Electrophysiological and electroanatomic characterization of the atria in sinus node disease: evidence of diffuse atrial remodeling.
BACKGROUND
The normal sinus pacemaker complex is an extensive structure within the right atrium. We hypothesized that patients with sinus node disease (SND) would have evidence of diffuse atrial abnormalities.


RESULTS
Sixteen patients with symptomatic SND and 16 age-matched controls were studied. The following were evaluated: effective refractory periods (ERPs) from the high and low lateral right atrium (RA), high septal RA, and distal coronary sinus (CS); conduction time along the CS and lateral RA; P-wave duration; and conduction at the crista terminalis. Electroanatomic mapping was performed to define the sinus node complex and determine regional conduction velocity, double potentials, fractionated electrograms, regional voltage, and areas of electrical silence. Patients with SND demonstrated significant increase in atrial ERP at all right atrial sites, increased atrial conduction time along the lateral RA and CS, prolongation of the P-wave duration, and greater number and duration of double potentials along the crista terminalis. Electroanatomic mapping demonstrated the sinus node complex in SND to be more often unicentric, localized to the low crista terminalis at the site of the largest residual voltage amplitude. There was significant regional conduction slowing with double potentials and fractionation associated with areas of low voltage and electrical silence (or scar).


CONCLUSIONS
SND is associated with diffuse atrial remodeling characterized by structural change, conduction abnormalities, and increased right atrial refractoriness. There was a change in the nature of sinus pacemaker activity with loss of the normal multicentric pattern of activation, caudal shift of the pacemaker complex, and abnormal and circuitous conduction around lines of conduction block.
Department of Cardiology, Royal Melbourne Hospital, University of Melbourne, Melbourne, Australia.
Prashanthan
P
Sanders
Joseph B
JB
Morton
Peter M
PM
Kistler
Steven J
SJ
Spence
Neil C
NC
Davidson
Azlan
A
Hussin
Jitendra K
JK
Vohra
Paul B
PB
Sparks
Jonathan M
JM
Kalman
D000200:Action Potentials; D000368:Aged; D001145:Arrhythmias, Cardiac / Q000473:pathology* / Q000503:physiopathology; D001281:Atrial Fibrillation / Q000209:etiology / Q000473:pathology / Q000503:physiopathology; D016280:Atrial Function, Right; D002304:Cardiac Pacing, Artificial; D004562:Electrocardiography; D005260:Female; D006325:Heart Atria / Q000473:pathology* / Q000503:physiopathology; D006329:Heart Conduction System / Q000503:physiopathology; D006801:Humans; D008297:Male; D008875:Middle Aged; D009431:Neural Conduction; D012849:Sinoatrial Node / Q000503:physiopathology*