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Division of Cardiology, Department of Internal Medicine, University of Cincinnati Medical Center, Cincinnati, Ohio 45267
The objective of this study was to examine the hypothesis that long-term, rapid atrial pacing produces a model of atrial systolic and diastolic dysfunction but does not alter ventricular function. Eight dogs were atrially paced at 400 beats/min (3:1-5:1 ventricular response) for 6 wk and subsequently instrumented with left atrial (LA) and left ventricular (LV) sonomicrometers and micromanometers. Data were compared with those from six sham-operated controls at matched heart rates and mean LA pressures of 10 mmHg. Dogs with rapid pacing had slightly greater LA volume (10.3 ± 4.0 vs. 7.9 ± 4.4 ml) and reduced ejection fraction (2.2 ± 1.4 vs. 13.0 ± 4.0, P < 0.05), systolic ejection rate (0.3 ± 0.1 vs. 2.8 ± 1.2 vol/s, P < 0.05), and reservoir fraction (0.07 ± 0.04 vs. 0.35 ± 0.06, P < 0.05) compared with controls. LA diastolic chamber stiffness was greater after rapid atrial pacing than before (stiffness constant kc, 5.7 ± 2.3 vs. 3.4 ± 0.6, P < 0.05), and the ratio of transesophageal echo-determined pulmonary venous systolic to diastolic integrated flow (a measure of relative reservoir to conduit function of the LA) was less in rapidly paced dogs compared with control dogs (0.41 ± 0.19 vs. 0.68 ± 0.23, P < 0.05). In contrast, rapid atrial pacing did not influence LV systolic performance or lusitropy, because the LV pressure time derivative and the time constant of LV relaxation were similar in both groups. In this model of isolated atrial myopathy, increased atrial stiffness and enhanced conduit function compensate for impaired atrial booster pump and reservoir functions.
dog; atrial function; left atrium; cardiac mechanics; heart failure
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