{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,15]],"date-time":"2026-10-15T23:46:06Z","timestamp":1792107966132,"version":"4.4.0"},"reference-count":67,"publisher":"Springer Science and Business Media LLC","issue":"3","license":[{"start":{"date-parts":[[2026,1,30]],"date-time":"2026-01-30T00:00:00Z","timestamp":1769731200000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0"},{"start":{"date-parts":[[2026,1,30]],"date-time":"2026-01-30T00:00:00Z","timestamp":1769731200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0"}],"content-domain":{"domain":["link.springer.com"],"crossmark-restriction":false},"short-container-title":["Pediatr Res"],"published-print":{"date-parts":[[2026,8]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Congenital heart disease (CHD) is a significant congenital anomaly, with ventricular septal defect (VSD) and transposition of the great arteries (TGA) being commonly encountered. Despite advancements in prenatal diagnosis and postnatal care, predicting neonatal outcomes remains difficult due to fetal compensatory mechanisms. This study utilizes and adapts existing mathematical models, without patient-specific parameters, to simulate the hemodynamic effects of VSD and TGA during the fetal-to-neonatal transition, validated against literature data.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Method<\/jats:title>\n                    <jats:p>The model uses a closed-loop 0D-1D cardiovascular system and an oxygen-carbon dioxide exchange model to retrieve clinically relevant information.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Results show realistic replication of flow, pressure profiles, oxygen saturation, and carbon dioxide levels for both normal and CHD-compromised fetuses.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>The mathematical model offers valuable insights into hemodynamic alterations during the fetal-to-neonatal transition, also under two pathophysiological conditions. It provides a non-invasive means of predicting clinically relevant parameters, which is essential for postnatal treatment planning in the prenatal period, especially given the potential need for immediate postnatal hemodynamic management. Overall, this model presents a promising tool for predicting the impact of CHD postnatally based on prenatal information and for guiding timely and effective treatment strategies. As such, the model may be considered as a potential basis for other applications in perinatal hemodynamics including fetal-to-neonatal transition.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Impact<\/jats:title>\n                    <jats:p>\n                      <jats:list list-type=\"bullet\">\n                        <jats:list-item>\n                          <jats:p>This study introduces a mathematical model that simulates the hemodynamic impact of congenital heart disease (CHD) during the fetal-to-neonatal transition, focusing on ventricular septal defect (VSD) and transposition of the great arteries (TGA). By integrating a one-fiber heart model and oxygen and carbon dioxide dynamics, the model gives a prediction of critical clinical parameters like flow, pressure, and oxygen saturation. This mathematical model has a potential to serve as non-invasive tool, providing valuable insights for prenatal planning and postnatal management, helping guide timely interventions for newborns affected by CHD.<\/jats:p>\n                        <\/jats:list-item>\n                      <\/jats:list>\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1038\/s41390-025-04565-1","type":"journal-article","created":{"date-parts":[[2026,1,30]],"date-time":"2026-01-30T12:22:02Z","timestamp":1769775722000},"page":"1056-1068","update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["The hemodynamic impact of congenital heart diseases during fetal-to-neonatal transition: an in-silico investigation"],"prefix":"10.1038","volume":"100","author":[{"given":"Bettine G.","family":"van Willigen","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Babette C.","family":"Krabben","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"M. 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