Electrophysiologic Characteristics of the Atrium in Sinus Node Dysfunction:

Abstract

Electrophysiologic Characteristics in Sinus Node Dysfunction. Introduction: Clinical electrophysiology (EP) has focused attention on the EP properties of atrial muscle in patients with atrial fibrillation (AF). Patients with sinus node dysfunction (SND) sometimes are included in these studies, but the characteristics of these patients with SND alone appear less well investigated. Methods and Results: We reviewed EP data of 46 patients (mean age 70 ± 8 years) with SND, who underwent EP study for evaluation of the atrial substrate. In 16 patients, a history of paroxysmal AF was documented, but not in the remaining 30 patients who had SND alone. We considered as control a group of 25 subjects (mean age 63 ± 14 years), who were referred to our EP laboratory for unexplained syncope or AV conduction disturbances. Following pharmacologic washout and at a drive cycle of 600 msec, effective (ERP) and functional refractory periods (FRP), S1-A1 and S2-A2 latency, A1 and A2 width, latent vulnerability index (ERP/A2), and P wave duration on the surface ECG were measured. Intra-atrial conduction times were measured from the stimulus artifact by pacing the high right atrium (HRA), to the corresponding atriograms at the AV node (HRA-AVN), low lateral atrium (HRA-LLA), and low interatrial septum close to the coronary sinus ostium (HRA-CSO). Compared with the control group, SND patients did not show differences in ERP (238 ± 26 msec vs 250 ± 29 msec), FRP (274 ± 25 msec vs 280 ± 32 msec), S1-A1 (38 ± 15 msec vs 33 ± 11 msec) and S2-A2 latency (67 ± 24 msec vs 63 ± 25 msec), or HRA-AVN (81 ± 24 msec vs 65 ± 19 msec), HRA-LLA (36 ± 30 msec vs 40 ± 27 msec), and HRA-CSO (77 ± 17 msec vs 80 ± 15 msec) conduction times. In contrast, we observed strong differences in atriogram durations Al (59 ± 19 msec vs 39 ± 13 msec; P < 0.001) and A2 (92 ± 28 msec vs 57 ± 18 msec; P < 0.001), as well as in the latent vulnerability index ERP/A2 (2.8 ± 1.2 msec vs 4.8 ± 1.7; P < 0.001). Also, the P wave was slightly longer (104 ± 18 msec vs 94 ± 45 msec; P < 0.05). No significant statistical difference in EP parameters was found between SND patients with or without documented AF. Conclusion: In patients with SND, atrial refractoriness appears similar to that of control subjects. The most important EP abnormality appears to be local conduction slowing disturbances, with prolonged basal and postextrastimuli atriograms, responsible for a lower vulnerability index. This could explain, at least in part, the tendency of patients with SND to develop AF during their natural history. Normality of atrial refractoriness, in contrast to atrial conduction disorders, might explain why atrial pacing shows a preventative effect on the development of AF and why antiarrhythmic drugs often are ineffective.