Computational modelling to optimize the hybrid configuration for hypoplastic left heart syndrome.

OBJECTIVES Hybrid palliation for hypoplastic left heart syndrome (HLHS) is associated with mortality and late ventricular dysfunction. Increased ventricular workload and coronary perfusion limitation may be the important factors. Using mathematical modelling, this study investigated the effects of differing hybrid configurations on the demands on this single ventricle circulation. METHODS A multicompartmental Windkessel model of hybrid HLH-aortic atresia circulation was adopted, with a time-varying elastance representing ventricular functionality. The effects of diameter increases in bilateral pulmonary artery bandings (PABs) (+0.5, 2.5-4 mm) and ductal stent (+1, 4-10 mm) on cardiovascular haemodynamics, systemic oxygenation and ventricular energetics were assessed. RESULTS Simulations showed that an increase in PAB diameter of 2.5-4 mm resulted in an increased Q (0.61-2.66), and diastolic stent backflow (-0.2 to -0.78 l/min) with reduced systemic perfusion (0.82-0.77 l/min) and diastolic pressures (48.3-41.2 mmHg). Arterial and venous saturations increased, SaO2 (%) was 62-88 and SvO(2) 41-65. To maintain mean systemic pressures, substantial increases in cardiac output (1.3-2.8 l/min) and ventricular stroke work (576-1360 mmHg ml) were required. A decrease in the ductal stent diameter over the range 10-7 mm had a negligible haemodynamic effect: reduced systemic systolic pressure (77-72 mmHg) and increase in ventricular stroke work (781-790 mmHg ml). When the ductal diameter was restricted to <7 mm, it resulted in a significant reduced systemic flow and increased stroke work. Optimal hybrid configuration was defined at PAB 3 mm and ductal stent ≥7 mm. CONCLUSIONS In this model, increasing the PAB diameter, or a stent diameter <7 mm, substantially increased single ventricle workload and reduced systemic perfusion and diastolic pressure. This may compromise myocardial oxygen demand-supply, particularly in the setting of retrograde-dependent coronary perfusion.