title: Interventional creation of an atrial septal defect and its impact on right ventricular function: an animal study with the pressure-volume conductance system.
abstract: 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.
authors.affiliation: Department of Pediatric Cardiology, University Hospital of Schleswig-Holstein, Campus Kiel, Kiel, Germany. a.uebing@rbht.nhs.uk
authors.forename: Anselm
authors.initials: A
authors.lastname: Uebing
authors.forename: Gunther
authors.initials: G
authors.lastname: Fischer
authors.forename: Jana
authors.initials: J
authors.lastname: Schlangen
authors.forename: Traudel
authors.initials: T
authors.lastname: Hansen
authors.forename: Ralph G
authors.initials: RG
authors.lastname: Grabitz
authors.forename: Kolja
authors.initials: K
authors.lastname: Becker
authors.forename: Paul
authors.initials: P
authors.lastname: Steendijk
authors.forename: Hans-Heiner
authors.initials: HH
authors.lastname: Kramer
mesh_terms: D000818:Animals; D006328:Cardiac Catheterization; D002306:Cardiac Volume / Q000502:physiology*; D002908:Chronic Disease; D004195:Disease Models, Animal; D006344:Heart Septal Defects, Atrial / Q000503:physiopathology* / Q000601:surgery*; D006439:Hemodynamics / Q000502:physiology; D008955:Models, Cardiovascular; D009200:Myocardial Contraction / Q000502:physiology; D055989:Septal Occluder Device; D034421:Sus scrofa; D016278:Ventricular Function, Right / Q000502:physiology*; D017725:Ventricular Pressure / Q000502:physiology*