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.
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.
A central (ascending aorta-to-pulmonary artery) shunt is a standard palliative operation for infants with cyanotic congenital heart disease. Thrombosis of these shunts can be life-threatening. We report our experience with catheter-directed thrombolysis using recombinant tissue plasminogen activator to locally treat totally occluded central shunts as an alternative to surgery. Ten patients (median age 47 days) successfully underwent the procedure. Following thrombolysis, shunt patency was verified by angiography. The arterial oxygen (O 2 ) saturations in 100% O 2 increased from a median value of 55% to 90%. Major bleeding did not occur in any patients. Computational fluid dynamics was used to identify a relationship between shunt hemodynamics and thrombosis. We retrospectively analyzed blood flow through simulations of these shunts as they would have appeared prior to obstruction. The calculations revealed that flow negotiating "angulated" portions of these central shunts produced wall shear stresses of 157-168 Pa (or N/m 2 ), with shear rates reaching 31,400-33,600/s. These values are easily high enough to initiate platelet activation/aggregation, leading to thrombus formation. We conclude that: 1) catheter-directed thrombolysis can be used to rapidly, effectively, and safely resolve total central shunt occlusion in critically ill neonates and 2) central shunts containing prominent angulation are at risk for developing shear stress-induced, plateletmediated thrombosis. This finding is clinically important as this flow-directed process is not affected by prophylactic aspirin against shunt thrombosis.
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