commonly enter fast-VT or VF therapy zones, where rate classification alone may favor shock-based treatment. Here, however, the stored electrograms remained regular and monomorphic. Successful ATP termination indicates that a very short tachycardia cycle length did not preclude sufficient circuit organization for pacing to interrupt the arrhythmia. This supports preservation of an ATP opportunity before shock, or during capacitor charging, for selected organized fast-zone rhythms when redetection and back-up defibrillation are maintained.

Case 3: δ-Sarcoglycan-Associated Dilated Cardiomyopathy with ATP-Terminated Electrical Storm

A man in his early fifties with δ-sarcoglycan-associated dilated cardiomyopathy presented with exertional syncope, positive signal-averaged ECG late potentials, inducible VT at electrophysiological study, low-voltage surface ECG features, and cardiac magnetic resonance evidence of fibrosis involving the mid/apical inferior, posterior, and lateral left ventricular segments. He subsequently developed multiple episodes of fast sustained monomorphic VT at approximately 240–250 beats/min, fulfilling an electrical storm phenotype (Figure 3). All documented episodes were terminated by ATP without ICD shocks.

Figure 3.

Recurrent fast VT episodes successfully treated by ATP in Case 3: (A) Device episode summary showing recurrent ventricular tachyarrhythmia episodes, including sustained VT-2 events successfully terminated by ATP without shock delivery, and (B) Representative stored intracardiac electrograms demonstrating a regular fast ventricular tachyarrhythmia with a cycle length of approximately 245 ms, detected in the fast VT/VF range. Delivery of ATP/stimulation during the episode terminates the tachycardia and restores a slower ventricular rhythm.

Abbreviations: ATP, antitachycardia pacing; VF, ventricular fibrillation; VT, ventricular tachycardia.

δ-sarcoglycan is a component of the dystrophin-glycoprotein complex that links the cytoskeleton to the extracellular matrix and contributes to sarcolemmal stability during contraction. Pathogenic variants in the human δ-sarcoglycan gene have been reported in familial and sporadic dilated cardiomyopathy.²² In this patient, late potentials, inducible VT, regional non-ischemic fibrosis, and recurrent sustained monomorphic VT form a coherent substrate-level phenotype: delayed activation identifies slow-conduction tissue, inducibility demonstrates ventricular arrhythmia susceptibility, and late gadolinium enhancement provides an anatomic correlate of myocardial fibrosis.

Repeated ATP termination during electrical storm suggests recurrent activation of organized ventricular tachycardia rather than repeated degeneration into disorganized ventricular arrhythmia. Importantly, avoidance of shocks does not attenuate the clinical significance of electrical storm. Recurrent ATP-treated sustained VT remains evidence of active substrate instability and warrants reassessment of reversible triggers, heart failure status, electrolyte disturbance, ICD programming, antiarrhythmic therapy, and candidacy for catheter ablation. This approach is consistent with the EHRA consensus on electrical storm, which emphasizes prompt device interrogation, arrhythmia characterization, optimization of programming, antiarrhythmic therapy, autonomic modulation, and ablation for recurrent scar-mediated VT.²³

Case 4: Severe Non-Ischemic Cardiomyopathy with Ring-Like Fibrosis and Recurrent ATP-Terminated VT After CRT-D Implantation

A 58-year-old man with severe non-ischemic cardiomyopathy, NYHA class III symptoms, syncope, left bundle branch block with a QRS duration of 170 ms, left ventricular dilatation, and an LVEF of approximately 27–30% underwent CRT-D implantation for primary prevention. Cardiac magnetic resonance demonstrated extensive circumferential ring-like non-ischemic fibrosis with septal involvement. During the first post-implant day, device interrogation documented 27 discrete sustained VT episodes. All recorded episodes were treated successfully with ATP, with no shock delivery or documented ATP failure. The patient was already receiving amiodarone at the time of the arrhythmic cluster. The device episode summary, corresponding timestamps, representative stored electrogram, and ATP programming are presented in Figure 4. Burst ATP consisted of 8 stimuli delivered at 85% of the tachycardia cycle length. Available intracardiac electrograms demonstrated a regular monomorphic VT phenotype.

Figure 4.

