Endothelial stress caused by blood flow dynamics, specifically abnormal wall shear stress and oscillatory shear index, affects the degeneration of autologous pericardium in reconstructed pulmonary arteries.
Hypothesis-generating for shear stress effects on pericardial patches; leaves open validation before guiding congenital repairs.
OBJECTIVES: To clarify the risk factors for abnormal degeneration of autologous pericardium, the mechanical stress on the endothelial tissue caused by turbulent blood flow in the pulmonary artery (PA) reconstructed with autologous pericardium and major aortopulmonary collateral arteries was assumed in pulmonary atresia and ventricular septal defect. METHODS: Patient-specific PA models were created for 6 patients based on their past computed tomography images taken after unifocalization of major aortopulmonary collateral arteries. Computational fluid dynamics models were created to simulate the physiological pulsatile flow including the peripheral reflection wave, characteristic impedance and autonomous regulation system. Flow streamline, wall shear stress (WSS) and the oscillatory shear index (OSI) were calculated from the simulated result. PA degeneration was evaluated with the computed tomography images before the intracardiac repair. RESULTS: Regions with physiological high WSS had fewer abnormal changes. Excessively high WSS was often detected at the anastomosis site of the reconstructed PA, and intimal thickening was found in these regions during intracardiac repair. Regions with high OSI and low WSS had dilated change within several months. In 1 patient, in particular, detached vortex flow occurred at the rectangular angle anastomosis site of the right PA in flow streamline, resulting in high OSI and low WSS with abnormal enlargement in the pericardium. CONCLUSIONS: Endothelial stress caused by blood flow would affect the degeneration of autologous pericardium and major aortopulmonary collateral arteries in the reconstructed PA. High OSI and low WSS might induce enlargement or dilatation, and excessively high WSS in the anastomosis site might induce intimal thickening.
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Kato et al. (2017) studied this question.
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