Sick sinus syndrome with and without atrial fibrillation: atrial refractoriness and conduction characteristics

Abstract

Background: Clinical electrophysiology has focused the attention on the electrophysiological properties of the atrial muscle in patients with atrial fibrillation: shortened and inhomogeneous refractoriness and local and regional conduction slowing, as well as prolonged intra- and interatrial conduction disturbances, are well described as electrophysiological parameters associated with the genesis of atrial fibrillation. Patients with sick sinus syndrome are variously included in these studies, but electrophysiological characteristics of patients with sick sinus syndrome alone appear less investigated, even if atrial fibrillation is part of its natural history. The aim of the present study was to define the electrophysiological characteristics of sick sinus syndrome patients with or without paroxysmal atrial fibrillation, compared to subjects without atrial fibrillation and sick sinus syndrome.

Methods: We reviewed the electrophysiological data of 39 patients with sick sinus syndrome (mean age 70 +/- 8 years), who underwent an electrophysiological study in sinus rhythm for the evaluation of the atrial substrate. In 12 patients an associated history of paroxysmal atrial fibrillation was documented. Twenty-seven patients were included in the study with a diagnosis of sinus node dysfunction alone. We also considered as control group 25 subjects (mean age 63 +/- 14 years), referred to our electrophysiological laboratory for unexplained syncope or atrioventricular disturbances. Following pharmacological wash-out and at a drive cycle of 600 ms, effective and functional refractory periods, S1-A1 and S2-A2 latency, A1 and A2 width, and the latent vulnerability index (effective refractory period/A2), were measured. In addition, the P-wave duration during spontaneous sinus rhythm on the surface ECG in D II/V1 leads was measured.

Results: Between sick sinus syndrome patients with or without atrial fibrillation, no significant statistical differences in electrophysiological parameters were found. When compared to the control group, sick sinus syndrome patients did not show any differences in effective refractory period (239 +/- 34 vs 250 +/- 29 ms), functional refractory period (276 +/- 28 vs 280 +/- 32 ms), S1-A1 (38 +/- 16 vs 33 +/- 11 ms), and S2-A2 latency (68 +/- 25 vs 63 +/- 25 ms). In contrast, we observed remarkable differences in terms of atriogram duration A1 (60 +/- 20 vs 39 +/- 13 ms, p < 0.001), A2 (95 +/- 34 vs 57 +/- 18 ms, p < 0.001), and effective refractory period/A2 (2.8 +/- 1.2 vs 4.8 +/- 1.7 cm, p < 0.001). Also the duration of the P wave was longer (103 +/- 17 vs 94 +/- 45 ms, p < 0.05).

Conclusions: In sick sinus syndrome patients with or without atrial fibrillation, electrophysiological characteristics appear homogeneous. When compared to the control group, refractoriness was quite similar. In contrast, the most important abnormalities appear based on conduction slowing disturbances, responsible for a low latent vulnerability index. This could explain, at least in part, the tendency of sick sinus syndrome to develop atrial fibrillation as a part of its natural history. At present, the influence of an altered electrophysiological substrate on pharmacological or pacing therapy in patients with sick sinus syndrome is not yet known.