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Aneurysm wall permeability has recently emerged as an in vivo marker of aneurysm wall remodeling. We sought to study the spatial relationship between hemodynamic forces derived from 4D-flow MRI and aneurysm wall permeability by DCE-MRI in a region-based analysis of unruptured saccular intracranial aneurysms (IAs). We performed 4D-flow MRI and DCE-MRI on patients with unruptured IAs of ≥ 5 mm to measure hemodynamic parameters, including wall shear stress (WSS), oscillatory shear index (OSI), WSS temporal (WSSGt) and spatial (WSSGs) gradient, and aneurysm wall permeability (Ktrans) in different sectors of aneurysm wall defined by evenly distributed radial lines emitted from the aneurysm center. The spatial association between Ktrans and hemodynamic parameters measured at the sector level was evaluated. Thirty-one patients were scanned. Ktrans not only varied between aneurysms but also demonstrated spatial heterogeneity within an aneurysm. Among all 159 sectors, higher Ktrans was associated with lower WSS, which was seen in both Spearman’s correlation analysis (rho = − 0.18, p = 0.025) and linear regression analysis using generalized estimating equation to account for correlations between multiple sectors of the same aneurysm (regression coefficient = − 0.33, p = 0.006). Aneurysm wall permeability by DCE-MRI was shown to be spatially heterogenous in unruptured saccular IAs and associated with local WSS by 4D-flow MRI.

Since the first endovascular aortic repair in 1990, endovascular devices and the indications for their use have significantly grown. Considerable progress has been made in endovascular devices and techniques, such that endovascular repair is now considered first-line treatment for patients with descending aortic disease. However, for patients with ascending aortic disease, open surgical repair with cardiopulmonary bypass and hypothermic cardiac arrest was the only option until recently. Although the outcomes for open surgical repair of the ascending aorta have improved over the years, approximately 30% of patients with an emergent surgical indication, such as type A aortic dissection, are considered to be too high risk for open repair. For these patients, endovascular repair of the ascending aorta offers a life-saving procedure. The ascending aorta is regarded as the final frontier for endovascular therapy. Endovascular repair of it has posed a formidable challenge thus far, due to its unique anatomy, hemodynamic forces, and lack of an appropriate stent-graft designed specifically for the ascending aorta. Although currently there are no comprehensive data from randomized clinical trials, there are several case series and case reports that have shown favorable outcomes. Improvements in available devices soon will drive an exponential increase in the number of patients undergoing endovascular ascending aortic repair. In this review, the authors discuss multiple aspects of endovascular ascending aortic repair including the unique surgical and anesthetic considerations, the devices used, and the available outcomes data, and future directions are also explored.

Mouse models have contributed significantly to understanding genetic and physiological factors involved in healthy cardiac function, how perturbations result in pathology, and how myocardial diseases may be treated. Cardiovascular magnetic resonance imaging (CMR) has become an indispensable tool for a comprehensive in vivo assessment of cardiac anatomy and function. This protocol shows detailed measurements of mouse heart left ventricular function, myocardial strain, and hemodynamic forces using 7-Tesla CMR. First, animal preparation and positioning in the scanner are demonstrated. Survey scans are performed for planning imaging slices in various short- and long-axis views. A series of prospective ECG-triggered short-axis (SA) movies (or CINE images) are acquired covering the heart from apex to base, capturing end-systolic and end-diastolic phases. Subsequently, single-slice, retrospectively gated CINE images are acquired in a midventricular SA view, and in 2-, 3-, and 4-chamber views, to be reconstructed into high-temporal resolution CINE images using custom-built and open-source software. CINE images are subsequently analyzed using dedicated CMR image analysis software. Delineating endomyocardial and epicardial borders in SA end-systolic and end-diastolic CINE images allows for the calculation of end-systolic and end-diastolic volumes, ejection fraction, and cardiac output. The midventricular SA CINE images are delineated for all cardiac time frames to extract a detailed volume-time curve. Its time derivative allows for the calculation of the diastolic function as the ratio of the early filling and atrial contraction waves. Finally, left ventricular endocardial walls in the 2-, 3-, and 4-chamber views are delineated using feature-tracking, from which longitudinal myocardial strain parameters and left ventricular hemodynamic forces are calculated. In conclusion, this protocol provides detailed in vivo quantification of the mouse cardiac parameters, which can be used to study temporal alterations in cardiac function in various mouse models of heart disease.

