Computer modelling of fetal blood flow distribution in hypoplastic left heart syndrome: effect of pulmonary trunk/ductal enlargement and aortic coarctation

  • Mr Jonathan Mynard, Heart Research Group, Murdoch Children's Research Institute, Australia
  • Mr Andrew Hattam, Heart Research Group, Murdoch Children's Research Institute, Australia
  • A/Prof Malcolm Davidson, Department of Chemical and Biomolecular Engineering, University of Melbourne, Australia
  • Prof Daniel Penny, Heart Research Group, Murdoch Children's Research Institute, Australia
  • A/Prof Joesph Smolich, Heart Research Group, Murdoch Children's Research Institute, Australia

    • Objective: Recently, we developed a computer model of the fetal circulation which produced blood flow distributions seen in vivo. The aim of this study was to use this model to investigate flow patterns in hypoplastic left heart syndrome (HLHS), a condition characterised by reduced left ventricular output and ascending aortic (AA) diameter, and which is often associated with pulmonary trunk (PT) and ductus arteriosus (DA) enlargement, and aortic isthmus (AI) coarctation. Particular attention was directed to changes in upper body (UB, including cerebral) flow.
    Methods: The computer model consisted of one-dimensional representations of left/right ventricles (LV/RV) and large arteries, and a lumped-parameter model of downstream circulations. A spectrum of HLHS severity was simulated by reducing LV output and AA diameter, from normal to aortic valve atresia (AVA, 10% of normal AA diameter and zero LV output). With AVA, PT/DA diameters were then progressively increased (to 80% above normal). Subsequently, AI diameter was reduced to simulate coarctation.
    Results: With increasing HLHS severity, combined ventricular output and UB flow fell progressively to 17% and 26% below normal respectively for AVA, despite RV output increasing by 29% and the appearance of retrograde AI flow. PT/DA enlargement increased RV output further (by 54%), thereby ameliorating UB flow reduction to 13%. However, superimposition of AI coarctation progressively reduced UB flow towards zero after AI diameter had been reduced below 40% of normal.
    Conclusions: Computer modelling of the fetal circulation suggests that PT/DA enlargement and aortic coarctation have a major impact on UB flow in HLHS.