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Research Papers

Simulations Reveal Adverse Hemodynamics in Patients With Multiple Systemic to Pulmonary Shunts

[+] Author and Article Information
Mahdi Esmaily-Moghadam, Alison Marsden

Mechanical and Aerospace
Engineering Department,
University of California,
San Diego, CA 92093

Bari Murtuza, Tain-Yen Hsia

Cardiac Unit,
Great Ormond Street Hospital for Children and Institute of Child Health,
London WC1N 3JH, UK

1Part of the Modeling of Congenital Hearts Alliance (MOCHA). MOCHA Investigators: Edward Bove and Adam Dorfman (University of Michigan); Andrew Taylor, Alessandro Giardini, Sachin Khambadkone, Marc de Leval, Silvia Schievano, and T.-Y. Hsia (Institute of Child Health, UK); G. Hamilton Baker and Anthony Hlavacek (Medical University of South Carolina); Francesco Migliavacca, Giancarlo Pennati, and Gabriele Dubini (Politecnico di Milano, Italy); Richard Figliola and John McGregor (Clemson University); Alison Marsden (University of California, San Diego); and Irene Vignon-Clementel (National Institute of Research in Informatics and Automation, France).

Manuscript received July 17, 2013; final manuscript received December 2, 2014; published online January 29, 2015. Assoc. Editor: Francis Loth.

J Biomech Eng 137(3), 031001 (Mar 01, 2015) (12 pages) Paper No: BIO-13-1320; doi: 10.1115/1.4029429 History: Received July 17, 2013; Revised December 02, 2014; Online January 29, 2015

For newborns diagnosed with pulmonary atresia or severe pulmonary stenosis leading to insufficient pulmonary blood flow, cyanosis can be mitigated with placement of a modified Blalock–Taussig shunt (MBTS) between the innominate and pulmonary arteries. In some clinical scenarios, patients receive two systemic-to-pulmonary connections, either by leaving the patent ductus arteriosus (PDA) open or by adding an additional central shunt (CS) in conjunction with the MBTS. This practice has been motivated by the thinking that an additional source of pulmonary blood flow could beneficially increase pulmonary flow and provide the security of an alternate pathway in case of thrombosis. However, there have been clinical reports of premature shunt occlusion when more than one shunt is employed, leading to speculation that multiple shunts may in fact lead to unfavorable hemodynamics and increased mortality. In this study, we hypothesize that multiple shunts may lead to undesirable flow competition, resulting in increased residence time (RT) and elevated risk of thrombosis, as well as pulmonary overcirculation. Computational fluid dynamics-based multiscale simulations were performed to compare a range of shunt configurations and systematically quantify flow competition, pulmonary circulation, and other clinically relevant parameters. In total, 23 cases were evaluated by systematically changing the PDA/CS diameter, pulmonary vascular resistance (PVR), and MBTS position and compared by quantifying oxygen delivery (OD) to the systemic and coronary beds, wall shear stress (WSS), oscillatory shear index (OSI), WSS gradient (WSSG), and RT in the pulmonary artery (PA), and MBTS. Results showed that smaller PDA/CS diameters can lead to flow conditions consistent with increased thrombus formation due to flow competition in the PA, and larger PDA/CS diameters can lead to insufficient OD due to pulmonary hyperfusion. In the worst case scenario, it was found that multiple shunts can lead to a 160% increase in RT and a 10% decrease in OD. Based on the simulation results presented in this study, clinical outcomes for patients receiving multiple shunts should be critically investigated, as this practice appears to provide no benefit in terms of OD and may actually increase thrombotic risk.

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References

Figures

Grahic Jump Location
Fig. 1

The constructed idealized models: (a) distal MBTS and a 4.0 mm PDA, (b) proximal MBTS and a 3.0 mm PDA, and (c) proximal MBTS and a 4.0 mm CS. The region between CS/PDA and MBTS inside the PA (red) and the region in the MBTS (blue) are used to compare the results of studied cases.

