Antonino Rinaudo

Difference in hemodynamic and wall stress of ascending thoracic aortic aneurysms with bicuspid and tricuspid aortic valve

The aortic dissection (AoD) of an ascending thoracic aortic aneurysm (ATAA) initiates when the hemodynamic loads exerted on the aneurysmal wall overcome the adhesive forces holding the elastic layers together. Parallel coupled, two-way fluid-structure interaction (FSI) analyses were performed on patient-specific ATAAs obtained from patients with either bicuspid aortic valve (BAV) or tricuspid aortic valve (TAV) to evaluate hemodynamic predictors and wall stresses imparting aneurysm enlargement and AoD. Results showed a left-handed circumferential flow with slower-moving helical pattern in the aneurysms center for BAV ATAAs whereas a slight deviation of the blood flow toward the anterolateral region of the ascending aorta was observed for TAV ATAAs. Blood pressure and wall shear stress were found key hemodynamic predictors of aneurysm dilatation, and their dissimilarities are likely associated to the morphological anatomy of the aortic valve. We also observed discontinues, wall stresses on aneurysmal aorta, which was modeled as a composite with two elastic layers (i.e., inhomogeneity of vessel structural organization). This stress distribution was caused by differences on elastic material properties of aortic layers. Wall stress distribution suggests AoD just above sinotubular junction. Moreover, abnormal flow and lower elastic material properties that are likely intrinsic in BAV individuals render the aneurysm susceptible to the initiation of AoD.

Regional variation of wall shear stress in ascending thoracic aortic aneurysms

The development of an ascending thoracic aortic aneurysm is likely caused by excessive hemodynamic loads exerted on the aneurysmal wall. Computational fluid-dynamic analyses were performed on patient-specific ascending thoracic aortic aneurysms obtained from patients with either bicuspid aortic valve or tricuspid aortic valve to evaluate hemodynamic and wall shear parameters, imparting aneurysm enlargement. Results showed an accelerated flow along the outer aortic wall with helical flow in the aneurysm center for bicuspid aortic valve ascending thoracic aortic aneurysms. In a different way, tricuspid aortic valve ascending thoracic aortic aneurysms exhibited normal systolic flow without substantial secondary pattern. Analysis of wall shear parameters evinced a high and locally varying wall shear stress on the outer aortic wall and high temporal oscillations in wall shear stress (oscillatory shear index) on either left or right side of aneurysmal aorta. These findings may explain the asymmetric dilatation typically observed in ascending thoracic aortic aneurysms. Simulations of a hypertensive scenario revealed an increase in wall shear stress upon 44% compared to normal systemic pressure models. Computational fluid-dynamics–based analysis may allow identification of wall shear parameters portending aneurysm dilatation and hence guide preventative intervention.

Haemodynamic predictors of a penetrating atherosclerotic ulcer rupture using fluid-structure interaction analysis.

We present preliminary data on the flow-induced haemodynamic and structural loads exerted on a penetrating atherosclerotic aortic ulcer (PAU). Specifically, one-way fluid-structure interaction analysis was performed on the aortic model reconstructed from a 66-year-old male patient with a PAU that evolved into an intramural haematoma and rupture of the thoracic aorta. The results show that elevated blood pressure (117 mmHg) and low flow velocity at the aortic wall (0.15 m/s(2)) occurred in the region of the PAU. We also found a low value of time-averaged wall shear stress (1.24 N/m(2)) and a high value of the temporal oscillation in the wall shear stress (oscillatory shear index = 0.13) in the region of the PAU. After endovascular treatment, these haemodynamic parameters were distributed uniformly on the luminal surface of the stent graft. These findings suggest that wall shear stress could be considered one of the major haemodynamic factors indicating the structural fragility of the PAU wall, which ultimately lead to PAU growth and rupture.

Computational fluid dynamics simulation to evaluate aortic coarctation gradient with contrast-enhanced CT.

Coarctation of aorta (CoA) is a narrowing of the aorta leading to a pressure gradient (ΔP) across the coarctation, increased afterload and reduced peripheral perfusion pressures. Indication to invasive treatment is based on values of maximal (systolic) trans-coarctation ΔP. A computational fluid dynamic (CFD) approach is herein presented for the non-invasive haemodynamic assessment of ΔP across CoA. Patient-specific CFD simulations were created from contrast-enhanced computed tomography (CT) and appropriate flow boundary conditions. Computed ΔP was validated with invasive intravascular trans-CoA pressure measurements. Haemodynamic indices, including pressure loss coefficient (PLc), time-averaged wall shear stress (TAWSS) and oscillatory shear index (OSI), were also quantified. CFD-estimated ΔP values were comparable to the invasive ones. Moreover, the aorta proximal to CoA was exposed to altered TAWSS and OSI suggesting hypertension. PLc was found as a further geometric marker of CoA severity. Finally, CFD-estimated ΔP confirmed a significant reduction after percutaneous balloon dilatation and stenting of the CoA in one patient (e.g. from ΔP∼52 mmHg to ΔP∼3 mmHg). The validation of the ΔP computations with catheterisation measurements suggests that CFD simulation, based on CT-derived anatomical data, is a useful tool to readily quantify CoA severity.

