Interventricular mechanical dyssynchrony determines abnormal heightening of plasma N-terminal probrain natriuretic peptide level in symptomatic bradyarrhythmia patients with chronic dual-chamber vs. single-chamber atrial pacing

Jih Min Lin, Ling Ping Lai, Chia Ti Tsai, Lung Chun Lin, Chuen Den Tseng, Jiunn Lee Lin

Research output: Contribution to journalArticle

2 Citations (Scopus)

Abstract

Objective: Debates about adverse effects of ventricular- vs. atrial-based pacing have never ended, especially regarding cardiovascular outcomes in common pacemaker populations. Methods: To investigate the contribution of right ventricular apical pacing to the left ventricular negative remodeling, we measured the inter- and intraventricular mechanical dyssynchrony by echocardiography as well as plasma N-terminal pro-brain natriuretic peptide (NT-proBNP) level in 116 consecutive patients of symptomatic bradyarrhythmias including sinus node dysfunction (SND) in 80 and atrioventricular block in 36. Dual-chamber rate-modulated pacing (DDDR) pacemakers were implanted in 76 patients (SND, 40), and single-chamber ventricular rate-modulated pacing (AAIR) pacemakers in 40 (all SND). Clinical manifestations were retrospectively correlated. Results: After 3.5 years of pacing, DDDR pacemaker patients demonstrated higher plasma NT-proBNP concentration (503 ± 111 pg/ml) than AAIR patients (194 ± 42 pg/ml, p = 0.002) despite similar cardiovascular function at baseline. Multivariate regression analysis revealed that the only predictor of the highest quartile of plasma NT-proBNP, i.e. ≥386 pg/ml, was the interventricular contraction time difference (p = 0.01). Reprograming to minimize ventricular pacing percentage in 8 patients of SND caused parallel reduction of plasma NT-proBNP. Conclusion: Interventricular mechanical dyssynchrony, imposed mostly by right ventricular apical pacing, could lead to abnormal heightening of plasma NT-proBNP concentration after chronic DDDR pacing in common pacemaker patients with normal baseline left ventricular function.

Original languageEnglish
Pages (from-to)167-173
Number of pages7
JournalCardiology
Volume110
Issue number3
DOIs
Publication statusPublished - Jun 1 2008
Externally publishedYes

Fingerprint

Natriuretic Peptides
Bradycardia
Brain Natriuretic Peptide
Sick Sinus Syndrome
Ventricular Remodeling
Atrioventricular Block
Left Ventricular Function
Echocardiography
Multivariate Analysis
Regression Analysis
Population

Keywords

  • Brain natriuretic peptide
  • Mechanical dyssynchrony
  • Permanent pacemaker

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

Interventricular mechanical dyssynchrony determines abnormal heightening of plasma N-terminal probrain natriuretic peptide level in symptomatic bradyarrhythmia patients with chronic dual-chamber vs. single-chamber atrial pacing. / Lin, Jih Min; Lai, Ling Ping; Tsai, Chia Ti; Lin, Lung Chun; Tseng, Chuen Den; Lin, Jiunn Lee.

In: Cardiology, Vol. 110, No. 3, 01.06.2008, p. 167-173.

Research output: Contribution to journalArticle

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abstract = "Objective: Debates about adverse effects of ventricular- vs. atrial-based pacing have never ended, especially regarding cardiovascular outcomes in common pacemaker populations. Methods: To investigate the contribution of right ventricular apical pacing to the left ventricular negative remodeling, we measured the inter- and intraventricular mechanical dyssynchrony by echocardiography as well as plasma N-terminal pro-brain natriuretic peptide (NT-proBNP) level in 116 consecutive patients of symptomatic bradyarrhythmias including sinus node dysfunction (SND) in 80 and atrioventricular block in 36. Dual-chamber rate-modulated pacing (DDDR) pacemakers were implanted in 76 patients (SND, 40), and single-chamber ventricular rate-modulated pacing (AAIR) pacemakers in 40 (all SND). Clinical manifestations were retrospectively correlated. Results: After 3.5 years of pacing, DDDR pacemaker patients demonstrated higher plasma NT-proBNP concentration (503 ± 111 pg/ml) than AAIR patients (194 ± 42 pg/ml, p = 0.002) despite similar cardiovascular function at baseline. Multivariate regression analysis revealed that the only predictor of the highest quartile of plasma NT-proBNP, i.e. ≥386 pg/ml, was the interventricular contraction time difference (p = 0.01). Reprograming to minimize ventricular pacing percentage in 8 patients of SND caused parallel reduction of plasma NT-proBNP. Conclusion: Interventricular mechanical dyssynchrony, imposed mostly by right ventricular apical pacing, could lead to abnormal heightening of plasma NT-proBNP concentration after chronic DDDR pacing in common pacemaker patients with normal baseline left ventricular function.",
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AU - Lai, Ling Ping

