Closure of atrial septal defect normalizes left and right ventricular hemodynamic forces in children and adolescents
Year: 2026
Type: article
Study design: Observational Study
Abstract: BACKGROUND: Atrial septal defect (ASD) is one of the most common congenital heart defects and leads to chronic right ventricular (RV) volume loading, which may progress to heart failure if untreated. Surgical or transcatheter closure unloads the RV and improves hemodynamics, but the impact on intraventricular hemodynamic forces (HDF) remains unclear. Here, we evaluated the effects of ASD closure on biventricular HDF. METHODS: Cardiac magnetic resonance imaging was performed at 1.5T on 21 patients and 11 sex- and age-matched healthy controls. Whole-heart 4D flow and cine images in standard views were acquired and used to compute HDF using custom software (Segment). Paired analysis was used to compare HDF pre-/post ASD closure. RESULTS: At baseline, patients showed aberrant RV HDF in both longitudinal and transverse directions (p<0.05 vs controls), largely explained by volume loading (R = 0.83-0.92 for volume parameters, p<0.0001). At 8-month follow-up (n = 16), LV HDF increased in the apical-basal and septal-lateral directions (p<0.05), while RV HDF decreased in all directions (p<0.05), effectively normalizing HDF to control levels (p>0.05). Changes in HDF were associated with remodeling of ventricular volumes and with shunt reduction. CONCLUSION: Children and adolescents with ASD exhibit a wide range of alterations to ventricular HDF partially reflective of altered loading conditions. Successful ASD closure normalizes HDF in many but not all cases, highlighting the potential of force analysis to improve our understanding of ventricular remodeling processes in congenital heart disease.
Authors: Per M. Arvidsson, Henning Clausen, Pia Sjöberg
Institutions: Lund University, Skåne University Hospital
Language: English
Subfield: Epidemiology
Field: Medicine
Domain: Health Sciences
Open Access status: gold
Estimated APC paid: $3,000
OpenAlex ID: W7128699614