Evaluation of ventricular wall stress and cardiac function in patients with dilated cardiomyopathy

Dilated cardiomyopathy is a heart disease characterized by both left ventricular dilatation and left ventricular systolic dysfunction, leading to cardiac remodeling and ultimately heart failure. We aimed to investigate the effect of dilated cardiomyopathy on the pump performance and myocardial wall mechanics using patient-specific finite element analysis. Results evinced pronounced end-systolic wall stress on left ventricular wall of patients with dilated cardiomyopathy as compared to that of normal hearts. In dilated cardiomyopathy, both end-diastolic and end-systolic pressure–volume relationships of left ventricle and right ventricle were shifted to the right compared to controls, suggesting reduced myocardial contractility. We hereby propose that finite element analysis represents a useful tool to assess the myocardial wall stress and cardiac work, which are responsible for progressive left ventricular deterioration and poor clinical course.

An In Vitro Phantom Study on the Role of the Bird-Beak Configuration in Endograft Infolding in the Aortic Arch

Purpose: To assess endograft infolding for excessive bird-beak configurations in the aortic arch in relation to hemodynamic variables by quantifying device displacement and rotation of oversized stent-grafts deployed in a phantom model. Methods: A patient-specific, compliant, phantom pulsatile flow model was reconstructed from a patient who presented with collapse of a Gore TAG thoracic endoprosthesis. Device infolding was measured under different flow and pressure conditions for 3 protrusion extensions (13, 19, and 24 mm) of the bird-beak configuration resulting from 2 TAG endografts with oversizing of 11% and 45%, respectively. Results: The bird-beak configuration with the greatest protrusion extension exhibited the maximum TAG device displacement (1.66 mm), while the lowest protrusion extension configuration led to the minimum amount of both displacement and rotation parameters (0.25 mm and 0.6°, respectively). A positive relationship was found between the infolding parameters and the flow circulating in the aorta and left subclavian artery. Similarly, TAG device displacement was positively and significantly (p<0.05) correlated with the pulse pressure for all bird-beak configurations and device sizes. However, no collapse was observed under chronic perfusion testing maintained for 30 days and pulse pressure of 100 mm Hg. Conclusion: These findings suggest that endograft infolding depends primarily on the amount of aortic pulsatility and flow rate and that physiological flows do not necessarily engender hemodynamic loads on the proximal bird-beak segment sufficient to cause TAG collapse. Hemodynamic variables may allow for identification of patients at high risk of endograft infolding and help guide preventive intervention to avert its occurrence.

Mechanics of pericardial effusion: a simulation study.

Pericardial effusion is a pathological accumulation of fluid within pericardial cavity, which may compress heart chambers with hemodynamic impairment. We sought to determine the mechanics underlying the physiology of the hemodynamic impairment due to pericardial effusion using patient-specific computational modeling. Computational models of left ventricle and right ventricle were based on magnetic resonance images obtained from patients with pericardial effusion and controls. Myocardial material parameters were adjusted, so that volumes of ventricular chambers and pericardial effusion agreed with magnetic resonance imaging data. End-diastolic and end-systolic pressure–volume relationships as well as stroke volume were determined to evaluate impaired cardiac function of biventricular model. Distributions of myocardial fiber stresses and their regional variation along left ventricular wall were compared between patient groups. Both end-diastolic and end-systolic pressure–volume relationships shifted to the left for patients with pericardial effusion, with right ventricle diastolic filling particularly restricted. Left ventricle function as estimated by Starling curve was reduced by pericardial effusion. End-systolic fiber stress of left ventricle was significantly reduced as compared to that found for healthy patients. Myocardial stress was found increased at interventricular septum when compared to that exerted at lateral wall of left ventricle. Right ventricular myocardial stress was reduced as a consequence of the pressure equalization between right ventricle and pericardial effusion. Diastolic right ventricle collapse in patients with pericardial effusion is related to higher myocardial fiber stress on interventricular septum and to an extensible pericardium reducing motion of ventricular chambers, with right ventricle particularly restrained. These findings likely portend progression of pericardial effusion to cardiac tamponade.

Biomechanical implications of excessive endograft protrusion into the aortic arch after thoracic endovascular repair

Endografts placed in the aorta for thoracic endovascular aortic repair (TEVAR) may determine malappositioning to the lesser curvature of the aortic wall, thus resulting in a devastating complication known as endograft collapse. This premature device failure commonly occurs in young individuals after TEVAR for traumatic aortic injuries as a result of applications outside the physical conditions for which the endograft was designed. In this study, an experimentally-calibrated fluid-structure interaction (FSI) model was developed to assess the hemodynamic and stress/strain distributions acting on the excessive protrusion extension (PE) of endografts deployed in four young patients underwent TEVAR. Endograft infolding was experimentally measured for different hemodynamic scenarios by perfusion testing and then used to numerically calibrate the mechanical behavior of endograft PE. Results evinced that the extent of endograft can severely alter the hemodynamic and structural loads exerted on the endograft PE. Specifically, PE determined a physiological aortic coarctation into the aortic arch characterized by a helical flow in the distal descending aorta. High device displacement and transmural pressure across the stent-graft wall were found for a PE longer than 21 mm. Finally, marked intramural stress and principal strain distributions on the protruded segment of the endograft wall may suggest failure due to material fatigue. These critical parameters may contribute to the endograft collapse observed clinically and can be used to design new devices more suitable for young individuals to be treated with an endoprosthesis for TEVAR of blunt traumatic aortic injuries.