Abnormal Response of Superior Sinoatrial Node to Sympathetic Stimulation Is a Characteristic Finding in Patients With Atrial Fibrillation and Symptomatic Bradycardia

Abstract

Background— We hypothesized that unresponsiveness of superior sinoatrial node (SAN) to sympathetic stimulation is strongly associated with the development of symptomatic bradycardia in patients with atrial fibrillation (AF). Methods and Results— We performed 3D endocardial mapping in healthy controls (group 1, n=10) and patients with AF without (group 2, n=57) or with (group 3, n=15) symptomatic bradycardia at baseline and during isoproterenol infusion. Corrected SAN recovery time was abnormal in 0%, 11%, and 36% of groups 1, 2, and 3, respectively ( P =0.02). At baseline, 90%, 26%, and 7% ( P <0.001) of the patients had multicentric SAN activation patterns. For groups 1, 2, and 3, the median distance from the superior vena cava-right atrial junction to the most cranial earliest activation site (EAS) was 5.0 (25–75 percentile range, 3.5–21.3), 10.0 (4–20), and 17.5 (12–34) mm at baseline ( P =0.01), respectively, and 4.0 (0–5), 5.0 (1–10), and 15.0 (5.4–33.3) mm, respectively, during isoproterenol infusion ( P =0.01), suggesting an upward shift of EAS during isoproterenol infusion. However, although the EAS during isoproterenol infusion was at the upper one third of the crista terminalis in 100% of group 1 and 78% of group 2 patients, only 20% of group 3 patients showed a move of the EAS to that region ( P <0.001). Conclusions— Superior SAN serves as the EAS during sympathetic stimulation in patients without AF and in most patients with AF without symptomatic bradycardia. In contrast, unresponsiveness of superior SAN to sympathetic stimulation is a characteristic finding in patients with AF and symptomatic bradycardia.