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Introduction: Ventricular tachycardia (VT) can occur following valvular interventions. There are limited data describing substrate and ablation approaches in such patients. We sought to describe the clinical, electrophysiologic, electroanatomic features and catheter ablation outcomes of patients with VT following aortic and/or mitral valve intervention. Methods: Over 12‐years, consecutive patients with aortic valve replacement (AVR) and/or mitral valve replacement (MVR) or repair, undergoing VT ablation, were identified from two centers. Clinical and procedural parameters and outcomes are described. Results: Twenty‐three patients (age 66 ± 14years, 78% male, left ventricular ejection fraction 37 ± 16%), with prior AVR (mechanical n = 6, bioprosthetic n = 2, transcatheter n = 1), MVR (mechanical n = 5, bioprosthetic n = 1), mitral valve repair (n = 6) and both mechanical AVR and MVR (n = 2), underwent VT ablation. Sixteen had concurrent ischemic cardiomyopathy, 10 with prior bypass surgery. Left ventricular access was obtained in 21/23 (91%) patients (transseptal n = 14, retrograde aortic n = 5, transapical n = 2), with perivalvular scar identified in 17/21 (81%). Re‐entrant VT isthmi involved the perivalvular regions in 12/23 (52%) patients, and regions remote from the valve in the remainder; 9% had nonscar‐related VT. Intramural substrate was ablated from adjacent chambers in 5/23 (22%) patients and with half‐normal saline irrigation in 8/23 (35%) patients. There were no instances of catheter entrapment. Following final ablation, VA‐free survival was 78% at 13‐months. Conclusion: Only half of VT circuits following valvular interventions involve the valve regions themselves, while the remainder involves unrelated regions. Catheter ablation is safe and efficacious at treating VT following valvular intervention, but novel strategies may be required. [ABSTRACT FROM AUTHOR]

Uraemic Cardiomyopathy (UC) is recognised as an intricate and multifactorial disease which portends a significant burden in patients with End-Stage Renal Disease (ESRD). The cardiovascular morbidity and mortality associated with UC is significant and can be associated with the development of arrythmias, cardiac failure and sudden cardiac death (SCD). The pathophysiology of UC involves a complex interplay of traditional implicative factors such as haemodynamic overload and circulating uraemic toxins as well as our evolving understanding of the Chronic Kidney Disease-Mineral Bone Disease pathway. There is an instrumental role for multi-modality imaging in the diagnostic process; including transthoracic echocardiography and cardiac magnetic resonance imaging in identifying the hallmarks of left ventricular hypertrophy and myocardial fibrosis that characterise UC. The appropriate utilisation of the aforementioned diagnostics in the ESRD population may help guide therapeutic approaches, such as pharmacotherapy including beta-blockers and aldosterone-antagonists as well as haemodialysis and renal transplantation. Despite this, there remains limitations in effective therapeutic interventions for UC and ongoing research on a cellular level is vital in establishing further therapies. [ABSTRACT FROM AUTHOR]

Introduction: Testing for inducible ventricular tachycardia (VT) pre‐ and postablation forms the cornerstone of contemporary scar‐related VT ablation procedures. There is significant heterogeneity in reported VT induction protocols. We examined the utility of an extensive induction protocol (up to 4 extra‐stimuli [ES] ± burst ventricular pacing) compared to the current guideline‐recommended protocol (up to 3ES, defined as limited induction protocol) in patients with scar‐related VT. Methods and Results: Sixty‐two patients (age: 64 ± 14 years; left ventricular ejection fraction: 37 ± 13%, ischemic cardiomyopathy: 31, nonischemic cardiomyopathy: 31) with at least one inducible VT were included. An extensive testing protocol induced 11%–17% more VTs, compared to the limited induction protocol before, and after the final ablation. VT recurred in 48% of patients during a mean follow up of 566 ± 428 days. Patients who were noninducible for any VT using the limited induction protocol had worse ventricular arrhythmia (VA)‐free survival (12 months, 43% vs. 82%; p =.03) and worse survival free of VA, transplantation and mortality (12 months 46% vs. 82%; p =.02), compared to patients who were noninducible for any VT using the extensive induction protocol. Conclusions: Between 11% and 17% of inducible VTs may be missed if 4ES and burst pacing are not performed in induction protocols before and after ablation. Noninducibility for any VT after an extensive induction protocol after the final ablation portends more favorable prognostic outcomes when compared with the current guideline‐recommended induction protocol of up to 3ES. This data suggests that the adoption of an extensive induction protocol is of prognostic benefit after VT ablation. [ABSTRACT FROM AUTHOR]