Femoral artery | EPFL Graph Search

The femoral artery is a large artery in the thigh and the main arterial supply to the thigh and leg. The femoral artery gives off the deep femoral artery and descends along the anteromedial part of the thigh in the femoral triangle. It enters and passes through the adductor canal, and becomes the popliteal artery as it passes through the adductor hiatus in the adductor magnus near the junction of the middle and distal thirds of the thigh. The femoral artery proximal to the origin of the deep femoral artery is referred to as the common femoral artery, whereas the femoral artery distal to this origin is referred to as the superficial femoral artery. Structure The femoral artery represents the continuation of the external iliac artery beyond the inguinal ligament underneath which the vessel passes to enter the thigh. The vessel passes under the inguinal ligament just medial of the midpoint of this ligament, midway between the anterior superi

Arterial in vitro remodeling

Gabriela Montorzi Thorell

Vascular remodeling is defined as any enduring change in the size and composition of an adult blood vessel, allowing adaptation or repair. The vascular remodeling response has been shown to depend on a variety of endogenous and environmental factors. Physiological remodeling is a tightly regulated process that mainly occurs in response to long-term changes in hemodynamic conditions. The adaptation to these hemodynamic changes implies the production of mediators that influence structure as well as function. A loss of regulation in the adaptive response underlies the pathogenesis of major cardiovascular diseases, including hypertension, atherosclerosis, restenosis and arterial aneurismal dilatation. Specialized enzymes called matrix metalloproteinases (MMPs) have been shown to have a predominant participation in the reorganization of the vessel structure, through the degradation of the extracellular matrix scaffold. The aim of this thesis is to gain insight in the biological and mechanical processes taking place in the vascular wall as an adaptive response to different biomechanical stimuli such as blood pressure and blood flow. This work proposes a new model for the study of vascular remodeling where physical factors acting on the arterial wall can be dissociated and analyzed, individually, in relation to the biological response. The results are presented in form of an introduction, three scientific papers and a conclusion section. The investigation has been designed around three different approaches: adaptation of a non-uniform artery to an in vitro environment, vascular adaptation to steady and pulsatile pressure and vascular adaptation to unidirectional and oscillatory flow. The adaptive response to each one of the variables chosen has been analyzed through biological and biomechanical remodeling indicators of the arterial wall. The introduction is an overview of the biological and biomechanical characteristics of arterial wall in relation to the remodeling process. The contribution of vascular smooth muscle cells and extracellular matrix to physiological and pathological arterial remodeling is discussed. Paper I assesses the relative remodeling of a non-axisymmetric artery in relation to its environment. The study considers the native circumferential asymmetry of the porcine right common carotid, which results from the non-homogenous mechanical and hemodynamic native environment. The adaptive response of the artery to an in vitro perfusion environment is analyzed. The study shows that in vitro perfusion leads, through remodeling, to a circumferentially uniform scleroprotein distribution and to a change in arterial compliance. This study emphasizes the link between structural changes, the biomechanical response and the enzymatic implication in the adaptive response. In paper II we investigate the role of continuous and cyclic stretch, produced by steady or pulsatile pressure acting on the arterial wall, on the remodeling response. The study shows that exposure to continuous and cyclic stretch differentially affects the relative scleroprotein content and leads to a change in arterial wall stiffness. The adaptive outcome is studied through an integrative approach taking into consideration the geometrical and structural adaptation, the biomechanical behavior and the enzymatic agents implicated in extracellular matrix turnover. Paper III analyzes the influence of different flow patterns on the arterial adaptive response. We investigate the differential effects of oscillatory flow, mimicking a plaque-prone hemodynamic environment, and unidirectional flow, to mimicking a physiologically protective (plaquefree) environment. The effect of these hemodynamic forces on the remodeling response are characterized through the study of endothelial and smooth muscle cell function as well as through assessment of agents influencing extracellular matrix turnover. The conclusions section presents a synthesis of the results and contribution of this thesis and proposes perspectives for future studies.

