title: Hemodynamic improvement is faster after percutaneous ASD closure than after surgery.
abstract: OBJECTIVE
  Hemodynamic effects of surgical and percutaneous closure of atrial septal defect (ASD) were evaluated.
  
  
  BACKGROUND
  ASD causes volume overload of right ventricle (RV) and is associated with distortion and dysfunction of left ventricle (LV). The amount and timing of hemodynamic changes after ASD closure are not well known.
  
  
  METHODS
  The study group consisted of 7 children treated surgically and 17 treated in the catheterization laboratory. In the control group, there were 51 healthy children. RV size and LV end-diastolic and systolic dimensions, volumes, and function were examined by two- and three- dimensional echocardiography and serum concentrations of natriuretic peptides measured prior to ASD closure, and 1, 6, and 12 months thereafter.
  
  
  RESULTS
  In all children with ASD, during the 1-year follow-up, the z score of RV end-diastolic diameter decreased from a median 5.00 SD to 2.25 SD (P < 0.001). Dilatation of RV did not resolve entirely during 1-year follow-up in either treatment group. End-diastolic LV diameter increased from -1.50 to -0.50 SD (P < 0.001). LV size increased slower in the surgical subgroup but reached control levels in both groups. Concentrations of natriuretic peptides increased during the first month after ASD closure and normalized thereafter in patients treated percutaneously but remained higher than in controls in patients treated surgically.
  
  
  CONCLUSIONS
  During 1-year follow-up after ASD closure, RV size decreases but does not normalize in all patients. The size of the LV normalizes after ASD closure but the increase in LV size is slower in patients treated surgically. Serum levels of ANPN and proBNP are elevated prior to ASD closure but decrease thereafter to control levels in patients treated with the percutaneous technique but not in those treated surgically.
authors.affiliation: Department of Pediatrics, University Hospital of Kuopio, Kuopio, Finland. anneli.eeroli@fimnet.fi
authors.forename: Anneli
authors.initials: A
authors.lastname: Eerola
authors.forename: Jaana I
authors.initials: JI
authors.lastname: Pihkala
authors.forename: Talvikki
authors.initials: T
authors.lastname: Boldt
authors.forename: Ilkka P
authors.initials: IP
authors.lastname: Mattila
authors.forename: Tuija
authors.initials: T
authors.lastname: Poutanen
authors.forename: Eero
authors.initials: E
authors.lastname: Jokinen
mesh_terms: D000293:Adolescent; D009320:Atrial Natriuretic Factor / Q000097:blood; D015415:Biomarkers / Q000097:blood; D006328:Cardiac Catheterization; D006348:Cardiac Surgical Procedures; D002315:Cardiopulmonary Bypass; D016022:Case-Control Studies; D002648:Child; D002675:Child, Preschool; D004452:Echocardiography / Q000379:methods; D005260:Female; D005500:Follow-Up Studies; D006344:Heart Septal Defects, Atrial / Q000150:complications / Q000000981:diagnostic imaging / Q000503:physiopathology* / Q000601:surgery*; D006352:Heart Ventricles / Q000503:physiopathology; D006801:Humans; D008297:Male; D020097:Natriuretic Peptide, Brain / Q000097:blood; D010446:Peptide Fragments / Q000097:blood; D011498:Protein Precursors / Q000097:blood; D013318:Stroke Volume; D013997:Time Factors; D016896:Treatment Outcome; D018487:Ventricular Dysfunction, Left / Q000209:etiology / Q000503:physiopathology; D018497:Ventricular Dysfunction, Right / Q000209:etiology / Q000503:physiopathology; D016277:Ventricular Function, Left; D016278:Ventricular Function, Right
chemical_list: D015415:Biomarkers; C099254:N-terminal proatrial natriuretic peptide; D010446:Peptide Fragments; D011498:Protein Precursors; C109794:pro-brain natriuretic peptide (1-76); D020097:Natriuretic Peptide, Brain; D009320:Atrial Natriuretic Factor