Micro-computed tomography and mathematical modelling of an AVSD heart revealed inferior displacement of the compact atrioventricular node and modified dual pathway physiology, serving as arrhythmogenic substrates.
Case Report (n=1)
No
High-resolution micro-CT and mathematical modeling of an AVSD heart reveal that displacement of the AV node and altered myocyte orientation flip the normal dual pathway physiology, providing an anatomical and electrical substrate for re-entrant arrhythmias.
Due to advances in corrective surgery, congenital heart disease has an ever growing patient population. Atrial arrhythmias are frequently observed pre- and post-surgical correction. Pharmaceutical antiarrhythmic therapy is not always effective, therefore many symptomatic patients undergo catheter ablation therapy. In patients with atrioventricular septal defects (AVSD), ablation therapy itself has mixed success; arrhythmogenic recurrences are common, and because of the anatomical displacement of the atrioventricular node, 3-degree heart block post-ablation is a real concern. In order to develop optimal and safe ablation strategies, the field of congenital cardiac electrophysiology must combine knowledge from clinical electrophysiology with a thorough understanding of the anatomical substrates for arrhythmias. Using image-based analysis and multi-cellular mathematical modelling of electrical activation, we show how the anatomical alterations characteristic of an AVSD serve as arrhythmogenic substrates. Using ex-vivo contrast enhanced micro-computed tomography we imaged post-mortem the heart of a 5 month old male with AVSD at an isometric spatial resolution of 38 µm. Morphological analysis revealed the 3D disposition of the cardiac conduction system for the first time in an intact heart with this human congenital malformation. We observed displacement of the compact atrioventricular node inferiorly to the ostium of the coronary sinus. Myocyte orientation analysis revealed that the normal arrangement of the major atrial muscle bundles was preserved but was modified in the septal region. Models of electrical activation suggest the disposition of the myocytes within the atrial muscle bundles associated with the ‘fast pathway’, together with the displaced AV node, serve as potential substrates for re-entry and possibly atrial fibrillation. This study used archived human hearts, showing them to be a valuable resource for the mathematical modelling community, and opening new possibilities for the investigations of arrhythmogenesis and ablation strategies in the congenitally malformed heart.
Stephenson et al. (Thu,) conducted a case report in Atrioventricular septal defect (AVSD) (n=1). Micro-computed tomography and mathematical modelling was evaluated on Anatomical disposition of the cardiac conduction system and inter-nodal conduction pathways. Micro-computed tomography and mathematical modelling of an AVSD heart revealed inferior displacement of the compact atrioventricular node and modified dual pathway physiology, serving as arrhythmogenic substrates.