Eoin R Hyde1, Jonathan M Behar1, Simon Claridge1, Tom Jackson1, Angela W C Lee1, Espen W Remme1, Manav Sohal1, Gernot Plank1, Reza Razavi1, Christopher A Rinaldi1, Steven A Niederer2. 1. From the Department of Biomedical Engineering, King's College London, London, United Kingdom (E.R.H., J.M.B., S.C., T.J., A.W.C.L., M.S., R.R., C.A.R., S.A.N.); Department of Cardiology, Guy's and St Thomas' NHS Foundation Trust, London, United Kingdom (J.M.B., S.C., T.J., M.S., C.A.R.); Institute for Surgical Research, Oslo University Hospital, Rikshospitalet and KG Jebsen Cardiac Research Centre, University of Oslo, Oslo, Norway (E.W.R.); and Institut für Biophysik, Medizinische Universität, Graz, Austria (G.P.). 2. From the Department of Biomedical Engineering, King's College London, London, United Kingdom (E.R.H., J.M.B., S.C., T.J., A.W.C.L., M.S., R.R., C.A.R., S.A.N.); Department of Cardiology, Guy's and St Thomas' NHS Foundation Trust, London, United Kingdom (J.M.B., S.C., T.J., M.S., C.A.R.); Institute for Surgical Research, Oslo University Hospital, Rikshospitalet and KG Jebsen Cardiac Research Centre, University of Oslo, Oslo, Norway (E.W.R.); and Institut für Biophysik, Medizinische Universität, Graz, Austria (G.P.). steven.niederer@kcl.ac.uk.
Abstract
BACKGROUND: Cardiac resynchronization therapy (CRT) delivered via left ventricular (LV) endocardial pacing (ENDO-CRT) is associated with improved acute hemodynamic response compared with LV epicardial pacing (EPI-CRT). The role of cardiac anatomy and physiology in this improved response remains controversial. We used computational electrophysiological models to quantify the role of cardiac geometry, tissue anisotropy, and the presence of fast endocardial conduction on myocardial activation during ENDO-CRT and EPI-CRT. METHODS AND RESULTS: Cardiac activation was simulated using the monodomain tissue excitation model in 2-dimensional (2D) canine and human and 3D canine biventricular models. The latest activation times (LATs) for LV endocardial and biventricular epicardial tissue were calculated (LVLAT and TLAT), as well the percentage decrease in LATs for endocardial (en) versus epicardial (ep) LV pacing (defined as %dLV=100×(LVLATep-LVLATen)/LVLATep and %dT=100×(TLATep-TLATen)/TLATep, respectively). Normal canine cardiac anatomy is responsible for %dLV and %dT values of 7.4% and 5.5%, respectively. Concentric and eccentric remodeled anatomies resulted in %dT values of 15.6% and 1.3%, respectively. The 3D biventricular-paced canine model resulted in %dLV and %dT values of -7.1% and 1.5%, in contrast to the experimental observations of 16% and 11%, respectively. Adding fast endocardial conduction to this model altered %dLV and %dT to 13.1% and 10.1%, respectively. CONCLUSIONS: Our results provide a physiological explanation for improved response to ENDO-CRT. We predict that patients with viable fast-conducting endocardial tissue or distal Purkinje network or both, as well as concentric remodeling, are more likely to benefit from reduced ATs and increased synchrony arising from endocardial pacing.
BACKGROUND: Cardiac resynchronization therapy (CRT) delivered via left ventricular (LV) endocardial pacing (ENDO-CRT) is associated with improved acute hemodynamic response compared with LV epicardial pacing (EPI-CRT). The role of cardiac anatomy and physiology in this improved response remains controversial. We used computational electrophysiological models to quantify the role of cardiac geometry, tissue anisotropy, and the presence of fast endocardial conduction on myocardial activation during ENDO-CRT and EPI-CRT. METHODS AND RESULTS: Cardiac activation was simulated using the monodomain tissue excitation model in 2-dimensional (2D) canine and human and 3D canine biventricular models. The latest activation times (LATs) for LV endocardial and biventricular epicardial tissue were calculated (LVLAT and TLAT), as well the percentage decrease in LATs for endocardial (en) versus epicardial (ep) LV pacing (defined as %dLV=100×(LVLATep-LVLATen)/LVLATep and %dT=100×(TLATep-TLATen)/TLATep, respectively). Normal canine cardiac anatomy is responsible for %dLV and %dT values of 7.4% and 5.5%, respectively. Concentric and eccentric remodeled anatomies resulted in %dT values of 15.6% and 1.3%, respectively. The 3D biventricular-paced canine model resulted in %dLV and %dT values of -7.1% and 1.5%, in contrast to the experimental observations of 16% and 11%, respectively. Adding fast endocardial conduction to this model altered %dLV and %dT to 13.1% and 10.1%, respectively. CONCLUSIONS: Our results provide a physiological explanation for improved response to ENDO-CRT. We predict that patients with viable fast-conducting endocardial tissue or distal Purkinje network or both, as well as concentric remodeling, are more likely to benefit from reduced ATs and increased synchrony arising from endocardial pacing.
Authors: Benjamin J Sieniewicz; Jonathan M Behar; Manav Sohal; Justin Gould; Simon Claridge; Bradley Porter; Steve Niederer; James H P Gamble; Tim R Betts; Pierre Jais; Nicolas Derval; David D Spragg; Paul Steendijk; Berry M van Gelder; Frank A Bracke; Christopher A Rinaldi Journal: Europace Date: 2018-12-01 Impact factor: 5.214
Authors: Jonathan M Behar; Tom Jackson; Eoin Hyde; Simon Claridge; Jaswinder Gill; Julian Bostock; Manav Sohal; Bradley Porter; Mark O'Neill; Reza Razavi; Steve Niederer; Christopher Aldo Rinaldi Journal: JACC Clin Electrophysiol Date: 2016-12
Authors: Angela W C Lee; Caroline Mendonca Costa; Marina Strocchi; Christopher A Rinaldi; Steven A Niederer Journal: J Cardiovasc Transl Res Date: 2018-01-11 Impact factor: 4.132
Authors: Eoin R Hyde; Jonathan M Behar; Andrew Crozier; Simon Claridge; Tom Jackson; Manav Sohal; Jaswinder S Gill; Mark D O'Neill; Reza Razavi; Steven A Niederer; Christopher A Rinaldi Journal: Pacing Clin Electrophysiol Date: 2016-05-09 Impact factor: 1.976