Functional Substrate-Only Guided VT Ablation

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

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