Three-dimensional computer model of the right atrium including the sinoatrial and atrioventricular nodes predicts classical nodal behaviours.
The aim of the study was to develop a three-dimensional (3D) anatomically-detailed model of the rabbit right atrium containing the sinoatrial and atrioventricular nodes to study the electrophysiology of the nodes. A model was generated based on 3D images of a rabbit heart (atria and part of ventricles), obtained using high-resolution magnetic resonance imaging. Segmentation was carried out semi-manually. A 3D right atrium array model (∼3.16 million elements), including eighteen objects, was constructed. For description of cellular electrophysiology, the Rogers-modified FitzHugh-Nagumo model was further modified to allow control of the major characteristics of the action potential with relatively low computational resource requirements. Model parameters were chosen to simulate the action potentials in the sinoatrial node, atrial muscle, inferior nodal extension and penetrating bundle. The block zone was simulated as passive tissue. The sinoatrial node, crista terminalis, main branch and roof bundle were considered as anisotropic. We have simulated normal and abnormal electrophysiology of the two nodes. In accordance with experimental findings: (i) during sinus rhythm, conduction occurs down the interatrial septum and into the atrioventricular node via the fast pathway (conduction down the crista terminalis and into the atrioventricular node via the slow pathway is slower); (ii) during atrial fibrillation, the sinoatrial node is protected from overdrive by its long refractory period; and (iii) during atrial fibrillation, the atrioventricular node reduces the frequency of action potentials reaching the ventricles. The model is able to simulate ventricular echo beats. In summary, a 3D anatomical model of the right atrium containing the cardiac conduction system is able to simulate a wide range of classical nodal behaviours.
Institute of Cardiovascular Sciences, University of Manchester, Core Technology Facility, Manchester, United Kingdom.
Jue
J
Li
Institute of Cardiovascular Sciences, University of Manchester, Core Technology Facility, Manchester, United Kingdom.
Shin
S
Inada
Institute of Cardiovascular Sciences, University of Manchester, Core Technology Facility, Manchester, United Kingdom.
Jurgen E
JE
Schneider
Institute of Cardiovascular Sciences, University of Manchester, Core Technology Facility, Manchester, United Kingdom.
Henggui
H
Zhang
Institute of Cardiovascular Sciences, University of Manchester, Core Technology Facility, Manchester, United Kingdom.
Halina
H
Dobrzynski
Institute of Cardiovascular Sciences, University of Manchester, Core Technology Facility, Manchester, United Kingdom.
Mark R
MR
Boyett
D000200:Action Potentials; D000818:Animals; D001281:Atrial Fibrillation / Q000503:physiopathology; D001283:Atrioventricular Node / Q000473:pathology / Q000503:physiopathology*; D003198:Computer Simulation; D006325:Heart Atria / Q000473:pathology / Q000503:physiopathology; D006329:Heart Conduction System / Q000503:physiopathology; D021621:Imaging, Three-Dimensional / Q000379:methods*; D008279:Magnetic Resonance Imaging; D008953:Models, Anatomic; D011817:Rabbits; D012849:Sinoatrial Node / Q000473:pathology / Q000503:physiopathology*