Computational fluid dynamics characterization of pulsatile flow in central and Sano shunts connected to the pulmonary arteries: importance of graft angulation on shear stress-induced, platelet-mediated thrombosis.

OBJECTIVES: Central (aorta) and Sano (right ventricle)-to-pulmonary artery (PA) shunts, palliative operations for infants with complex heart defects, can develop life-threatening thrombosis. We employed computational fluid dynamics (CFD) to study pulsatile flow in these shunts, with the goal to identify haemodynamic characteristics conducive to thrombus formation. METHODS: CFD, using the finite volume method with cardiac catheterization data, and computer simulations, based on angiography, were employed to determine flow-velocity field, wall shear stress (WSS) profile and oscillatory shear index (OSI). RESULTS: At prominent angulation, in central shunts (4 and 3.5 mm), WSS reached 245 and 123 (Pascal-Pa), peak systole and 137 and 46 Pa, end diastole; and, in Sano shunts (5 and 6 mm), WSS attained 203 and 133 Pa, peak systole and 1.6 and 1.5 Pa, end diastole. Counter-rotating flow vortices augmented WSS. These high WSSs can promote platelet aggregation, leading to thrombus formation. The OSIs averaged 0.39, indicative of multidirectional shearing forces. Shunt burden was assessed by averaging WSS, over its luminal area and the cardiac cycle. For the central shunts, these WSSs were 73.0 and 67.2 Pa; whereas, for the Sano shunts, 34.9 and 19.6 Pa. For modified Blalock-Taussig shunts (4 and 3.5 mm), the averaged WSSs were significantly lower at 26.0 and 27.5 Pa, respectively. CONCLUSIONS: CFD modelling is an important tool to determine blood flow behaviour in shunts. Graft angulation presents a risk for shear stress-induced, platelet- mediated thrombosis, which is more likely to occur in elongated central than in Sano shunts.

Computational fluid dynamics characterization of blood flow in central aorta to pulmonary artery connections: importance of shunt angulation as a determinant of shear stress-induced thrombosis.

The central aortic shunt, consisting of a Gore-Tex (polytetrafluoroethylene) tube (graft) connecting the ascending aorta to the pulmonary artery, is a palliative operation for neonates with cyanotic congenital heart disease. These tubes often have an extended length, and therefore must be angulated to complete the connection to the posterior pulmonary arteries. Thrombosis of the graft is not uncommon and can be life-threatening. We have shown that a viscous fluid (such as blood) traversing a curve or bend in a small-caliber vessel or conduit can give rise to marked increases in wall shear stress, which is the major mechanical factor responsible for vascular thrombosis. Thus, the objective of this study was to use computational fluid dynamics to investigate whether wall shear stress (and shear rate) generated in angulated central aorta-to-pulmonary artery connections, in vivo, can be of magnitude and distribution to initiate platelet activation/aggregation, ultimately leading to thrombus formation. Anatomical features required to construct the computer-simulated blood flow pathways were verified from angiograms of central aortic shunts in patients. For the modeled central aortic shunts, we found wall shear stresses of (80-200 N/m(2)), with shear rates of (16,000-40,000/s), at sites of even modest curvature, to be high enough to cause platelet-mediated shunt thrombosis. The corresponding energy losses for the fluid transitions through the aorta-to-pulmonary connections constituted (70 %) of the incoming flow's mechanical energy. The associated velocity fields within these shunts exhibited vortices, eddies, and flow stagnation/recirculation, which are thrombogenic in nature and conducive to energy dissipation. Angulation-induced, shear stress-mediated shunt thrombosis is insensitive to aspirin therapy alone. Thus, for patients with central aortic shunts of longer length and with angulation, aspirin alone will provide insufficient protection against clotting. These patients are at risk for shunt thrombosis and significant morbidity and mortality, unless their anticoagulation regimen includes additional antiplatelet medications.