Inhibition of the Na+/H+ exchanger delays the development of rapid pacing-induced atrial contractile dysfunction

Gregory T. Altemose, Douglas P. Zipes, Juan Weksler, John Miller, Jeffrey E. Olgin

Research output: Contribution to journalArticle

24 Citations (Scopus)

Abstract

Background - Atrial mechanical stunning due to atrial fibrillation may persist after restoration of sinus rhythm. Although the mechanism of rapid rate-related contractile dysfunction remains unknown, ischemia, pH changes, and calcium overload have been postulated as potential mechanisms. We hypothesized that blockade of the Na+/H+ exchanger (NHE) would alter atrial contractile dysfunction from rapid rates. Methods and Results - Twenty-three anesthetized dogs were studied and subjected to 5 hours of rapid right atrial pacing. Ten received an inhibitor of the NHE, 10 received saline, and 3 received nifedipine. All animals underwent placement of 2 sonomicrometers on the left atrium, transesophageal echocardiography, and invasive hemodynamic monitoring. All measurements were made in sinus rhythm. Except for baseline and postdrug measurements, reduction in left atrial fractional shortening was significantly less at all time points in the NHEI group than in the control and nifedipine groups (P=0.05). The percent change from baseline of left atrial function at all time intervals as assessed by left atrial appendage contraction velocity (LAACV) was significantly less in the NHEI group than in the control (P=0.05) group. LAACV was significantly preserved at all time intervals (except 300 minutes) in the NHEI group compared with the nifedipine group (P=0.05). The only significant difference in hemodynamics among the groups was between the control and the nifedipine groups at 30 minutes after drug (P=0.05). Conclusions - Treatment with HOE642 significantly blunts the decline in left atrial mechanical function from rapid atrial rates compared with both control and nifedipine-treated groups.

Original languageEnglish
Pages (from-to)762-768
Number of pages7
JournalCirculation
Volume103
Issue number5
StatePublished - Feb 6 2001

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Sodium-Hydrogen Antiporter
Nifedipine
Left Atrial Function
Atrial Appendage
Control Groups
Hemodynamics
Transesophageal Echocardiography
Heart Atria
Atrial Fibrillation
Ischemia
Dogs
Calcium
Pharmaceutical Preparations

Keywords

  • Arrhythmias
  • Contractility
  • Fibrillation
  • Sodium

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine

Cite this

Inhibition of the Na+/H+ exchanger delays the development of rapid pacing-induced atrial contractile dysfunction. / Altemose, Gregory T.; Zipes, Douglas P.; Weksler, Juan; Miller, John; Olgin, Jeffrey E.

In: Circulation, Vol. 103, No. 5, 06.02.2001, p. 762-768.

Research output: Contribution to journalArticle

Altemose, Gregory T. ; Zipes, Douglas P. ; Weksler, Juan ; Miller, John ; Olgin, Jeffrey E. / Inhibition of the Na+/H+ exchanger delays the development of rapid pacing-induced atrial contractile dysfunction. In: Circulation. 2001 ; Vol. 103, No. 5. pp. 762-768.
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N2 - Background - Atrial mechanical stunning due to atrial fibrillation may persist after restoration of sinus rhythm. Although the mechanism of rapid rate-related contractile dysfunction remains unknown, ischemia, pH changes, and calcium overload have been postulated as potential mechanisms. We hypothesized that blockade of the Na+/H+ exchanger (NHE) would alter atrial contractile dysfunction from rapid rates. Methods and Results - Twenty-three anesthetized dogs were studied and subjected to 5 hours of rapid right atrial pacing. Ten received an inhibitor of the NHE, 10 received saline, and 3 received nifedipine. All animals underwent placement of 2 sonomicrometers on the left atrium, transesophageal echocardiography, and invasive hemodynamic monitoring. All measurements were made in sinus rhythm. Except for baseline and postdrug measurements, reduction in left atrial fractional shortening was significantly less at all time points in the NHEI group than in the control and nifedipine groups (P=0.05). The percent change from baseline of left atrial function at all time intervals as assessed by left atrial appendage contraction velocity (LAACV) was significantly less in the NHEI group than in the control (P=0.05) group. LAACV was significantly preserved at all time intervals (except 300 minutes) in the NHEI group compared with the nifedipine group (P=0.05). The only significant difference in hemodynamics among the groups was between the control and the nifedipine groups at 30 minutes after drug (P=0.05). Conclusions - Treatment with HOE642 significantly blunts the decline in left atrial mechanical function from rapid atrial rates compared with both control and nifedipine-treated groups.

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