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Longitudinal Measurement of Extracellular Matrix Rigidity in 3D Tumor Models Using Particle-tracking Microrheology
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Fontan Route Remodeling over Time: A Longitudinal Quantitative 3D Case Series.

Raquel Dos Santos1, Amartya Dave2, Mohammed Usmaan Siddiqi3

  • 1Section of Cardiac Surgery, Department of Surgery, The University of Chicago, Chicago, IL 60637, USA.

Journal of Cardiovascular Development and Disease
|January 27, 2026
PubMed
Summary

Fontan remodeling involves complex anatomical changes beyond simple somatic growth. Quantitative 3D modeling reveals individualized Fontan route trajectories influenced by multiple factors, not just growth.

Keywords:
3D modelingFontan procedurecardiovascular biomechanicsconduit propertiescongenital heart diseasegrowth mappingremodelingshape analysissingle-ventricle physiologysomatic growth

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Area of Science:

  • Cardiovascular Research
  • Medical Imaging
  • Pediatric Cardiology

Background:

  • Fontan-associated anatomical remodeling is a known complication, but its underlying mechanisms are not fully understood.
  • Existing research lacks detailed characterization of the Fontan pathway's longitudinal changes.
  • The interplay between somatic growth and other factors in Fontan remodeling requires further investigation.

Purpose of the Study:

  • To quantitatively characterize the anatomical remodeling of the Fontan pathway over time.
  • To determine if observed morphological changes are solely due to somatic growth or influenced by other factors.
  • To explore the utility of 3D geometric analysis in understanding Fontan pathway dynamics.

Main Methods:

  • Retrospective analysis of five Fontan patients (four extracardiac, one lateral tunnel) using serial MRI-derived 3D models (1-4 years apart).
  • Assessment of directional displacement via 3D shape overlays and surface geometry using the Koenderink Shape Index (KSI).
  • Patient-specific growth mapping to estimate localized tissue dynamics and statistical analysis of geometric changes.

Main Results:

  • All patients demonstrated anterior displacement of the Fontan pathway, with a mean shift of 0.29″ ± 0.33″.
  • Four out of five patients exhibited increased convexity of the Fontan pathway over time.
  • Localized native-tissue expansion was minimal and heterogeneous, indicating remodeling is not solely driven by somatic growth.

Conclusions:

  • Fontan pathway remodeling is a highly individualized process, not explained by somatic growth alone.
  • Conduit properties, surgical design, thoracic anatomy, and mechanical forces likely contribute to remodeling.
  • Quantitative 3D geometric tools are valuable for assessing subtle Fontan remodeling and support patient-specific modeling in single-ventricle physiology.