OBJECTIVEAneurysm wall enhancement (AWE) on 3D vessel wall MRI (VWMRI) has been suggested as an imaging biomarker for intracranial aneurysms (IAs) at higher risk of rupture. While computational fluid dynamics (CFD) studies have been used to investigate the association between hemodynamic forces and rupture status of IAs, the role of hemodynamic forces in unruptured IAs with AWE is poorly understood. The authors investigated the role and implications of abnormal hemodynamics related to aneurysm pathophysiology in patients with AWE in unruptured IAs.METHODSTwenty-five patients who had undergone digital subtraction angiography (DSA) and VWMRI studies from September 2016 to September 2017 were included, resulting in 22 patients with 25 IAs, 9 with and 16 without AWE. High-resolution CFD models of hemodynamics were created from DSA images. Univariate and multivariate analyses were performed to investigate the association between AWE and conventional morphological and hemodynamic parameters. Normalized MRI signal intensity was quantified and quantitatively associated with wall shear stresses (WSSs) for the entire aneurysm sac, and in regions of low, intermediate, and high WSS.RESULTSThe AWE group had lower WSS (p < 0.01) and sac-averaged velocity (p < 0.01) and larger aneurysm size (p < 0.001) and size ratio (p = 0.0251) than the non-AWE group. From multivariate analysis of both hemodynamic and morphological factors, only low WSS was found to be independently associated with AWE. Sac-averaged normalized MRI signal intensity correlated with WSS and was significantly different in regions of low WSS compared to regions of intermediate (p = 0.018) and high (p < 0.001) WSS.CONCLUSIONSThe presence of AWE was associated with morphological and hemodynamic factors related to rupture risk. Low WSS was found to be an independent predictor of AWE. Our findings support the hypothesis that low WSS in IAs with AWE may indicate a growth and remodeling process that may predispose such aneurysms to rupture; however, a causality between the two cannot be established.

Middle cerebral aneurysms constitute almost one-third of all anterior circulation aneurysms. Most of the saccular aneurysms originate from the arterial branching sites, but origins other than at the branching site are extremely rare. In this article, we are describing a unique M1 segment middle cerebral artery aneurysm which is not related with any branching site. Our literature search suggests that atherosclerotic changes in the arterial wall and local hemodynamic forces play an important role in the development of these types of aneurysm. Surgical management is not so unique in this type of aneurysm, but due to atherosclerotic parent arterial wall and thin-walled aneurysm sac, a neurosurgeon should be more cautious.

Mechanical hallmarks of fibrotic microenvironments are both outcomes and causes of fibrosis progression. Understanding how cells sense and transmit mechanical cues in the interplay with extracellular matrix (ECM) and hemodynamic forces is a significant challenge. Recent advances highlight the evolvement of intracellular mechanotransduction pathways responding to ECM remodeling and abnormal hemodynamics (i.e., low and disturbed shear stress, pathological stretch, and increased pressure), which are prevalent biomechanical characteristics of fibrosis in multiple organs (e.g., liver, lung, and heart). Here, we envisage the mechanical communication in cell–ECM, cell–hemodynamics and cell–ECM–cell crosstalk (namely paratensile signaling) during fibrosis expansion. We also provide a comprehensive overview of in vitro and in silico engineering systems for disease modeling that will aid the identification and prediction of mechano-based therapeutic targets to ameliorate fibrosis progression.