EPFL2004

A force-sensing device for assistance in soft-tissue balancing during knee arthroplasty

Denis Crottet

Nowadays, the large majority of the instrumentation for orthopaedic surgery consists of mechanical tools with varying degrees of complexity. To increase the accuracy and the safety of orthopaedic interventions, sensors and computers were recently introduced in the operating room. Computer Assisted Orthopaedic Surgery (CAOS) uses a navigation system that tracks the movements of surgical instruments in real-time and displays their exact location in relation to the operative area. Such technology improved the quality of orthopaedic arthroplasties, but it is still limited to the measurement of kinematic parameters such as axial alignments, position and angle measurements. In Total Knee Arthroplasty (TKA), the ligament balance, which is crucial for the stability and lifetime of implants, is currently only qualitatively assessed. The goal of this thesis was therefore to demonstrate the importance of intraoperative measurement of musculoskeletal forces through the development of a force-sensing device designed to improve the ligament balancing procedure during TKA. Three possible device designs were proposed and evaluated using finite element analysis in an iterative optimization process. The final design consists of two sensitive plates, one for each condyle, a tibial base plate and a set of spacers to adapt the device thickness to the patient-specific tibiofemoral gaps. Each sensitive plate is equipped with three deformable bridges instrumented with thick-film piezoresistive sensors, which allow accurate measurements of the amplitude and location of the tibiofemoral contact forces. The net varus-valgus moment is then computed to characterize the ligament imbalance. Laboratory experiments showed that the device has appropriate accuracy and dynamic range for the intended application. The first experimental trials on a plastic knee joint model and on a cadaver specimen demonstrated the proper in-situ functioning of the device. The performance and surgical advantages of the device were then evaluated in an in-vitro study including four different experiments: 1) Six knee joints were axially loaded. Comparing applied and measured compressive forces demonstrated the accuracy and reliability of in-situ measurements. 2) To estimate the importance of keeping the patella in its anatomical place during imbalance assessment, the effect of patellar eversion on the mediolateral distribution of tibiofemoral contact forces was measured. One fourth of the patellar load was shifted to the lateral compartment. 3) Assessment of knee stability based on condyle contact forces or varus-valgus moments were compared to the current surgical method (difference of varus-valgus loads causing condyle lift-off). The force-based assessment found to be equivalent to the surgical method while the moment-based technique, which is considered optimal, showed a tendency of lateral imbalance. 4) Finally the effect of minor and major medial collateral ligament releases was biomechanically quantified. Large variation among specimens reflected the difficulty of ligament release and the need for intraoperative force monitoring. Two clinical trials were carried out to evaluate the device performance in a surgical environment. After the tibial cut, the medial and lateral tibiofemoral gaps ensuring the knee stability were determined from the device measurements and compared to the femoral cuts performed on the basis of standard instrumentation. The agreement between the two approaches was generally good. The only significant difference was measured on the first patient at 90° flexion. At this point, the surgeon also estimated that the knee was not optimally balanced, thus demonstrating the consistency between his perception and the device measurements. In conclusion, the proposed force-sensing device for assistance in ligament balancing during TKA provides accurate, reliable and useful measurements. In addition to the precise imbalance assessment based on the measurement of forces and moments, important clinical advantages, such as the possibility to keep the patella in its anatomical place during the measurement or the real-time force monitoring during the delicate phase of ligament release, were demonstrated. The encouraging results of the in-vivo trial proved the usability of the device in a surgical environment and opens the way for larger clinical studies. The developed device has thus potential to improve the ligament balancing procedure, the consistency of surgery and the lifetime of TKA, illustrating thereby the clinical benefit of measuring forces during orthopaedic surgeries.