Device programming and recurrent ATP-terminated VT in Case 4: (A) CRT-D zone configuration showing VT-1 monitor zone, VT-2 therapy zone, and VF zone with ATP before shock therapy. Burst ATP was programmed with 8 stimuli at 85% of the tachycardia cycle length; (B) Surface ECG during wide-complex tachycardia consistent with sustained monomorphic VT; (C) Representative stored intracardiac electrogram showing VT-2 at 190 beats/min with successful termination by ATP and restoration of ventricular sensed rhythm, and (D) Episode summary demonstrating clustered VT-2 episodes on the same day, all successfully treated with ATP without shock delivery.

Abbreviations: ATP, antitachycardia pacing; CRT-D, cardiac resynchronization therapy-defibrillator; VF, ventricular fibrillation; VT, ventricular tachycardia.

The marked temporal clustering of these episodes immediately after CRT-D implantation raises the possibility of an early post-implant proarrhythmic contribution superimposed on a pre-existing arrhythmogenic substrate. CRT-associated proarrhythmia has been described early after implantation and may present as monomorphic VT or electrical storm, particularly when epicardial LV pacing interacts with scar or border-zone myocardium.^24,25 Nevertheless, the extensive circumferential fibrosis present before implantation provides a compelling chronic substrate for reentry, and temporal proximity to CRT initiation alone cannot establish causality. In the absence of evidence that VT was reproducibly induced or suppressed by modification of LV pacing, the episodes are best interpreted as an early post-implant electrical storm arising from a highly arrhythmogenic scar substrate, with a possible contribution from CRT-related triggering that cannot be definitively established.

The reproducible ATP response is nevertheless mechanistically informative. Ring-like late gadolinium enhancement may create broad regions of conduction slowing, functional block, and anatomically constrained reentrant pathways. Muser et al associated non-ischemic ring-like left ventricular scar with malignant ventricular arrhythmic events in patients initially presenting with apparently idiopathic non-sustained ventricular arrhythmias.¹² More broadly, late gadolinium enhancement in dilated cardiomyopathy is associated with increased risk of ventricular arrhythmia and sudden cardiac death,²⁶ while mid-wall fibrosis carries prognostic information even when systolic dysfunction is above conventional ICD thresholds.²⁷

Importantly, the 27 episodes represent recurrent events within a single patient and should not be considered independent demonstrations of ATP efficacy. Rather, their repeated termination by the same programmed ATP strategy suggests a reproducible, pacing-accessible arrhythmic phenotype. Extensive scar does not necessarily imply ATP resistance; a stable reentrant circuit with a consistent exit and accessible excitable gap may remain repeatedly pace-terminable. Septal scar involvement may also facilitate interaction between right ventricular pacing and the reentrant circuit, although this cannot be established from device electrograms alone. The clinical significance of the episode cluster therefore lies not in the absolute number of successful ATP therapies, but in the coexistence of a highly active arrhythmogenic substrate with remarkably reproducible pacing susceptibility.

Case 5: Hypertrophic Cardiomyopathy with Apical Aneurysm and Shock-Free Electrical Storm

A 59-year-old man with hypertrophic cardiomyopathy, an apical left ventricular aneurysm, left atrial enlargement, diffuse late gadolinium enhancement, paroxysmal atrial fibrillation, and prior ischemic stroke had undergone ICD implantation for primary prevention. Over a four-day period, he developed multiple episodes of sustained VT, all successfully terminated by ATP without shock delivery (Figure 5). He remained functionally active and initially attributed his symptoms to recurrent atrial fibrillation; remote device interrogation instead demonstrated recurrent sustained VT requiring appropriate therapy.

Figure 5.

Shock-free electrical storm treated by ATP in Case 5. Remote monitoring/device summary showing multiple alerts for ATP therapy delivered to terminate ventricular tachyarrhythmia over a 4-day period. The representative stored electrogram demonstrates onset of a regular ventricular tachycardia with ventricular cycle lengths in the fast VT range, followed by ATP-mediated termination without shock delivery.

Abbreviations: ATP, antitachycardia pacing; VT, ventricular tachycardia.

