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 language | English |
|---|---|
| Pages (from-to) | 762-768 |
| Number of pages | 7 |
| Journal | Circulation |
| Volume | 103 |
| Issue number | 5 |
| State | Published - Feb 6 2001 |
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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 journal › Article
}
TY - JOUR
T1 - Inhibition of the Na+/H+ exchanger delays the development of rapid pacing-induced atrial contractile dysfunction
AU - Altemose, Gregory T.
AU - Zipes, Douglas P.
AU - Weksler, Juan
AU - Miller, John
AU - Olgin, Jeffrey E.
PY - 2001/2/6
Y1 - 2001/2/6
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.
AB - 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.
KW - Arrhythmias
KW - Contractility
KW - Fibrillation
KW - Sodium
UR - http://www.scopus.com/inward/record.url?scp=0035814746&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0035814746&partnerID=8YFLogxK
M3 - Article
C2 - 11156891
AN - SCOPUS:0035814746
VL - 103
SP - 762
EP - 768
JO - Circulation
JF - Circulation
SN - 0009-7322
IS - 5
ER -