AU - Tsai, Chia Ti

AU - Lin, Lung Chun

AU - Tseng, Chuen Den

AU - Lin, Jiunn Lee

PY - 2008/6/1

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N2 - Objective: Debates about adverse effects of ventricular- vs. atrial-based pacing have never ended, especially regarding cardiovascular outcomes in common pacemaker populations. Methods: To investigate the contribution of right ventricular apical pacing to the left ventricular negative remodeling, we measured the inter- and intraventricular mechanical dyssynchrony by echocardiography as well as plasma N-terminal pro-brain natriuretic peptide (NT-proBNP) level in 116 consecutive patients of symptomatic bradyarrhythmias including sinus node dysfunction (SND) in 80 and atrioventricular block in 36. Dual-chamber rate-modulated pacing (DDDR) pacemakers were implanted in 76 patients (SND, 40), and single-chamber ventricular rate-modulated pacing (AAIR) pacemakers in 40 (all SND). Clinical manifestations were retrospectively correlated. Results: After 3.5 years of pacing, DDDR pacemaker patients demonstrated higher plasma NT-proBNP concentration (503 ± 111 pg/ml) than AAIR patients (194 ± 42 pg/ml, p = 0.002) despite similar cardiovascular function at baseline. Multivariate regression analysis revealed that the only predictor of the highest quartile of plasma NT-proBNP, i.e. ≥386 pg/ml, was the interventricular contraction time difference (p = 0.01). Reprograming to minimize ventricular pacing percentage in 8 patients of SND caused parallel reduction of plasma NT-proBNP. Conclusion: Interventricular mechanical dyssynchrony, imposed mostly by right ventricular apical pacing, could lead to abnormal heightening of plasma NT-proBNP concentration after chronic DDDR pacing in common pacemaker patients with normal baseline left ventricular function.

AB - Objective: Debates about adverse effects of ventricular- vs. atrial-based pacing have never ended, especially regarding cardiovascular outcomes in common pacemaker populations. Methods: To investigate the contribution of right ventricular apical pacing to the left ventricular negative remodeling, we measured the inter- and intraventricular mechanical dyssynchrony by echocardiography as well as plasma N-terminal pro-brain natriuretic peptide (NT-proBNP) level in 116 consecutive patients of symptomatic bradyarrhythmias including sinus node dysfunction (SND) in 80 and atrioventricular block in 36. Dual-chamber rate-modulated pacing (DDDR) pacemakers were implanted in 76 patients (SND, 40), and single-chamber ventricular rate-modulated pacing (AAIR) pacemakers in 40 (all SND). Clinical manifestations were retrospectively correlated. Results: After 3.5 years of pacing, DDDR pacemaker patients demonstrated higher plasma NT-proBNP concentration (503 ± 111 pg/ml) than AAIR patients (194 ± 42 pg/ml, p = 0.002) despite similar cardiovascular function at baseline. Multivariate regression analysis revealed that the only predictor of the highest quartile of plasma NT-proBNP, i.e. ≥386 pg/ml, was the interventricular contraction time difference (p = 0.01). Reprograming to minimize ventricular pacing percentage in 8 patients of SND caused parallel reduction of plasma NT-proBNP. Conclusion: Interventricular mechanical dyssynchrony, imposed mostly by right ventricular apical pacing, could lead to abnormal heightening of plasma NT-proBNP concentration after chronic DDDR pacing in common pacemaker patients with normal baseline left ventricular function.

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