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Interventional creation of an atrial septal defect and its impact on right ventricular function: An animal study with the pressure-volume conductance system
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Abstract
Methods: Thirteen ASD and six control animals were studied. An ASD was created by balloon dilatation (BD) of the fossa ovalis (n = 4) or by implantation of a multi-perforated Amplatzer Septal Occluder (n = 4) or a patch-less nitinol device (n = 5). After 4.8 (3.9–6.0) weeks, the amounts of left-to-right shunting (Qp/Qs) and RV contractility (end systolic elastance — Ees) were assessed.
Results: In the ASD group, a significant left-to-right shunt could be documented (Qp/Qs 1.5 ± ± 0.4). However, a shunt was absent in the BD subgroup (Qp/Qs 1.1 ± 0.1). In animals with devices implanted, a significant relationship between the post-mortem ASD area and Qp/Qs was found (r = 0.68, p < 0.05). Compared to controls, RV contractility was not significantly impaired at rest and during dobutamine in ASD animals (Ees: 0.40 ± 0.20 vs 0.54 ± 0.12 and 0.75 ± 0.29 vs 1.04 ± 0.24 mm Hg/mL, p = NS for both).
Conclusions: Device implantation is necessary to create a patent ASD resulting in significant left-to-right shunting. In an experimental ASD model, a five week period of chronic RV volume overload does not alter RV contractility significantly. (Cardiol J 2011; 18, 3: 289–296)
Abstract
Methods: Thirteen ASD and six control animals were studied. An ASD was created by balloon dilatation (BD) of the fossa ovalis (n = 4) or by implantation of a multi-perforated Amplatzer Septal Occluder (n = 4) or a patch-less nitinol device (n = 5). After 4.8 (3.9–6.0) weeks, the amounts of left-to-right shunting (Qp/Qs) and RV contractility (end systolic elastance — Ees) were assessed.
Results: In the ASD group, a significant left-to-right shunt could be documented (Qp/Qs 1.5 ± ± 0.4). However, a shunt was absent in the BD subgroup (Qp/Qs 1.1 ± 0.1). In animals with devices implanted, a significant relationship between the post-mortem ASD area and Qp/Qs was found (r = 0.68, p < 0.05). Compared to controls, RV contractility was not significantly impaired at rest and during dobutamine in ASD animals (Ees: 0.40 ± 0.20 vs 0.54 ± 0.12 and 0.75 ± 0.29 vs 1.04 ± 0.24 mm Hg/mL, p = NS for both).
Conclusions: Device implantation is necessary to create a patent ASD resulting in significant left-to-right shunting. In an experimental ASD model, a five week period of chronic RV volume overload does not alter RV contractility significantly. (Cardiol J 2011; 18, 3: 289–296)
Keywords
atrial septal defect; right ventricular volume load; right ventricular function
About this articleTitle
Interventional creation of an atrial septal defect and its impact on right ventricular function: An animal study with the pressure-volume conductance system
Journal
Issue
Pages
289-296
Published online
2011-06-09
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Bibliographic record
Cardiol J 2011;18(3):289-296.
Keywords
atrial septal defect
right ventricular volume load
right ventricular function
Authors
Anselm Uebing
Gunther Fischer
Jana Schlangen
Traudel Hansen
Ralph G. Grabitz
Kolja Becker
Paul Steendijk
Hans-Heiner Kramer
