Abstract
Introduction: Surgical/ablation treatment for atrial arrhythmias such as anatomic sinoatrial node (SAN) tachycardia and atrial fibrillation either target or preserve the SAN. However, defining SAN is challenging because clinical electrophysiological (EP) mapping can visualize only exits of SAN activation as early activation sites (EAS) and not the leading pacemaker (LP) within the 3D intramural SAN. Methods: High resolution (300-900μm 2 ) including epi/endocardial (Epi/Endo) dual sided near infrared optical mapping (NIOM) was conducted on coronary perfused explanted human atria (n=26, 19-69 y.o.). SAN was defined by optical action potential morphologies as the region of slow diastolic depolarization (slow upstroke) preceding atrial excitation. Serial histology and contrast enhanced MRI (CE-MRI, 100μm 3 resolution) were used to define the 3D fibrotic structure of the SAN pacemaker complex. Results: During sinus rhythm (SR) (83±22 bpm), the LP was primarily located in the SAN center. Electrical impulses exit from SAN to atria through 1-2 sinoatrial conduction pathways (SACP), leading to discrete EAS along crista terminalis (CT), preferentially from lateral superior/middle SACPs. The distance between SAN LP and EAS varied from 3.5-23 mm. Heterogeneous atrial wall thickness, fibrosis content and myofiber orientation along the SAN and CT (5-15mm thick) regions led to complex intramural conduction from SAN LP to EAS and substantial Epi-Endo activation dyssynchrony. Conclusions: EAS visualized on both Epi/Endo mapping mainly distributed along thick CT, but not on the surface projection of SAN, due to intramural fiber orientation of preferential SACPs. The higher fibrotic content in the human SAN than CT detected by CE-MRI, integrated with EP mapping can be helpful to accurately define SAN structure and pathways for reentrant SAN arrhythmias ablations.
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