Intracardiac hemodynamic forces have been proposed to influence remodeling and be a marker of ventricular dysfunction. We aimed to quantify the hemodynamic forces in patients with repaired tetralogy of Fallot (rToF) to further understand the pathophysiological mechanisms as this could be a potential marker for pulmonary valve replacement (PVR) in these patients. Patients with rToF and pulmonary regurgitation (PR) > 20% ( n = 18) and healthy control subjects ( n = 15) underwent MRI, including four-dimensional flow. A subset of patients ( n = 8) underwent PVR and MRI after surgery. Time-resolved hemodynamic forces were quantified using 4D-flow data and indexed to ventricular volume. Patients had higher systolic and diastolic left ventricular (LV) hemodynamic forces compared with control subjects in the lateral-septal/LV outflow tract ( P = 0.011 and P = 0.0031) and inferior-anterior ( P < 0.0001 and P < 0.0001) directions, which are forces not aligned with blood flow. Forces did not change after PVR. Patients had higher RV diastolic forces compared with control subjects in the diaphragm-right ventricular (RV) outflow tract (RVOT; P < 0.001) and apical-basal ( P = 0.0017) directions. After PVR, RV systolic forces in the diaphragm-RVOT direction decreased ( P = 0.039) to lower levels than in control subjects ( P = 0.0064). RV diastolic forces decreased in all directions ( P = 0.0078, P = 0.0078, and P = 0.039) but were still higher than in control subjects in the diaphragm-RVOT direction ( P = 0.046). In conclusion, patients with rToF and PR had LV hemodynamic forces less aligned with intraventricular blood flow compared with control subjects and higher diastolic RV forces along the regurgitant flow direction in the RVOT and that of tricuspid inflow. Remaining force differences in the LV and RV after PVR suggest that biventricular pumping does not normalize after surgery. NEW & NOTEWORTHY Biventricular hemodynamic forces in patients with repaired tetralogy of Fallot and pulmonary regurgitation were quantified for the first time. Left ventricular hemodynamic forces were less aligned to the main blood flow direction in patients compared with control subjects. Higher right ventricular forces were seen along the pulmonary regurgitant and tricuspid inflow directions. Differences in forces versus control subjects remain after pulmonary valve replacement, suggesting that altered biventricular pumping does not normalize after surgery.

(1) Background: Traumatic brain injury (TBI) frequently occurs worldwide, resulting in high morbidity and mortality. Here, we hypothesized that TBI impairs an autoregulatory mechanism, namely the flow-induced constriction of isolated rat middle cerebral arteries (MCAs). (2) Methods: TBI was induced in anaesthetized rats by weight drop model, and then MCAs were isolated and transferred into a pressure-flow chamber. The internal diameter was measured by a video-microscopy. (3) Results: In MCAs from intact rats, increases in flow and pressure + flow elicited constrictions (−26 ± 1.9 µm and −52 ± 2.8 µm, p &lt, 0.05), which were significantly reduced after TBI or in the presence of thromboxane-prostanoid (TP receptor) antagonist SQ 29,548. Flow-induced constrictions were significantly reduced by HET0016, inhibitor of cytochrome P450 4A (CYP450 4A). Arachidonic acid, (AA, 10−7 M), and CYP-450 4A metabolite 20-hydroxyeicosatetraenoic acid (20-HETE) elicited constrictions of intact MCA (−26 ± 2.3% and −31 ± 3.6%), which were significantly reduced after TBI (to 11 ± 1.3% and −16 ±2.5%). The TP receptor agonist U46619 (10−7 M) elicited substantial constrictions of MCA from intact rats (−21 ± 3.3%), which were also significantly reduced, after TBI (to −16 ± 2.4%). (4) Conclusions: Flow-induced constrictor response of MCA is impaired by traumatic brain injury, likely due to the reduced ability of cytochrome P450 4A to convert arachidonic acid to constrictor prostaglandins and the mitigated sensitivity of thromboxane-prostanoid receptors.

