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Research Papers

Fluid Structure Interaction With Contact Surface Methodology for Evaluation of Endovascular Carotid Implants for Drug-Resistant Hypertension Treatment

[+] Author and Article Information
Dinesh A. Peter, Yared Alemu, Michalis Xenos

Department of Biomedical Engineering,  Stony Brook University, Stony Brook, NY 11794

Ori Weisberg, Itzhak Avneri, Moshe Eshkol, Tal Oren, Moshe Elazar, Yaron Assaf

 Vascular Dynamics Ltd., Herzelia, Israel

Danny Bluestein1

Department of Biomedical Engineering,  Stony Brook University, Stony Brook, NY 11794danny.bluestein@sunysb.edu

1

Corresponding author.

J Biomech Eng 134(4), 041001 (Apr 12, 2012) (10 pages) doi:10.1115/1.4006339 History: Received August 31, 2011; Revised February 23, 2012; Posted March 14, 2012; Published April 09, 2012; Online April 12, 2012

Drug-resistant hypertensive patients may be treated by mechanical stimulation of stretch-sensitive baroreceptors located in the sinus of carotid arteries. To evaluate the efficacy of endovascular devices to stretch the carotid sinus such that the induced strain might trigger baroreceptors to increase action potential firing rate and thereby reduce systemic blood pressure, numerical simulations were conducted of devices deployed in subject-specific carotid models. Two models were chosen—a typical physiologic carotid and a diminutive atypical physiologic model representing a clinically worst case scenario—to evaluate the effects of device deployment in normal and extreme cases, respectively. Based on the anatomical dimensions of the carotids, two different device sizes were chosen out of five total device sizes available. A fluid structure interaction (FSI) simulation methodology with contact surface between the device and the arterial wall was implemented for resolving the stresses and strains induced by device deployment. Results indicate that device deployment in the carotid sinus of the physiologic model induces an increase of 2.5% and 7.5% in circumferential and longitudinal wall stretch, respectively, and a maximum of 54% increase in von Mises arterial stress at the sinus wall baroreceptor region. The second device, deployed in the diminutive carotid model, induces an increase of 6% in both circumferential and longitudinal stretch and a 50% maximum increase in von Mises stress at the sinus wall baroreceptor region. Device deployment has a minimal effect on blood-flow patterns, indicating that it does not adversely affect carotid bifurcation hemodynamics in the physiologic model. In the smaller carotid model, deployment of the device lowers wall shear stress at sinus by 16% while accelerating flow entering the external carotid artery branch. Our FSI simulations of carotid arteries with deployed device show that the device induces localized increase in wall stretch at the sinus, suggesting that this will activate baroreceptors and subsequently may control hypertension in drug-resistant hypertensive patients, with no consequential deleterious effects on the carotid sinus hemodynamics.

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Copyright © 2012 by American Society of Mechanical Engineers
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Figures

Grahic Jump Location
Figure 5

Comparative analysis of the effect of device deployment on wall stress distribution in the sinus of the diminutive carotid is shown, for the control and deployed device case. The stress distribution is depicted distal to the carotid bifurcation to highlight the effects of the device in the sinus region only. The bottom images depict the overall stress distribution pattern on the inner surface of the arterial wall of the complete carotid geometry. Peak wall stress caused by device deployment at the sinus (indicated by a triangle, location pointed out by an arrow) is 90 kPa, whereas the peak stress in the sinus of the carotid without the device is approximately 60 kPa. For the overall carotid model (bottom), peak stress occurring at the bifurcation in deployed device case is 622 kPa, whereas that in the control is 211 kPa.

Grahic Jump Location
Figure 4

Comparative analysis of the effect of device deployment on the wall stress in the sinus region of the physiologic carotid model (top) is shown. Stress distribution is mapped for the control (left, without device) and the deployed device case (right). Stress is mapped distal to the carotid bifurcation to highlight the effects of the device in the sinus region only. The bottom images depict the overall stress distribution pattern on the inner surface of the arterial wall of the complete carotid geometry. Peak wall stress caused by device deployment at the sinus (indicated by a triangle and pointed out by an arrow) is 305 kPa, whereas the peak stress in the sinus of the carotid without the device is approximately 198 kPa. For both the control and deployed device cases the maximum stress is approximately 347 kPa.

Grahic Jump Location
Figure 3

(a) Velocity and pressure waveforms (boundary conditions) applied to the physiologic carotid model are shown (top). Peak ICA velocity is 22 cm/s and peak ECA velocity is 52 cm/s (velocity waveform shown above pertains to the geometric dimensions of the physiologic carotid model only). (b) Von Mises stress–stretch behavior curve of Mooney Rivlin material model of the carotid arterial wall.

