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<p><h3>Aortofemoral Normal</h3></p>
<li><a href="#sec1">Clinical Significance</a></li>
<li><a href="#sec2">Clinical Data</a></li>
<li><a href="#sec3">Model Description</a></li>
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<div><section id="sec1" class="group"><h1>Aortofemoral Normal - 2</h1>
<h2>Clinical Significance</h2>
<p>Studying the hemodynamics of the vasculature distal to the abdominal aorta may be important in understanding common diseases in peripheral arteries downstream of the thoracic aorta. Diseases in the peripheral vasculature affect millions of people in the U.S and can have a profound effect on daily quality of life. </p>
<p>Peripheral arterial disease is the build-up of fatty tissue, or atherosclerosis, in lower extremity arteries. By 2001 at least 10 million people in the U.S were estimated to have peripheral arterial disease. The prevalence of peripheral arterial occlusive disease increases with age and can increase to up to 20% of the population in the geriatric population. Up to 4 million people in the U.S suffer from intermittent claudication causing pain in the legs during exercise. Atherosclerotic occlusive disease of the lower extremity arteries is a major cause of walking impairment, pain, ulcerations and gangrene. </p>
<p>Renal artery stenosis can have a prevalence of up to 45% in selective populations, specifically populations with other vascular disease. Prevalence can be from 1-6% in hypertensive patients to 30-45% in patients with aortoiliac occlusive disease or abdominal aortic aneurysms. It is most often caused by atherosclerosis in the renal arteries and is often undetected until symptoms become severe. The most common symptom of renal artery stenosis is hypertension, which can have significant effects on the entire vasculature. Up to 24% of patients with renal insufficiency, which can lead to end-stage renal disease renal disease, had renal artery stenosis, suggesting that renal artery stenosis may play an important role in kidney failure.</p>
</section>
<section id="sec2" class="group"><h2>Clinical Data</h2>
<p>Patient-specific volumetric image data was obtained to create physiological models and blood flow simulations. The RAS coordinate system was assumed for the image data orientation. Voxel Spacing, voxel dimensions, and physical dimensions are provided in the Right-Left (R ), Anterior-Posterior (A), and Superior-Inferior (S) direction. The patient was 21 years old and female. Details of the image data are listed as below:</p>
<p><strong>Volumetric image data details (CT)</strong>
<table class="table table-bordered">
<tr><th></th><th>R</th><th>A</th><th>S</th></tr>
<tr><th>Voxel Spacing (mm)</th><td>0.6445</td><td>0.6445</td><td>0.8</td></tr>
<tr><th>Voxel Dimensions</th><td>512</td><td>512</td><td>737</td></tr>
<tr><th>Physical Dimensions (mm)</th><td>330</td><td>330</td><td>589.6</td></tr>
</table></p>
<p><strong>Volume image:</strong></p>
<figure>
<img class="svImg svImgMd" src="clinical/aortofemoral2/imgs/volume.png">
<figcaption class="svCaption" ></figcaption>
</figure>
</section>
<section id="sec3" class="group"><h2>Model Description</h2>
<p>The aortofemoral model extends from the ascending or thoracic aorta to the femoral arteries. Using <strong>Simvascular</strong> and the image data above, the geometrical models are generated by selecting centerline paths along the vessels, creating 2D segmentations along each of these paths, and then lofting the segmentations together to create a solid model. A separate solid model was created for each vessel and Boolean addition was used to generate a single model representing the complete aortofemoral model. The vessel junctions were then blended to create a smoothed model.</p>
<p><strong>Geometric model details</strong>
<table class="table table-bordered">
<thead>
<tr>
<th>Number of inlets</th>
<th>Number of outlets</th>
<th>Volume(cm<sup>3</sup>)</th>
<th>Surface Area(cm<sup>2</sup>)</th>
<th>Number of Vessel Paths</th>
<th>Number of 2-D Segmentations</th>
</tr>
</thead>
<tr>
<td>1</td>
<td>17</td>
<td>128.8597</td>
<td>443.9319</td>
<td>18</td>
<td>198</td>
</tr>
</table></p>
<p><strong>Physiological Assumption</strong>
<table class="table table-bordered">
<thead>
<tr>
<th>Blood Viscosity</th>
<th>Blood Density</th>
</tr>
</thead>
<tr>
<td>0.04 g/cm•s<sup>2</sup></td>
<td>1.06 g/cm<sup>3</sup></td>
</tr>
</table></p>
<p><strong>Vessel Paths:</strong></p>
<figure>
<img class="svImg svImgMd" src="clinical/aortofemoral2/imgs/paths.jpg">
<figcaption class="svCaption" ></figcaption>
</figure>
<p><strong>Vessel Segmentations:</strong></p>
<figure>
<img class="svImg svImgMd" src="clinical/aortofemoral2/imgs/segmentations.jpg">
