Abstract

Introduction: Central shunts (aorta) and Sano shunts (right ventricle) connected to the pulmonary arteries (PAs) are vital operations for infants with complex heart defects. However, they can become thrombosed. Hypothesis: At sites of prominent angulation, flow augments wall shear stress (WSS), a determinate of platelet-mediated thrombosis. Methods: We employed a patient-based computational model (Fluent) of pulsatile flow (viscosity 5 cPa-s), using a finite volume method and cardiac catheterization data, and geometric simulations (Autodesk Inventor), using angiography, to study flow behavior and WSS. Two central (4.0 and 3.5 mm) and Sano (5 and 6 mm) shunts were assessed. At the inlet to the central and Sano shunts, ascending aorta (AAo, 87/40 and 93/35 mmHg) and right ventricle (RV, 99/10 and 84/10 mmHg) pressures were used, respectively. At the outlets, measured PA pressures were used. Results: For central shunts, Fig 1, WSS reached 245 Pa and 123 Pa, peak systole. For Sano shunts, Fig 2, WSS attained 203 Pa and 133 Pa, peak systole. At sites of angulation, we identified flow vortices augmenting WSS (>100 Pa), and downstream regions of flow stagnation and recirculation, which are conducive to platelet aggregation and thrombus formation. Shunt burden, assessed by averaging WSS over the luminal surface of the shunts and the cardiac cycle, was 73.0 Pa and 67.2 Pa for central shunts, and 34.9 Pa and 19.6 Pa for Sano shunts. Conclusions: Our results indicate central shunts present a higher risk for thrombosis than Sano shunts. Importantly, WSS induced, platelet-mediated thrombosis is insensitive to aspirin, as the process does not involve the cyclooxygenase pathway.

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