Grahic Jump Location
Figure 2

Two intra-luminal device designs, both in crimped state (left) and before deployment to distend the vascular wall of the corresponding carotid ICA from within the sinus region, are shown. Dimensions of the device (shown on the extreme left) designed to be deployed in a physiologic carotid: height, 17 mm; internal diameter, 6.6 mm; and strut thickness, 0.2 mm. Central image depicts the crimped state design of device, custom made for the extreme carotid model case, with height, 13 mm; internal diameter, 2.8 mm; and strut thickness, 0.2 mm. (Right) Image shows the model setup with the crimped device inside the sinus prior to deployment by radial expansion. The arterial wall is shown after being prestretched 18% axially along the z direction. Radial displacement boundary condition (along the x and y axes) is then applied to the vertical struts of the device (which are aligned with the z axis) such that the device would expand to 20% more than the sinus diameter of the carotid model. Similar setup and model boundary conditions are prescribed for the diminutive carotid and the second device.

Grahic Jump Location
Figure 1

Subject specific carotid model, with typical physiological carotid contours and dimensions of CCA internal diameter (ID), 9.5 mm; ICA ID, 8.3 mm; ECA ID, 5.3 mm; and wall thickness of 0.8–1 mm is shown on left. Height of reconstructed model is 44 mm. Image on right is the second subject specific extreme carotid model that lacks physiologic sinus contours and has ICA and ECA branches running in parallel and at close proximity to each other. Dimensions of this diminutive model are CCA ID, 5.5 mm; ICA ID, 3.8 mm; ECA ID, 2.4 mm; wall thickness, 0.6 mm; and height of model from CCA to ICA exit, 53 mm.

Grahic Jump Location
Figure 11

Velocity vector plot (left, during early diastole) and the wall shear stress contours (right, during peak systole) are shown for the deployed device case of the second carotid. The inset shows cross-sectional WSS in the sinus region. Velocity decreases towards inner wall of CCA with no apparent recirculation zones visible. WSS is approximately 16 dyn/cm2 in the sinus, 10–12 dyn/cm2 in the CCA, and 100 dyn/cm2 in the ECA (the scale for the WSS distribution shown appears in Pa).

Grahic Jump Location
Figure 6

Wall stress distribution, on the inner surface of each carotid is mapped (in units of Pa) with the custom devices deployed within the respective sinuses. The range of the stress distributions depicted (not in the same scale) are meant to provide a perspective of the device in relation to the artery, as well as to show the regions of high stresses that occur in segments of the wall that are in contact with the device once it is deployed.

Grahic Jump Location
Figure 7

Cross sections of the sinus wall, between the device struts, are highlighted for (a) the physiologic model and (d) the diminutive model. The highlighted sections are chosen for depicting the resulting wall stretch variation during the carotid bifurcation flow cycle. Wall stretch plots for the physiologic model are shown in (b) and (c), and for the diminutive model in (e) and (f). Reported stretch values are absolute maximum in the domains of interest. In all cases, the carotid without the device (control) has wall pulsatility. For the physiologic model with the deployed device, the carotid sinus pulsation is attenuated as shown in (b) and (c) Pulsatility for the diminutive model, shown in (e) and (f), is also attenuated compared to the control.

Grahic Jump Location
Figure 8

Cross sections of the carotid sinus, for the planes shown in (a) and (d ), are chosen for depicting the resulting wall stretch variation. For the physiologic model with the deployed device, the carotid sinus pulsatility is attenuated as shown in (b) and (c). Pulsatility for the diminutive model is either completely absent or extremely attenuated as shown in (e) and (f).

Grahic Jump Location
Figure 9

Velocity contour plots, at systole, for (a) control and (b) deployed device case of the physiologic carotid, (c) control and (d) deployed device case of the diminutive model are shown. The plane for the velocity contour representation was specifically chosen to depict the peak velocity at the ECA entrance region, and does not reflect the centerline peak velocity in the branches. Peak systolic velocity in the ICA and the ECA of the physiologic carotid, in both the control and the deployed device case, is 22 cm/s and 52 cm/s, respectively. Device deployment in the physiologic carotid slightly increases the sinus cross section area, marginally augmenting the size of the characteristic recirculation zone in the sinus. In the second carotid, the device induces local velocity drop at the sinus as compared to the control. No flow separation is observed. The device also induces higher velocity at the entrance of the ECA (peak of 74 cm/s) as compared to approximately 54 cm/s at the ECA entrance region of the control.

Grahic Jump Location
Figure 10

Velocity vector plot (left, during early diastole) and the wall shear stress contours (right, during peak systole) are shown for the deployed device case of the first carotid model. The inset shows cross-sectional WSS in the sinus region. The velocity vector field depicts regions of flow separation close to the arterial wall at the ICA–CCA junction. WSS is in the range of 2–3 dyn/cm2 in the sinus, 10–14 dyn/cm2 in the ECA, and 2–5 dyn/cm2 in the CCA (the scale for the WSS distribution shown appears in Pa).

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