Background The impact of catheter ablation of ventricular tachycardia (VT) on all-cause mortality remains unknown. Objective To examine the association between VT recurrence after ablation and survival in patients with scar-related VT. Methods Analysis of 2,061 patients with structural heart disease referred for catheter ablation of scar-related VT from 12 international centers was performed. Data on clinical and procedural variables, VT recurrence, and mortality were analyzed. Kaplan-Meier analysis was used to estimate freedom from recurrent VT, transplant, and death. Cox proportional hazards frailty models were used to analyze the effect of risk factors on VT recurrence and mortality. Results One-year freedom from VT recurrence was 70% (72% in ischemic and 68% in non-ischemic cardiomyopathy). 57 (3%) patients underwent cardiac transplantation and 216 (10%) died during follow-up. At one year, the estimated rate of transplant and/or mortality was 15% (same for ischemic and non-ischemic cardiomyopathy). Transplant-free survival was significantly higher in patients without VT recurrence compared to those with recurrence (90% vs. 71%, p<0.001). In multivariable analysis, recurrence of VT after ablation showed the highest risk for transplant and/or mortality (HR 6.9 (5.3-9.0); p<0.001). In patients with EF<30% and across all NYHA classes, improved transplant-free survival was seen in those without VT recurrence. Conclusions Catheter ablation of VT in patients with structural heart disease results in 70% freedom from VT recurrence, with an overall transplant and/or mortality rate of 15% at 1 year. Freedom from VT recurrence is associated with improved transplant-free survival, independent of heart failure severity.

Immune system activation contributes to the pathogenesis of hypertension and the resulting progression of chronic kidney disease (CKD). In this regard, we recently identified a role for pro-inflammatory Th1 T lymphocyte responses in hypertensive kidney injury. As Th1 cells generate IFN-γ and TNF-α, we hypothesized that IFN-γ and TNF-α propagate renal damage during hypertension induced by activation of the renin-angiotensin system (RAS). Therefore, after confirming that mice genetically deficient of Th1 immunity were protected from kidney glomerular injury despite a preserved hypertensive response, we subjected mice lacking IFN-γ or TNF-α to our model of hypertensive CKD. IFN-deficiency had no impact on blood pressure elevation or urinary albumin excretion during chronic angiotensin II infusion. By contrast, TNF-deficient (KO) mice had blunted hypertensive responses and reduced end-organ damage in our model. As Ang II-infused TNF KO mice had exaggerated eNOS expression in the kidney and enhanced nitric oxide (NO) bioavailability, we examined the actions of TNF-α generated from renal parenchymal cells in hypertension by transplanting wild-type or TNF KO kidneys into wild-type recipients prior to the induction of hypertension. Transplant recipients lacking TNF solely in the kidney had blunted hypertensive responses to Ang II and augmented renal eNOS expression, confirming a role for kidney-derived TNF-α to promote Ang II-induced blood pressure elevation by limiting renal NO generation.