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Fig. 2

The LPN, which is coupled to the MBTS anatomy, contains blocks for the upper body arteries (UBA), upper body capillary bed (UBB), upper body veins (UBV), pulmonary artery bed (PAB), pulmonary vein bed (PVB), lower body arteries (LBA), lower body capillary bed (LBB), lower body veins (LBV), two coronary arteries (CA1 and CA2), coronary capillary bed (CB), coronary veins (CV), left atrium (LA), right atrium (RA), and single ventricle (SV). The ascending aorta (AA), descending aorta (AoD), brachiocephalic artery (BA), right common carotid artery (RCCA), left common carotid artery (LCCA), left subclavian artery (LSA), left PA (LPA), right PA (RPA), and right coronary artery (RCA) are shown in the 3D model. Note the left coronary artery, which is omitted here to make the schematic less crowded, is connected to an LPN block identical to that of the RCA.

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Fig. 3

Wall thickness is calculated by solving the Laplace equation (left figure). Then, the wall of the fluid domain mesh is extruded in the normal direction to generate the solid domain mesh, i.e., vasculature wall (middle and right figures).

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Fig. 4

Deformation of the vessel walls at the peak systole

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Fig. 5

Systemic (top plot) and coronary oxygen deliveries (bottom plot) for proximal (solid) and distal (dashed) MBTS and normal PVR (black) and high PVR (red) versus PDA/CS diameter. Note the single MBTS corresponds to DPDA = 0. The results of three simulations with CS are shown with red circles, in which DPDA denotes CS diameter. (For interpretation of the references to color in this figure legend, the reader is referred to the web version of this article.)

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Fig. 6

Time averaged velocity field in normal PVR (top row) and high PVR (bottom row), and a single proximal MBTS (left column), a proximal MBTS and a 2 mm PDA (middle column), and a proximal MBTS and a 4 mm PDA (right column)

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Fig. 7

(a) Pressure contours for normal PVR (top row) and high PVR (bottom row), and a single proximal MBTS (left column), a proximal MBTS and a 2 mm PDA (middle column) cases, and a proximal MBTS and a 4 mm PDA (right column). (b) Averaged pressure in the PA outlets (top plot) and in the AA (bottom plot). See Fig. 5 caption for more details.

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Fig. 8

(a) RT contours for normal PVR (top row) and high PVR (bottom row), and a single proximal MBTS (left column), a proximal MBTS and a 2 mm PDA (middle column), and a proximal MBTS and a 4 mm PDA (right column). (b) Spatially averaged RT in the PA segment (top plot) and in the MBTS (bottom plot). See Fig. 5 caption for more details.

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Fig. 9

(a) WSS contours for normal PVR (top row) and high PVR (bottom row), and a single proximal MBTS (left column), a proximal MBTS and a 2 mm PDA (middle column), and a proximal MBTS and a 4 mm PDA (right column). (b) Spatially averaged WSS in the PA segment (top plot) and in the MBTS (bottom plot). See Fig. 5 caption for more details.

Grahic Jump Location
Fig. 10

(a) WSSG contours for normal PVR (top row) and high PVR (bottom row), and a single proximal MBTS (left column), a proximal MBTS and a 2 mm PDA (middle column), and a proximal MBTS and a 4 mm PDA (right column). (b) Spatially averaged WSSG in the PA segment (top plot) and in the MBTS (bottom plot). See Fig. 5 caption for more details.

Grahic Jump Location
Fig. 11

(a) OSI contours for normal PVR (top row) and high PVR (bottom row), and a single proximal MBTS (left column), a proximal MBTS and a 2 mm PDA (middle column), and a proximal MBTS and a 4 mm PDA (right column). (b) Spatially averaged OSI in the PA segment (top plot) and in the MBTS (bottom plot). See Fig. 5 caption for more details.

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