Ventricular tachycardia (VT), and Catheter Ablation:
Catheter ablation is an established therapeutic option for the treatment of VT but remains challenging. This is in part due to inadequate mapping of the VT due to lack of inducibility or to hemodynamic instability during the arrhythmia. Thus, modification of the arrhythmogenic substrate during sinus rhythm is by far the most routinely performed approach for post-MI VT ablation. Scar tissue is most commonly identified, during the ablation procedure, by catheter mapping of the endocardial surface voltage in the EP lab, but this approach adds significant time to procedural duration, thereby increasing ablation complications and morbidity. Furthermore, this approach is highly dependent on catheter reach, stability and contact with the endocardium, which significantly affects the accuracy of anatomic definition. The border zone of the scar is often the site of VT exit and thus ablation is performed in that region. In addition, ablation of local abnormal ventricular activations which represent areas of residual viability within the scar is believed to increase procedural success, but catheter mapping to identify of these sites during the ablation procedure is tedious and time-consuming.
Dual Isotope Perfusion/Denervation:
In patients with VT, intracavity electrical abnormalities frequently originate at the site of viable but denervated regions and represent ultimate ablation targets. In a clinical study, quantitative uptake of a sympathetic-targeted radiotracer in the infarct border zone predicted VT inducibility on EP testing with promising accuracy.
We hypothesize using use Tl-201 for perfusion and 18F-FBBG to assess the area of denervation. Intra-ventricular detection of the boundary would be performent by the Atheron’s multi-detector catheter.