Reasons for Recurrent Ventricular Tachycardia After Catheter Ablation of Post-Infarction Ventricular Tachycardia

Objectives rpose of this study was to assess the determinants of ventricular tachycardia (VT) recurrence in patients who underwent VT ablation for post-infarction VT. ound ctors that predict recurrence of VT after catheter ablation in patients with prior infarctions are not well described. s er ablation was performed in 98 consecutive patients (88 males [90%]; mean age 67 ± 10 years; ejection fraction 27 ± 13%) with post-infarction VT. Electrograms from the implantable cardioverter-defibrillator were analyzed, and VTs were classified as clinical, nonclinical, or new clinical. s l of 725 VTs were induced during the ablation procedure. All VTs were targeted. In 76 patients, 105 clinical VTs were inducible. Critical sites were identified with entrainment mapping and pace-mapping (≥10 of 12 matching leads) for 75 of 105 clinical VTs (71%) and for 278 of 620 nonclinical VTs (45%). Post-ablation, the clinical VT was not inducible in any patient, and all VTs were rendered noninducible in 63% of the patients. Over a mean follow-up period of 35 ± 23 months, 65 of 98 patients (66%) had no recurrent VTs and 33 (34%) had VT recurrence. A new VT occurred in 26 of 33 patients (79%), and a prior clinical VT recurred in 7 patients (21%). Patients with recurrent VT had a larger scar area as assessed by electroanatomic mapping compared with patients without recurrent VTs (93 ± 40 cm2 vs. 69 ± 30 cm2; p = 0.002). In patients with repeat procedures, the majority of inducible VTs for which a critical area could be identified were at a distance of 6 ± 3 mm to the prior ablation lesions. sions ts with recurrent VTs have a larger scar as assessed by electroanatomic mapping. Most recurrent VTs were new, and the majority of these VTs were mapped to the vicinity of prior ablation lesions in patients with repeat procedures.