Abstract
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. To test the hypothesis that increased LVS is associated with worsened clinical outcomes and reduced survival after VT ablation. 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. 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. LVS burden derived from 12-lead ECGs is a significant and independent predictor of mortality and clinical outcomes in subjects with infarct-related VT.
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