Electrocardiographic left ventricular scar burden predicts clinical outcomes following infarct-related ventricular tachycardia ablation

Background: Conducting channels within scars form the substrate for infarct-related ventricular tachycardia (VT) and are targeted during catheter ablation. Whether the amount of left ventricular scar (LVS) affects outcomes after VT ablation is not known.

Objective: To test the hypothesis that increased LVS is associated with worsened clinical outcomes and reduced survival after VT ablation.

Methods: Patients with coronary artery disease and intrinsic AV nodal conduction undergoing infarct-related VT ablation were studied. A validated 32-point scoring system was used to measure LVS from 12-lead ECGs. Primary endpoint was all-cause mortality or transplantation. Secondary endpoint was a composite of death, transplantation, or readmission due to VT recurrence within 1 year of discharge.

Results: Of 356 patients undergoing 466 infarct-related VT ablations screened, 192 (84% male, age 66 ± 11 years, 52% prior coronary artery bypass graft, ejection fraction 28% ± 11%) who underwent 245 procedures for VT (2.4 ± 1.5 VTs per patient, 31% with VT storm, refractory to 2.7 ± 1.2 antiarrhythmic drugs) between 1999 and 2009 were included. During mapping, all patients had low-voltage areas. Mean LVS was 21.4% ± 15.0%. Over 3.4 ± 3.1 years, 78 patients (41%) reached the primary endpoint (73 deaths, 5 transplants). In the first year after discharge, the secondary endpoint was reached in 56 subjects (29%). In a multivariate model, larger LVS (hazard ratio [HR] 1.03 for every 3% increase in LVS, P < .01), renal dysfunction (HR 2.66, P <.01), and increased age (HR 1.05 per year, P < .01) predicted mortality, whereas noninducibility of any VT was protective. (HR 0.36, P < .01) Larger LVS and renal dysfunction were associated with worsened 1-year outcomes, whereas noninducibility was protective.

Conclusion: LVS burden derived from 12-lead ECGs is a significant and independent predictor of mortality and clinical outcomes in subjects with infarct-related VT.