<figcaption class="svCaption" ></figcaption>
</figure>
<p><strong>Vessel Geometric Model:</strong></p>
<figure>
<img class="svImg svImgMd" src="clinical/aortofemoral2/imgs/model.jpg">
<figcaption class="svCaption" ></figcaption>
</figure>
</section>
<section id="sec4" class="group"><h2>Boundary Conditions</h2>
<h3>Inlet Boundary Conditions</h3>
<p>The inflow waveform was adapted from literature and then smoothed. The mean value of the inflow waveform was reasonably in the range of mean cardiac output of 4.6 L/min given for women and the standard 5.0 L/min. The inflow waveform was prescribed to the inlet of the computational fluid dynamics (CFD) models</p>
<p><strong>Flow Waveform:</strong></p>
<figure>
<img class="svImg svImgMd" src="clinical/aortofemoral2/imgs/inflow.jpg">
<figcaption class="svCaption" ></figcaption>
</figure>
<p><strong>Period and Cardiac Output:</strong>
<table class="table table-bordered">
<thead>
<tr>
<th>Period (s)</th>
<th>Cardiac Output (L/min)</th>
<th>Profile Type</th>
</tr>
</thead>
<tr>
<td>1.0</td>
<td>4.90</td>
<td>Womersley</td>
</tr>
</table></p>
<h3>Outlet Boundary Conditions</h3>
<p>In order to represent the effects of vessels distal to the CFD model, a three-element Windkessel model can be applied at each outlet. This model consists of proximal resistance (Rp), capacitance (C ), and distal resistance (Rd) representing the resistance of the proximal vessels, the capacitance of the proximal vessels, and the resistance of the distal vessels downstream of each outlet, respectively. </p>
<p><strong>Windkessel Model:</strong>
<figure>
<img class="svImg svImgMd" src="clinical/aortofemoral2/imgs/windkessel.jpg">
<figcaption class="svCaption" ></figcaption>
</figure></p>
<p>These parameters are defined using the mean flow to each outlet calculated from PC-MRI. RCR values are shown on the table.</p>
<p><strong>RCR Values for Each Outlet:</strong>
<table class="table table-bordered">
<tr><th>Face Name </th><th>R<sub>p</sub> </th><th>C </th><th>R<sub>d</sub> </th></tr>
<tr><td>Brachiocephalic_Right_Subclavian </td><td>788.82</td><td>0.0002090</td><td>13297.26</td></tr>
<tr><td>Right_Common_Carotid </td><td>6697.69</td><td>0.0001235</td><td>17222.63</td></tr>
<tr><td>Left_Common_Carotid </td><td>6708.98</td><td>0.0001235</td><td>17251.66</td></tr>
<tr><td>Left_Subclavian </td><td>788.87</td><td>0.0002090</td><td>13298.17</td></tr>
<tr><td>Celiac_Hepatic </td><td>1114.61</td><td>0.0001456</td><td>18789.07</td></tr>
<tr><td>Splenic </td><td>1086.33</td><td>0.0001456</td><td>18312.39</td></tr>
<tr><td>SMA </td><td>829.30</td><td>0.0001970</td><td>13979.66</td></tr>
<tr><td>Left_Renal </td><td>4102.96</td><td>0.0001970</td><td>10550.48</td></tr>
<tr><td>Right_Renal </td><td>4141.67</td><td>0.0001970</td><td>10650.01</td></tr>
<tr><td>Left_Internal </td><td>3108.73</td><td>0.0000529</td><td>52404.23</td></tr>
<tr><td>Right_Internal </td><td>3109.10</td><td>0.0000529</td><td>52410.58</td></tr>
<tr><td>Left_Profunda </td><td>6620.49</td><td>0.0000247</td><td>111602.55</td></tr>
<tr><td>Right_Profunda </td><td>6570.55</td><td>0.0000247</td><td>110760.65</td></tr>
<tr><td>Left_Profunda_2 </td><td>3316.24</td><td>0.0000494</td><td>55902.32</td></tr>
<tr><td>Right_Profunda_2 </td><td>3299.25</td><td>0.0000494</td><td>55615.95</td></tr>
<tr><td>Aorta_Smoothed </td><td>3322.05</td><td>0.0000494</td><td>56000.20</td></tr>
<tr><td>Common_External_Femoral </td><td>3312.96</td><td>0.0000494</td><td>55847.04</td></tr>
</table></p>
</section>
<section id="sec5" class="group"><h2>Simulation & Results</h2>
<p>Conservation of mass and Navier-Stokes equations were solved using 3D finite element methods assuming rigid and non-slip walls. The number of time steps per cycle is 3200 with fixed time step size. The simulation was run in cgs units for several cardiac cycles to allow the flow rate and pressure fields to stabilize. Simulation results were quantified for the last cardiac cycle. Paraview, an open-source scientific visualization application, was used to visualize the results. A volume rendering of velocity magnitude for three time points during the cardiac cycle can be seen.</p>
<figure>
<img class="svImg svImgXl" src="clinical/aortofemoral2/imgs/vel.jpg">
<figcaption class="svCaption" >(a)Peak Systole; (b)End Systole; (\(c\))End Diastole</figcaption>
</figure>
<p>Surface distribution of time-averaged blood pressure (TABP), time-averaged wall shear stress (TAWSS) and oscillatory shear index (OSI) were also visualized and can be seen.</p>
<figure>
<img class="svImg svImgXl" src="clinical/aortofemoral2/imgs/timeaverage.jpg">
<figcaption class="svCaption" >(a)TABP; (b)TAWSS; (\(c\))OSI</figcaption>
</figure>
<p><br>
<br></p>
</section>
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