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Pulmonary arterial hypertension (PAH) is a progressive disease of the small pulmonary arteries characterized by vascular proliferation and remodeling, increased pulmonary vascular resistance (PVR) and endothelial dysfunction [1]. Previous studies have demonstrated by means of computational fluid dynamic (CFD) analysis and 4D-flow magnetic resonance imaging (MRI) that wall shear stress (WSS) is involved both in the progression and maintenance of pulmonary arterial hypertension (PAH) [2-3]. Previous computational analyses have demonstrated that WSS in pulmonary artery of PAH patients were lower than those in healthy subjects [4]. Current diagnostic techniques used to assess PAH severity and therapy effectiveness, as transthoracic echocardiography and right heart catheterization are graved by a number of drawbacks including operator’s dependence and invasiveness. The therapeutic response to Bosentan 125 is a die was monitored in a 65-year old man affected by post-embolic PAH at intermediate risk (WHO III class) by using computed tomography-derived WSS at main pulmonary artery bifurcation. Specific pulmonary artery geometries for each tertile of mPAP have been reconstructed using the mean values of the areas, lengths, and diameters of the MPA, left (LPA) and right pulmonary artery (RPA). The geometrical domain of interest for the study included the MPA from its origin until its bifurcation. Geometrical analysis, segmentation, and reconstruction have been performed using Osiri X (Pixmeo, Geneva, Switzerland) and Rhinoceros v. 4.0 Evaluation software (McNeel & Associates, Indianapolis, IN). To analyze the spatially resolved WSS, blood was modeled as a non-Newtonian viscous and incompressible fluid. The numeric grid was created from the 3-D geometry using ANSYS Meshing 14.0 (Ansys, Inc., Canonsburg, PA) while the simulations were conducted using the commercial software ANSYS FLUENT 14.0 (Ansys, Inc., Canonsburg, PA). After 12-month therapy, the mean area of high WSS was larger (Figure panel C –external and D –internal three dimensional reconstruction) at the main pulmonary artery (MPA) bifurcation and D) than before the start of the treatment (Figure panel A –external and B –internal three dimensional reconstruction) whereas the mean WSS value decreased. This was congruent with a decreasing of mean pulmonary artery pressure and mean wedge pressure and an increase of cardiac index from 45. mm Hg, 10.2 mmHg and 2.2 to 35.6 mmHg, 7.1 mmHg and 2.5, respectively. Although extensive studies are needed, mean WSS area calculated by computed tomography-derived CFD analysis has the potential to represent a complete non-invasive rapidly computed-calculated tool to monitor drug’s effectiveness in patients with PAH.
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1.
1.
Lai YC, Potoka KC, Champion HC, Mora AL, Gladwin MT. Pulmonary arterial
hypertension: the clinical syndrome. Circ Res. 2014;115:115-30
2.
Tang BT, Pickard SS, Chan FP, Tsao PS, Taylor CA,
Feinstein JA. Wall shear stress is decreased in the pulmonary arteries of
patients with pulmonary arterial hypertension: An image-based, computational
fluid dynamics study. Pulm Circ. 2012;2:470-6
3. Barker AJ,
Roldán-Alzate A, Entezari P, Shah SJ, Chesler NC, Wieben O, Markl M, François
CJ. Four-dimensional flow assessment of pulmonary artery flow and wall shear
stress in adult pulmonary arterial hypertension: results from two institutions.
Magn Reson Med. 2015;73:1904-13.
4. Truong U,
Fonseca B, Dunning J, Burgett S, Lanning C, Ivy DD, Shandas R, Hunter K, Barker
AJ. Wall shear stress measured by phase contrast cardiovascular magnetic
resonance in children and adolescents with pulmonary arterial hypertension. J
Cardiovasc Magn Reson. 2013;15:81
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