Hypertrophic cardiomyopathy with left ventricular apical aneurysm represents a distinct high-risk arrhythmogenic phenotype. Dense replacement fibrosis at the aneurysm and transition zone can generate conduction slowing, fractionated activation, and protected channels capable of supporting scar-mediated monomorphic VT. Although non-ischemic in origin, this architecture shares mechanistic features with infarct-border-zone reentry. Rowin et al demonstrated increased risks of arrhythmic sudden death and thromboembolic events in this phenotype,¹⁷ and contemporary hypertrophic cardiomyopathy guidelines recognize apical aneurysm as a major risk marker relevant to ICD decision-making.²⁸

The case also illustrates the limitations of symptom-based rhythm attribution in patients with coexisting atrial and ventricular arrhythmias. Palpitations, fatigue, presyncope, or nonspecific discomfort may be ascribed to atrial fibrillation, whereas stored intracardiac electrograms may reveal sustained VT. Remote monitoring therefore provides clinically decisive information. Recurrent ATP-treated VT should not be considered benign simply because shocks are avoided; it documents an active ventricular arrhythmic substrate and should prompt reassessment of antiarrhythmic therapy, device programming, and the role of VT ablation when episodes recur despite optimized management.

Discussion

The principal contribution of this case series is not to demonstrate that ATP can terminate fast VT—this has already been established in randomized ICD studies—but to show the breadth of non-ischemic substrates in which very rapid, rate-defined fast-VT or VF-zone events may remain organized and pacing-susceptible. Across five markedly different cardiomyopathic phenotypes, successful ATP was associated with a common electrical pattern: regular, sustained, monomorphic ventricular tachycardia occurring in the setting of structural scar. These cases therefore reinforce a mechanism-centered interpretation of device-detected ventricular tachyarrhythmias, in which rate informs urgency but does not, by itself, define the optimal therapy.

The mechanistic basis for this observation is the requirement for circuit accessibility. ATP can terminate reentry only when paced wavefronts reach excitable tissue within, or sufficiently close to, the tachycardia circuit.²⁹ Tachycardia cycle length is therefore one component of a broader system that includes electrogram stability, excitable-gap duration, scar-channel geometry, conduction velocity, pacing-site proximity, and the timing and structure of the ATP sequence. Non-ischemic scar may be especially heterogeneous—mid-wall, septal, subepicardial, patchy, or circumferential—yet this heterogeneity can still create protected channels and functional barriers capable of supporting stable reentry. Computational work similarly suggests that ATP success depends on scar-specific delivery, circuit proximity, and avoidance of re-initiation rather than on rate alone.⁶

The randomized programming literature provides the appropriate clinical context. PainFREE Rx II directly demonstrated that empirical ATP can terminate a large proportion of fast VT episodes and substantially reduce shock use without an excess of syncope, acceleration, or sudden death.¹⁹ PITAGORA ICD subsequently showed greater efficacy of burst than ramp pacing for fast ventricular tachyarrhythmias.³⁰ MADIT-RIT and ADVANCE III established the complementary value of higher rate thresholds and longer detection intervals in reducing unnecessary ICD therapy.^31,32 More recently, APPRAISE ATP showed that, even in contemporary primary-prevention ICD recipients programmed with long detection, ATP before shock prolonged the time to first all-cause shock compared with a shock-only strategy.³³ Taken together, these trials support a programming paradigm in which organized fast VT is given a reasonable opportunity for painless termination before high-energy therapy is delivered.³⁴

The genetic cases emphasize that ATP susceptibility can coexist with substrates carrying substantial arrhythmic risk. In LMNA cardiomyopathy, conduction disease and fibrosis may precede severe systolic dysfunction, and ventricular arrhythmic risk is not adequately captured by LVEF alone.^13,21 TTN truncating variant-associated cardiomyopathy likewise has an arrhythmic dimension beyond adverse remodeling and pump failure.^14,15 In the δ-sarcoglycan case, late potentials, inducible VT, regional fibrosis, and recurrent monomorphic VT converged on a plausible reentrant substrate.^16,22 In each setting, successful ATP should be interpreted as evidence of a treatable arrhythmia mechanism—not as evidence of a low-risk disease phenotype.

The imaging phenotypes in Cases 4 and 5 provide a complementary structural perspective. Circumferential ring-like fibrosis is associated with malignant ventricular arrhythmic risk and may form extensive corridors of slow conduction.^12,26,27 In hypertrophic cardiomyopathy with apical aneurysm, dense fibrosis at the aneurysm border can similarly create anatomically constrained circuits amenable to monomorphic reentry and, when recurrent, to substrate-based ablation.^17,18,28 These observations highlight an important distinction: scar burden may increase the propensity to develop VT, whereas ATP susceptibility depends on whether the resulting circuit remains sufficiently organized and accessible to pacing.

