Abstract 2661: Excitation Origin of the Human Sinus Node: Optical Mapping of Conduction in the Node, Sino-Atrial Exit Pathways, and Atria
INTRODUCTION: The origin of excitation and conduction pathway(s) within the human sino-atrial node (SAN) remain debatable due to the absence of direct intramural nodal mapping data. Using multimodal biophotonic imaging, we recently demonstrated that the canine SAN is functionally insulated from the surrounding atrial myocardium except for several exit pathways. We hypothesized that human SAN has similar exit pathways, which are important in the modulation of sinus rhythm in health and disease.
METHODS: The SAN coronary perfused preparations were prepared from the explanted non-failing human hearts (n=4, age 54 ±15 years) and optically mapped from the epicardium with near infrared dye Di-4-ANBDQBS. The SAN 3D structure was mapped using histology.
RESULTS: SAN optical action potentials had diastolic depolarization and multiple upstroke components, which corresponded to the separate excitations of SAN and atrial layers. Excitation originated in the SAN (66 ±17 BPM), then slowly (1–18 cm/s) and anisotropically spread within the node. After a 82±17 ms conduction delay within the SAN, the atrial myocardium excitation (epicardial breakthrough) occurred via the superior, middle and/or inferior sinoatrial exit pathways 9.4 ±4.2 mm from the leading pacemaker site. The ellipsoidal 15.3 ±1.5 × 6.7±1.6 × 1.0±0.2 mm SAN structure was functionally insulated from the atrium by connective tissue, fat, and coronary arteries.
CONCLUSION: This data demonstrated for the first time the location of the leading pacemaker and the conduction pattern inside and outside of the human SAN. Existence of anatomically-defined SAN exit pathways explained why, during normal sinus rhythm, atrial breakthroughs could arise from a region along the CT that is larger (23.5±3.1 mm) than the area of the anatomical SAN. Conduction failure in exit pathways leads to the SAN exit block and is a modulator of heart rate.
This research has received full or partial funding support from the American Heart Association, Midwest Affiliate (Illinois, Indiana, Iowa, Kansas, Michigan, Minnesota, Missouri, Nebraska, North Dakota, South Dakota & Wisconsin).