Dispersion of atrial refractoriness in patients with sinus node dysfunction.

Abstract

SUMMARY Abnormal atrial refractoriness was examined as a cause of atrial fibrillation/flutter (AFF) in patients with bradycardia. Refractory periods at three disparate right atrial sites were compared in 17 patients with sinus node dysfunction (SND) and 16 controls. Atrial pacing shortened refractory periods, but failed to decrease dispersion of refractoriness significantly. During sinus rhythm, duration and dispersion of refractoriness were greater in SND patients than in controls. These differences persisted with atrial pacing. For example, at the paced rate, dispersion of effective refractory periods in SND patients was greater than in controls (62.9 ± 34 vs 36.6 ± 21 msec,p < 0.01). Six SND patients had AFF, but they did not have greater dispersion than other SND patients, or unusually short or long refractory periods. Thus, prolonged and nonuniform refractoriness were features of SND. Abnormal refractoriness in SND reflected atrial disease and persisted with pacing. These abnormalities were not unique to patients with AFF.EARLY ATRIAL EXTRASYSTOLES are critical to the initiation of atrial fibrillation and flutter (AFF).1, 2 According to one theory, AFF results from nonuniform recovery of excitability3 4 and nonhomogeheous spread of the early excitation.5 Thus, AFF results when there is dispersion of atrial refractoriness. Because slower heart rates have been shown to increase the normal dispersion of canine atrial refractoriness,6 bradycardia should predispose to ectopic atrial rhythms.7 A clinical model of this theory would be the bradycardia-tachycardia sequences in some patients with sinus node dysfunction (SND).6 9 HIowever, faster heart rates curtail atrial refractoriness in man, exposing the vulnerable zone to excitation.'0 Thus, vulnerability to AFF from early extrasystoles could reflect a shortened refractory period rather than dispersion of refractory periods. Alternative explanations for atrial tachycardias include enhanced automaticity or tachycardias triggered from afterpotentials." These mechanisms suggest that faster, not slower heart rates, predispose to AFF.In this investigation we assess atrial refractoriness in patients with SND to delineate the role of bradycardia in determining dispersion of refractoriness and arrhythmia in man. In this preliminary investigation, measurements were limited to the right atrium of patients without obvious hemodynamic abnormalities.

Electrophysiological and Electroanatomic Characterization of the Atria in Sinus Node Disease

“…Thus, the development of AF in SND has been attributed to bradycardia-related inhomogeneous refractoriness, which enhances the AF vulnerability of the atrium to atrial premature beats. 21 The present study demonstrates that the primary underlying substrate for sinus node dysfunction includes abnormalities that might also predispose to AF. Thus, the development of slowed conduction, regional conduction block, and anatomic obstacles (electrical silence) with propagation detours in the context of atrial enlargement would be expected to predispose to maintenance of multiple wavelet reentry.…”

Alterations in atrial electrophysiology associated with chronic atrial fibrillation in man

“…Sinus node dysfunction is associated with prolonged and non-uniform atrial refractoriness [25] . Atrial fibrillation is associated with a reduction in the atrial refractory period.…”

Slow Sinus Heart Rate as a Potential Predictive Factor of Paroxysmal Atrial Fibrillation in Stroke Patients

“…These pathological features are likely to be represented in electrophysiological tests by the dispersion or heterogeneity of effective refractory periods in the right atrium [11,12]. Consequently, abnormal atrial refractoriness is considered to play a crucial role in the pathogenesis of atrial arrhythmia such as PAF in sinus node disorders [11,12].…”