EPFL2006

Pressure and Flow Wave Propagation in Patient-Specific Models of the Arterial Tree

Philippe Reymond

Blood flow in the arterial circulation induces hemodynamic forces that play an important role in various forms of vascular diseases. Temporal variation of the wall shear stress seems to play a significant role in atherogenesis and plaque stability. Flow induced wall shear stress has been linked to growth and possibly rupture of the aneurysm wall. Hemodynamic forces are patient-specific and difficult to assess in the clinic. At present, there is no in vivo measurement technique that enables measurement of hemodynamic forces to the degree of precision needed. However, when imaging modalities used frequently in clinical routine re-create high-definition, patient geometric quantification of the blood vessel, they can be employed as a base for creating predictive hemodynamic models. Which in the case of understanding healthy vs. pathologic blood flow within the cerebral or systemic circulation, renders this an interesting approach. First, we developed a "generic 1D" distributed model of the human arterial tree including the primary systemic arteries and coupled this to a heart model. The fluid mechanics equations were solved numerically to obtain pressure and flow throughout the arterial tree. A nonlinear viscoelastic constitutive law for the arterial wall was considered while distal vessels were terminated with a three-element Windkessel model. The coronary arteries were modeled assuming a systolic flow impediment proportional to ventricular varying elastance. The model predictions were validated with noninvasive measurements of pressure and flow performed in young volunteers. Flow in the large arteries was visualized with magnetic resonance imaging, cerebral flow detected with ultrasound Doppler and blood pressure measured with applanation tonometry. Model predictions at different arterial locations compared well to measured flow and pressure waves at the same anatomical points. Thus, the generic 1D model reflected the flow and pressure measurements of the "average subject" of our volunteer population. Following the same approach as the generic 1D model, we built and validated a patient-specific model. In this case, geometric data, flow and pressure measurements were obtained for one person. The model predicted pressure and flow waveforms in good agreement with the in-vivo measurements with regards to wave shape and features. Comparison with a generic 1-D model has shown that the patient-specific model better predicted pressure and flow at specific arterial sites. Overall, the patient-specific 1-D model was able to predict pressure and flow waveforms in the main systemic circulation, whereas this was not always the case for a generic 1-D model. The inherent underestimation of energy losses of the 1-D wave propagation model, due to bifurcations, non-planarity and complex geometry, were examined. The 1-D model was compared to a rigid wall 3-D computational fluid dynamic model. Newtonian and non-Newtonian blood properties were studied and the longitudinal pressure distribution along the arteries was compared with the 1-D patient-specific model mean pressure prediction. The results indicated that pressure drop is significant only in small diameter vessels such as the precerebral and cerebral arteries. In these vessels the 1-D model in comparison to 3-D models consistently underestimated pressure drop. The complex flow patterns resulting from asymmetry and bifurcation yield shear stresses in the 3-D model that were greater than the 1-D model. A 3-D unsteady fluid structure interaction simulation in a patient-specific model was performed to simultaneously capture the flow details, given by the 3-D model, and wave propagation phenomena, provided by the 1-D model. The 3-D unsteady fluid structure interaction approach is the most computationally intense and cumbersome, but it allows physiological simulations with a high level of detail and accuracy. For instance, this approach could be relevant to obtain blood flow details in regions that are prone to atherosclerotic plaques or development of aneurysms. The 3-D fluid structure interaction simulation was performed for a patient-specific aorta. Important clinical parameters such as wall shear stress were quantified and significant differences were found in comparison to the rigid wall 3-D simulation indicating the relevance of a fluid structure interaction approach. A comparison of the fluid structure interaction to an equivalent 1-D model resulted in good reproduction of the pressure and flow waveforms. The effect of a decreased compliance of the arterial tree on hemodynamical parameters has been assessed with the use of a 1-D model. Local, proximal aorta and global stiffening of the arterial tree were modeled and led to two different mechanisms that contribute to the increase in central pulse pressure. They probably both contribute to systolic hypertension and their relative contribution depends on the topology of arterial stiffening and geometrical alterations taking place in aging or in disease. All these patient-specific models are about to being in use in a clinical environment and will be useful for providing better diagnostics and treatment planning in a near future.

EPFL2011