Mechanical remodeling of the left atrium after loss of atrioventricular synchrony. A long-term study in humans.
BACKGROUND
Tachycardia-mediated mechanical remodeling of the atrium is considered central to the pathogenesis of thromboembolism associated with chronic atrial fibrillation. Whether atrial mechanical remodeling also occurs in response to atrial stretch induced by chronic asynchronous ventricular pacing in patients with permanent pacemakers is unknown.


RESULTS
The study design was a prospective randomized comparison between 21 patients paced chronically in the VVI mode and 11 patients paced chronically in the DDD mode for 3 months. Left atrial appendage (LAA) function and the presence of spontaneous echo contrast (SEC) were determined with transesophageal echocardiography (TEE) within 24 hours of pacemaker implantation and after 3 months. The VVI patients were then programmed to DDD and underwent a third TEE after DDD pacing for an additional 3 months. After chronic VVI pacing, LAA velocity decreased from 82.4+/-29.0 to 42.1+/-25.4 cm/s (P<0.01), LAA fractional area change decreased from 74.9+/-17.2% to 49.8+/-22.0% (P<0.01), and 4 patients (19%) developed left atrial SEC (P<0.05). With the reestablishment of chronic AV synchrony, LAA velocity increased to 61.6+/-18.5 cm/s (P<0.01), LAA fractional area change increased to 76.4+/-18.1% (P<0.01), and SEC resolved. In the 11 patients undergoing chronic DDD pacing, no significant changes in LAA velocity (baseline, 86.0+/-28.8 cm/s versus 3 months, 79.6+/-14. 9 cm/s) or LAA fractional area change (baseline, 76.2+/-19.4% versus 72.5+/-15.7%) were demonstrated, and SEC did not develop.


CONCLUSIONS
Chronic loss of AV synchrony induced by VVI pacing is associated with mechanical remodeling of the left atrium, which may reverse after the reestablishment of AV synchrony with DDD pacing. This process may be partly responsible for the higher incidence of thromboembolism observed in patients undergoing VVI pacing compared with AV sequential pacing.
Sparks
P B
PB
Royal Melbourne Hospital, Department of Cardiology, The University of Melbourne, Melbourne, Australia. sparks@ep4.ucsf.edu
Mond
H G
HG
Vohra
J K
JK
Yapanis
A G
AG
Grigg
L E
LE
Kalman
J M
JM
D000368:Aged; D016279:Atrial Function, Left / Q000502:physiology*; D001283:Atrioventricular Node / Q000503:physiopathology*; D001919:Bradycardia / Q000628:therapy*; D017548:Echocardiography, Transesophageal; D004562:Electrocardiography; D004867:Equipment Design; D005260:Female; D005500:Follow-Up Studies; D006327:Heart Block / Q000628:therapy*; D006801:Humans; D008297:Male; D010138:Pacemaker, Artificial; D011446:Prospective Studies; D013997:Time Factors