Several programming implications follow. Fast-VT zones should preserve an ATP opportunity when clinically appropriate, particularly when stored electrograms show a stable monomorphic rhythm, while reliable redetection and back-up shock therapy are maintained. In rate zones conventionally labeled as VF, ATP during capacitor charging may provide shock avoidance without materially delaying defibrillation if the rhythm fails to terminate. Successful ATP should also be evaluated beyond a binary success/failure label: the number of sequences required, timing of termination, redetection behavior, acceleration, and early recurrence can provide clinically useful information about the arrhythmia-device interaction.

The cases also demonstrate why treatment burden cannot be inferred from symptoms. Several episodes were clinically silent or initially attributed to atrial fibrillation, yet interrogation documented sustained VT requiring therapy. Remote monitoring and stored electrograms are therefore central not only to diagnosis but also to longitudinal risk assessment. Conversely, recurrent ATP-treated VT should not be dismissed because shocks were avoided. ATP reduces the morbidity of therapy; it does not remove the prognostic significance of recurrent sustained ventricular arrhythmia or electrical storm.

This issue has renewed relevance as defibrillator platforms diversify. Subcutaneous defibrillators avoid transvenous lead-related complications but do not provide conventional ATP, creating an important trade-off for patients at risk of recurrent monomorphic VT. The PRAETORIAN appropriate-therapy analysis and APPRAISE ATP underscore this trade-off from different perspectives.^33,35 Device selection and programming should therefore account not only for the risk of ventricular fibrillation and sudden death, but also for the likelihood that a patient may develop organized monomorphic VT for which ATP could meaningfully reduce shock exposure.

The present series must be interpreted within the limitations of a descriptive case series. It includes only five selected patients and, by design, cannot estimate ATP efficacy, identify predictors of success, or compare alternative programming strategies. Repeated episodes within the same patient—most notably the 27 episodes in Case 4—are correlated observations and should not be treated as independent events. In addition, a scar-mediated reentrant mechanism is inferred from rhythm regularity, monomorphic electrograms, imaging substrate, and ATP response; invasive circuit mapping was not available for every episode. The series should therefore be regarded as mechanistically illustrative and hypothesis-generating rather than confirmatory.

These limitations also help define the principal implication of the present series. Most directly, our observations suggest that some extensively scarred non-ischemic substrates can sustain very rapid yet sufficiently organized reentrant VT to remain amenable to ATP. Successful ATP should therefore be interpreted primarily as evidence of circuit organization and accessibility rather than as a marker of benign arrhythmic disease or, conversely, as a sudden-death equivalent. Nevertheless, a high burden of ATP-treated VT may identify a more active arrhythmogenic phenotype: in a recent PARTITA subanalysis, ≥5 ATP-treated episodes within 6 months were associated with a markedly increased subsequent risk of ICD shock and cardiovascular events.³⁶ Whether reproducible ATP responsiveness itself carries independent prognostic significance, however, remains uncertain. Prospective studies integrating device electrograms, scar imaging, invasive mapping, and standardized ATP programming are needed to determine whether ATP responsiveness defines a clinically meaningful electrophysiological phenotype beyond the prognostic information conveyed by recurrent VT burden.

Conclusion

Fast scar-mediated monomorphic VT in non-ischemic cardiomyopathy may remain amenable to ATP even at rates conventionally assigned to fast-VT or VF therapy zones. The present cases suggest that ATP is most relevant when the ventricular tachyarrhythmia is sustained, regular, monomorphic, and supported by a structural scar substrate, with preserved electrogram organization and appropriate device detection, redetection, and back-up defibrillation. These features should be regarded as mechanistic considerations rather than validated selection criteria, as no predictive model for ATP success was tested in this series. ATP may therefore provide an important shock-sparing strategy in appropriately characterized ventricular tachyarrhythmias, while successful termination does not diminish the clinical significance of the underlying arrhythmogenic substrate.

Funding Statement

This research received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors.

Data Sharing Statement

No additional dataset was generated for this descriptive case series beyond the clinical information presented in the article.

Patient Consent

Written informed consent for publication of anonymized clinical information, device-interrogation data, and accompanying images was obtained from all patients included in this case series. All data were de-identified before manuscript preparation. In accordance with local institutional policy, formal institutional review board approval was not required for this retrospective descriptive case series because no experimental intervention was performed and no identifiable patient information is presented.

Disclosure

The authors report no conflicts of interest in this work.