Does the mechanism of action of biatrial pacing for atrial fibrillation involve changes in cardiac haemodynamics? Assessment by Doppler echocardiography and natriuretic peptide measurements.
OBJECTIVE
The antifibrillatory mechanism of biatrial (BI) pacing has not been fully elucidated. We investigated the role of a haemodynamic mechanism in eight patients implanted with a BI pacemaker (Chorus RM) by comparing changes in mitral Doppler flow and atrial and B-type natriuretic peptide levels (ANP, BNP) with BI pacing compared with sinus rhythm and right atrial (RA) pacing.


RESULTS
Measurements were taken after 60 min in the supine position in each of two pairs of randomized pacing modes: (a) AAI40 beats x min(-1), (allows sinus rhythm mean rate 56 beats x min(-1), SR) vs AAI 40 beats x min(-1) with synchronized left atrial pacing (SRSync); (b) overdrive AAI RA pacing (89 beats x min(-1) (n = 6) or 70 beats x min(-1) (n = 2)) vs overdrive AAI BI pacing. Within each pair there was significant earlier activation of the left atrial Doppler signal in relation to the surface ECG P wave with BI pacing (SR 163 +/- 10 ms vs SRSync 144 +/- 21 ms (P = 0.02), and RA 232 +/- 14 ms vs BI 196 +/- 16 ms (P = 0.001)), and significant shortening of the P-R interval (SR 163 +/- 29 ms vs SRSync 148 +/- 20 (P = 0.007) and RA 261 +/- 27 ms vs BI 232 +/- 23 (P = 0.001)). The net observed effect was of no change in the atrioventricular timing sequence (delay of peak E or A to QRS/ mitral valve closure) and no change in other Doppler echo parameters. Levels of the cardiac peptides ANP and BNP were raised compared with healthy controls, but did not significantly change during the study.


CONCLUSIONS
Acute BI pacing shortens the P-R interval and causes earlier left atrial contraction in relation to the surface electrocardiogram P wave. It does not alter the atrioventricular timing cycle, any other Doppler measurements or change cardiac peptide levels. This suggests that BI pacing does not cause haemodynamic changes that could account for any antifibrillatory properties.
Levy
T
T
Department of Cardiology, Royal Brompton and Harefield NHS Trust, Harefield Hospital, Middlesex, UK.
Jenkins
G H
GH
Walker
S
S
Grieve
L
L
Webb
C
C
Buckley
M G
MG
Singer
D R
DR
Paul
V
V
D000368:Aged; D001281:Atrial Fibrillation / Q000097:blood / Q000503:physiopathology* / Q000628:therapy*; D009320:Atrial Natriuretic Factor / Q000097:blood; D002304:Cardiac Pacing, Artificial / Q000379:methods*; D004562:Electrocardiography; D005260:Female; D006439:Hemodynamics; D006801:Humans; D008297:Male; D008875:Middle Aged; D020097:Natriuretic Peptide, Brain; D010138:Pacemaker, Artificial
D020097:Natriuretic Peptide, Brain; D009320:Atrial Natriuretic Factor