Does the mechanism of action of biatrial pacing for atrial fibrillation involve changes in cardiac haemodynamics? Assessment by Doppler echocardiography and natriuretic peptide measurements

Citation
T. Levy et al., Does the mechanism of action of biatrial pacing for atrial fibrillation involve changes in cardiac haemodynamics? Assessment by Doppler echocardiography and natriuretic peptide measurements, EUROPACE, 2(2), 2000, pp. 127-135
Citations number
38
Categorie Soggetti
Cardiovascular & Respiratory Systems
Journal title
EUROPACE
ISSN journal
10995129 → ACNP
Volume
2
Issue
2
Year of publication
2000
Pages
127 - 135
Database
ISI
SICI code
1099-5129(200004)2:2<127:DTMOAO>2.0.ZU;2-K
Abstract
Aims The antifibrillatory mechanism of biatrial (BI) pacing has not been fu lly elucidated. We investigated the role of a haemodynamic mechanism in eig ht patients implanted with a BI pacemaker (Chorus RM) by comparing changes in mitral Doppler flow and atrial and B-type natriuretic peptide levels (AN P, BNP) with BI pacing compared with sinus rhythm and right atrial (RA) pac ing. Methods and Results Measurements were taken after 60 min in the supine posi tion in each of two pairs of randomized pacing modes: (a) AAI 40 beats.min( -1), (allows sinus rhythm mean rate 56 beats.min(-1). SR) vs AAI 40 beats.m in(-1) with synchronized left atrial pacing (SRSync), (b) overdrive AAI RA pacing (89 beats.min(-1) (n=6) or 70 beats.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 p acing (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 i nterval (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 v alve closure) and no change in other Doppler echo parameters. Levels of the cardiac peptides ANP and BNP were raised compared with healthy controls, b ut did not significantly change during the study. Conclusion Acute BI pacing shortens the P-R interval and causes earlier lef t atrial contraction in relation to the surface electrocardiogram P wave. I t does not alter the atrioventricular timing cycle, any other Doppler measu rements or change cardiac peptide levels. This suggests that BI pacing does not cause haemodynamic changes that could account for any antifibrillatory properties. (Europace 2000; 2: 127-135) (C) 2000 The European Society of C ardiology.