Cardiology journal · 2011
Interventional creation of an atrial septal defect and its impact on right ventricular function: an animal study with the pressure-volume conductance system.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Uebing Anselm, Fischer Gunther, Schlangen Jana, Hansen Traudel, Grabitz Ralph G, Becker Kolja, Steendijk Paul, Kramer Hans-Heiner
Аннотация
BACKGROUND: The aim of our study was to assess the suitability of different interventional techniques to create an atrial septal defect (ASD) and to evaluate the short-term effects of right ventricular (RV) volume overload on RV contractility in the growing swine.
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.
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.