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Functional Substrate-Only Guided VT Ablation

Not Applicable
Not yet recruiting
Conditions
Sudden Cardiac Death
Ventricular Tachycardia
Interventions
Procedure: Standard-of-Care Mapping/Imaging
Procedure: Functional Substrate-Only Mapping without VT Induction
Registration Number
NCT06464315
Lead Sponsor
VA Office of Research and Development
Brief Summary

Ventricular tachycardia (VT) is a leading cause of death and suffering in the Veteran population. Currently, ablation procedures are performed to destroy the diseased tissue that causes this problem. This study will test to see if an experimental strategy of only targeting regions of slow conduction without the induction of VT can improve the efficacy and safety of VT ablation. Once this study is completed, the investigators will know whether this ablation strategy could help increase the efficacy, safety and efficiency of ablation therapy of fatal heart rhythms.

Detailed Description

Ventricular tachycardia (VT) remains a leading cause of death and morbidity in the veteran population, but current ablation procedures to treat VT are limited by hemodynamic instability of induced VT during standard invasive activation mapping (up to 80% of induced VT), lengthy ablation procedures (\~8 hours), and difficulty in accurately localizing the critical origination sites of VT. The long-term goal is to simplify VT ablation using invasive functional substrate mapping techniques to improve the safety, efficacy, and efficiency of VT catheter ablation. The overall objectives in this application are to i) perform a randomized clinical trial to test whether performing simplified VT ablation guided only by invasive functional substrate mapping without VT induction improves the safety and efficiency of VT ablation while maintaining similar efficacy compared to standard ablation and ii) mechanistically correlate abnormal functional substrate with VT origination sites localized using gold standard invasive activation mapping. The central hypothesis is that ablation of slowly conducting tissue characterized by high frequency signals is sufficient to eliminate VT and improves clinical outcomes of VT ablation. The rationale is that recently developed sophisticated techniques to characterize functionally abnormal tissue can localize critical VT-sustaining substrate without needing to subjecting patients to mapping of hemodynamically unstable VT which is routinely done during standard of care ablation. The central hypothesis will be tested by pursuing one primary specific aim: Perform a randomized clinical trial to determine whether VT ablation guided only by invasive functional substrate mapping without VT induction decreases procedure time, fluoroscopy time, and procedural complications while maintaining similar efficacy compared to standard VT ablation controls. This study also includes 2 sub-aims to uncover VT mechanisms characterizing the distance of slowly conducting tissue to VT exit sites and provide a method to unmask critical arrhythmogenic substrate in non-ischemic cardiomyopathy patients in whom scar is not easily identified. The research proposed is innovative because it tests a novel strategy using new algorithms that can identify the critical tissue sustaining VT without requiring the induction of VT. The proposed research is significant because a functional substrate-guided only approach to VT ablation while still localizing the critical tissue causing VT is expected to increase the safety, efficacy, and efficiency of treating a fatal heart rhythm disorder

Recruitment & Eligibility

Status
NOT_YET_RECRUITING
Sex
All
Target Recruitment
36
Inclusion Criteria
  • Men and women >18 years of age referred for clinically indicated VT ablation and experience monomorphic or polymorphic scar-based VT documented by telemetry, ICD interrogation, ECG or event monitoring.
  • Scar-based VT is defined as VT in patients with structural heart disease (assessed with either abnormal nuclear perfusion imaging (>5% defect), late gadolinium uptake on cardiac MRI, wall thinning <10mm or calcified myocardium on cardiac CT, akinesis or hypokinesis on echocardiogram, presence of Q waves on ECG, history of myocardial infarct).
  • Patients undergoing epicardial VT ablation and who undergo prophylactic percutaneous hemodynamic support devices will also be included.
Exclusion Criteria
  • Patients without structural heart disease will be excluded from the pri-mary analysis, but enrolled in a prospective registry
  • Patients who are pregnant
  • Presence of intracardiac thrombus
  • active acute coronary ischemia with unrevascularized coronary artery disease (CAD >70% stenosis)
  • Active bacteremia
  • Inaccessible ventricles due to dual mechanical valves
  • Inability to tolerate and inability to tolerate anticoagulation during ablation and for at least 1 month after ablation

Study & Design

Study Type
INTERVENTIONAL
Study Design
PARALLEL
Arm && Interventions
GroupInterventionDescription
Standard VT MappingStandard-of-Care Mapping/ImagingStandard-of-care mapping, including voltage mapping of intrinsic rhythm, entrainment, activation, and/or pace mapping, will be performed to guide VT ablation. Standard VT induction protocols will be performed.
Functional substrate mapping only without VT inductionFunctional Substrate-Only Mapping without VT InductionIn this experimental arm, only functional substrate mapping will be used to guide ablation of conduction slowing regions, without VT induction or mapping during VT. Ablation targets of conduction slowing will be identified as: 1) deceleration zones of conduction slowing, previously defined as 3 isochrones coalescing within 1cm radius. 2) wavefront discontinuities represented by lines of conduction block, previously defined as late potentials with at least 20ms of isoelectric segment, and 3) regions of slow conduction characterized by high peak frequency (220-500Hz), which uses spectral frequency analysis to identify signals with highest frequency as a surrogate for slow conduction. All regions exhibiting any of these 3 surrogates of slow conduction will be ablated.
Primary Outcome Measures
NameTimeMethod
Time to composite endpoint (VT recurrence, death, or acute hemodynamic decompensation)6 months

Ventricular arrhythmia recurrence is defined by an episode of sustained VT lasting 30 seconds or appropriate implantable cardioverter-defibrillator therapy including anti-tachycardia pacing or shock.

Acute hemodynamic decompensation is defined by escalation of at least 1 new high dose inotrope/pressor occurring after anesthesia induction with persistent requirement during stable rhythm, \>20% drop in cardiac index, unplanned insertion of percutaneous hemodynamic support device.

Secondary Outcome Measures
NameTimeMethod
VT burden (ICD therapy including shocks and ATP, sustained VT episodes >30 seconds)6 months

Total number of ICD therapies (ATP and shocks) and recorded sustained VT episodes\>30 seconds, compared 6 months before and 6 months after ablation.

Total Mapping Timeimmediately at the end of the procedure

dwell time of multi-electrode mapping catheters

total procedural timeimmediately at the end of the procedure

time from introduction of catheters to removal of catheters

Total fluoroscopy timeimmediately at the end of the procedure

Total amount of fluoroscopy time during the entire procedure

Procedural adverse events or complications1 month

Major complications include: new acute pericardial effusion requiring intervention, vascular complication requiring intervention, embolic stroke confirmed by brain imaging, limb ischemia requiring intervention, or bacteremia.

Major adverse events include: cardiogenic shock (requiring escalation of inotropes or salvage mechanical circulatory support)

Use of general anesthesiaimmediately at the end of the procedure

Whether general anesthesia (intubation) is required/used during the procedure

Trial Locations

Locations (1)

VA San Diego Healthcare System, San Diego, CA

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San Diego, California, United States

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