• Decrement Evoked Potential Mapping to Guide Ventricular Tachycardia Ablation: Elucidating the Functional Substrate.

      Bhaskaran, Abhishek; Fitzgerald, John; Jackson, Nicholas; Gizurarson, Sigfus; Nanthakumar, Kumaraswamy; Porta-Sánchez, Andreu; 1University Health Network, University of Toronto, Ontario, Canada. 2University of Adelaide, Australia. 3John Hunter Hospital, Newcastle, Australia. 4Landspitali, Reykjavik, Iceland. 5Hospital Universitario Quirónsalud Madrid, Molecular Cardiology Laboratory, Centro Nacional de Investigaciones Cardiovasculares, Spain. (Radcliffe Cardiology, 2020-12)
      Empirical approaches to targeting the ventricular tachycardia (VT) substrate include mapping of late potentials, local abnormal electrogram, pace-mapping and homogenisation of the abnormal signals. These approaches do not try to differentiate between the passive or active role of local signals as the critical components of the VT circuit. By not considering the functional components, these approaches often view the substrate as a fixed anatomical barrier. Strategies to improve the success of VT ablation need to include the identification of critical functional substrate. Decrement-evoked potential (DeEP) mapping has been developed to elucidate this using an extra-stimulus added to a pacing drive train. With knowledge translation in mind, the authors detail the evolution of the DeEP concept by way of a study of simultaneous panoramic endocardial mapping in VT ablation; an in silico modelling study to demonstrate the factors influencing DeEPs; a multicentre VT ablation validation study; a practical approach to DeEP mapping; the potential utility of DeEPs to identify arrhythmogenic atrial substrate; and, finally, other functional mapping strategies.
    • Obstructive sleep apnoea treatment and fasting lipids: a comparative effectiveness study.

      Keenan, Brendan T; Maislin, Greg; Sunwoo, Bernie Y; Arnardottir, Erna Sif; Jackson, Nicholas; Olafsson, Isleifur; Juliusson, Sigurdur; Schwab, Richard J; Gislason, Thorarinn; Benediktsdottir, Bryndis; et al. (European Respiratory Society, 2014-08)
      Obstructive sleep apnoea (OSA) is associated with cardiovascular disease. Dyslipidaemia has been implicated as a mechanism linking OSA with atherosclerosis, but no consistent associations with lipids exist for OSA or positive airway pressure treatment. We assessed the relationships between fasting lipid levels and obesity and OSA severity, and explored the impact of positive airway pressure treatment on 2-year fasting lipid level changes. Analyses included moderate-to-severe OSA patients from the Icelandic Sleep Apnoea Cohort. Fasting morning lipids were analysed in 613 untreated participants not on lipid-lowering medications at baseline. Patients were then initiated on positive airway pressure and followed for 2 years. Sub-classification using propensity score quintiles, which aimed to replicate covariate balance associated with randomised trials and, therefore, minimise selection bias and allow causal inference, was used to design the treatment group comparisons. 199 positive airway pressure adherent patients and 118 non-users were identified. At baseline, obesity was positively correlated with triglycerides and negatively correlated with total cholesterol, and low-density and high-density lipoprotein cholesterol. A small correlation was observed between the apnoea/hypopnoea index and high-density lipoprotein cholesterol. No effect of positive airway pressure adherence on 2-year fasting lipid changes was observed. Results do not support the concept of changes in fasting lipids as a primary mechanism for the increased risk of atherosclerotic cardiovascular disease in OSA.