Medicine (RMH) - Theses
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ItemVentricular Tachycardia: From Mechanisms to Therapies( 2021)Ventricular arrhythmias (VA) and sudden cardiac death (SCD) are responsible for one-half of all deaths in patients with heart disease. It is estimated that up to 40% of SCD is attributed to VA, highlighting a clear need for additional strategies to reduce this figure. Despite the systematic and escalated use of antiarrhythmic drugs (AADs) and implantable cardioverter defibrillators (ICD), VA incidence continues to rise. Catheter ablation (CA) has been shown to be a superior treatment for VA compared to AAD therapy in regards to reducing ICD shocks and ventricular tachycardia (VT) storm. However, a mortality benefit has not been demonstrated in randomized controlled trials. Advancements in catheter and electroanatomical mapping technology has led to new frontiers in delineating VT mechanisms and substrate characterisation translating to improvements to targeted ablation strategies. The aim of this thesis was to expand on the diagnostic, mechanistic, substrate characterisation and ablative techniques used for VT in the presence and absence of structural heart disease (SHD). Initially, we evaluate pre-procedural prediction of idiopathic outflow tract VAs using the surface electrocardiogram (ECG). We then perform studies involving scar-related VT. These include assessing the current evidence for the role of CA in VT ablation including assessment of Australian procedural trends, exploration of VT mechanisms and the effect of wavefront directionality on delineating scar substrate in an ovine-infarct model. Finally, we assess procedural characteristics and outcomes of implementing simultaneous high output pacing during substrate-based CA as an expedited lesion endpoint. Chapter 1 outlines our understanding of VT and ventricular fibrillation (VF) mechanisms. We discuss VT in the absence of the SHD (idiopathic VT) with particular emphasis on morphological ECG ‘signatures’ and prediction algorithms used differentiate outflow tract premature ventricular complexes (PVC) and VT (OTVT) sites of origin (SOO). We then explore VT in the setting of SHD providing a summary of current techniques used to characterise arrhythmogenic substrate, high density mapping and use of CA in both ischaemic and non-ischaemic cardiomyopathies and use of novel ablative techniques. Chapter 2 prospectively evaluates a modified high-precordial ECG configuration compared to standard ECG positions in 50 patients with OTVT. The study is divided into 3 phases assessing the anatomical relationship of the modified leads to the outflow tracts using multiplanar computer tomography (CT) followed by an algorithm development phase and validation review. We develop an algorithm that differentiated the right ventricular outflow tract and left ventricular outflow tract PVCs and VT with high accuracy – the modified lead R-wave deflection interval (RWDI). The RWDI was superior to all previously developed algorithms and anatomically closer to the outflow tracts compared to standard precordial lead positions. Chapter 3 assess the impact of CA as compared to medical therapy on outcomes in patients with VT and SHD. We perform a systematic review and meta-analysis of 8 randomized controlled trials (RCTs) enrolling 797 patients with predominantly ischaemic scar-related VT reporting VT recurrence and mortality. We compared RCTs to 4 contemporary, large observational studies including 3065 patients. We conclude CA is superior to medical therapy with significant reductions in VT recurrence and electrical VT storm, however, there was no difference in terms of all-cause or cardiac-specific mortality. The proportion of patients with non-ischaemic cardiomyopathy (NICM) and electrical storm (ES) was much higher in the observational studies; however, despite this, there was further reductions in VT recurrence and mortality compared to RCT meta-analysis. Chapter 4 analyses procedural trends of VT ablation procedures in Australia using two major data sources (Australian Institute of Health, Wealth and Aging and Medicare Australia) over a 10-year period. We calculated population-adjusted procedures per year and applied a regression model to calculate percentage change per year. We report growth of VT ablations have surpassed atrial fibrillation (AF) and percutaneous coronary intervention (PCI) procedures and discuss possible explanations for VT ablation growth and health care implications. Chapter 5 examines procedural characteristics and outcomes in patients undergoing ventricular assist device (VAD)-related VT ablation. We performed a systematic review of 18 studies including 110 patients demonstrating that scar-related re-entrant VT was the predominant mechanism in >90% cases followed by cannula-adjacent VT in approximately 20% of VTs. Furthermore, the haemodynamic tolerability of the VAD allowed an activation and entrainment mapping strategy as compared to a substrate-based approach. Perceived procedural difficulties during CA of VT were rare and complications comparable to a non-VAD cohort; however, need for cardiac transplantation and mortality were expectedly high underscoring the severe underlying disease in this group. Chapter 6 focuses on the prevalence of a primary or co-existent focal mechanism in patients with SHD who historically are exclusively thought to have scar-related reentry. Using an extended VT induction protocol incorporating catecholamine stimulation and right ventricle (RV) burst pacing in 112 patients over a 2-year period, we show 16% had a focal mechanism elucidated. Focal VTs commonly co-existed with re-entrant VTs and typically localised to scar borderzone or remote regions usually attributed to “idiopathic” locations. We found a high rate of failure of device therapies including repetitive initiation which was unique to this group with CA a highly effective treatment for durable outcomes. Chapter 7 examines the effect of directional influence of substrate characterisation using a multielectrode catheter (HD Grid) in a post infarct ovine model using proprietary software which selects the highest voltage from orthogonal bipolar pairs (HD wave solution). We compare this catheter to a validated linear duodecapolar catheter. We conclude that varying the wavefront of activation results in significant differences in the percentage of scar and abnormal electrograms (EGM) using the HD grid catheter, despite the HD wave solution. The HD grid demonstrated a higher proportion of normal voltage compared to the duodecapolar catheter, across all activation wavefronts. Compared to the duodecapolar catheter, we show abnormal EGMs, specifically local abnormal ventricular activations (LAVA) were significantly less using the HD grid catheter. Chapter 8 evaluates simultaneous high-output pacing and ablation adopting a substrate-based scar homogenisation strategy to achieve scar inexcitability for lesion endpoints. We assess the procedural characteristics and ablation parameters in 10 patients and show this technique is safe and effective with high acute procedural success for VT non-inducibility with no recurrence or repeat procedure in short-term (6 month) follow-up.