The frequent association of atrial fibrillation (AF) with sinus node dysfunction (SND) has
long been recognized ( ). However, to date the mechanisms of AF-associated SND have not
been fully elucidated. The sinoatrial node (SAN) is conventionally considered to be located at
the base of the superior vena cava (SVC). Detailed animal and human mapping has
demonstrated that normal cardiac pacemaker activity is widely distributed in the right atrium.
In the human atrium, the pacemaker complex extends for up to 75 mm along the long axis of
the sulcus terminalis and precaval band. Recently atrial activation maps by Boineau JP.
revealed that the sinus pacemaker activity could arise from an extensive structure along the
long axis of the crista terminalis (CT) from the superior to the inferior vena cava (IVC) in
humans. Several lines of evidence demonstrated that anatomic and structural changes along
the CT have been implicated in a reduction in functional sinus node reserve in patients with
sick sinus syndrome and congestive heart failure. In addition, extensive modification ablation
of the sinus node targeting this structure has been established as a treatment for inappropriate
sinus tachycardia. Thus, the CT is believed to be an important anatomic structure in the
initiation and propagation of sinus impulse. Previous studies in AF-induced SND have
focused on the electrophysiological parameters such as sinus node recovery time (SNRT)
and/or SACT, but have not characterized the electrophysiology of this structure in this
condition. In the present study, we evaluated the detailed electrophysiological and
electroanatomic changes in the sinus pacemaker complex and, in particular, conduction
properties of the CT in patients with AF by electrophysiological and non-contact mapping
studies performed after electrocardioversion and compared these changes with those in
age-matched control subjects without history of AF.