Background: Diastolic function in patients with heart failure is usually impaired, resulting in increased left ventricular (LV) filling pressures, whose gold standard assessment is right heart catheterization (RHC). Hemodynamic force (HDF) analysis is a novel echocardiographic tool, providing an original approach to cardiac function assessment through the speckle-tracking technology. The aim of our study was to evaluate the use of HDFs, both alone and included in a new predictive model, as a potential novel diagnostic tool of the diastolic function. Methods: HDF analysis was retrospectively performed in 67 patients enrolled in the “Right1 study.” All patients underwent RHC and echocardiography up to 2 h apart. Increased LV filling pressure (ILFP) was defined as pulmonary capillary wedge pressure (PCWP) ≥ 15 mmHg. Results: Out of 67 patients, 33 (49.2%) showed ILFP at RHC. Diastolic longitudinal force (DLF), the mean amplitude of longitudinal forces during diastole, was associated with the presence of ILFP (OR = 0.84 [0.70; 0.99], p = 0.046). The PCWP prediction score we built including DLF, ejection fraction, left atrial enlargement, and e' septal showed an AUC of 0.83 [0.76–0.89], with an optimal internal validation. When applied to our population, the score showed a sensitivity of 72.7% and a specificity of 85.3%, which became 66.7 and 94.4%, respectively, when applied to patients classified with “indeterminate diastolic function” according to the current recommendations. Conclusion: HDF analysis could be an additional useful tool in diastolic function assessment. A scoring system including HDFs might improve echocardiographic accuracy in estimating LV filling pressures. Further carefully designed studies could be useful to clarify the additional value of this new technology., Graphical Abstract Risk variation of presenting increased left ventricular filling pressure (upper graph) and PCWP variation (lower graph), according to the proposed scoring system. EF, ejection fraction; DLF, diastolic longitudinal force; LAe, left atrial enlargement; ILFP, increased left ventricular filling pressure; NLFP, normal left ventricular filling pressure; PCWP, postcapillary wedge pressure.

The development of experimental models represent an excellent tool for the study and understanding of arterial and venous injuries associated with vascular pathologies as diverse as atherosclerosis and transplant rejection. With these models it was possible to understand the interference of the environment on vascular biology as well as to identify the the role of several regulatory factors from the initiation to the formation of complex lesions as atherosclerosis. The increase in hemodynamic forces, especially flow and pressure, triggers endothelial damage in the vascular bed, leading to vascular remodeling and ultimately to graft failure. In this chapter, we describe several experimental models available for in vivo, in vitro, and ex vivo studies. So far, many advances have been made, but more research is still needed. Due to methodological limitations, a multipronged approach is necessary for a comprehensive understanding of the mechanisms involved with vascular diseases, especially in the processes of stenosis, restenosis, and venous graft occlusion.

The Hippo-Yap pathway regulates multiple cellular processes in response to mechanical and other stimuli. In Drosophila, the polarity protein Lethal (2) giant larvae [L(2)gl], negatively regulates Hippo-mediated transcriptional output. However, in vertebrates, little is known about its homolog Llgl1. Here, we define a novel role for vertebrate Llgl1 in regulating Yap stability in cardiomyocytes, which impacts heart development. In contrast to the role of Drosophila L(2)gl, Llgl1 depletion in cultured rat cardiomyocytes decreased Yap protein levels and blunted target gene transcription without affecting Yap transcript abundance. Llgl1 depletion in zebrafish resulted in larger and dysmorphic cardiomyocytes, pericardial effusion, impaired blood flow and aberrant valvulogenesis. Cardiomyocyte Yap protein levels were decreased in llgl1 morphants, whereas Notch, which is regulated by hemodynamic forces and participates in valvulogenesis, was more broadly activated. Consistent with the role of Llgl1 in regulating Yap stability, cardiomyocyte-specific overexpression of Yap in Llgl1-depleted embryos ameliorated pericardial effusion and restored blood flow velocity. Altogether, our data reveal that vertebrate Llgl1 is crucial for Yap stability in cardiomyocytes and its absence impairs cardiac development.

Endothelium of blood vessels is continuously exposed to various hemodynamic forces. Flow-mediated epigenetic plasticity regulates vascular endothelial function. Recent studies have highlighted the significant role of mechanosensing-related epigenetics in localized endothelial dysfunction and the regional susceptibility for lesions in vascular diseases. In this article, we review the epigenetic mechanisms such as DNA de/methylation, histone modifications, as well as non-coding RNAs in promoting endothelial dysfunction in major arterial and venous diseases, consequent to hemodynamic alterations. We also discuss the current challenges and future prospects for the use of mechanoepigenetic mediators as biomarkers of early stages of vascular diseases and dysregulated mechanosensing-related epigenetic regulators as therapeutic targets in various vascular diseases.

Summary: During metastasis, cancer cells are exposed to potentially destructive hemodynamic forces including fluid shear stress (FSS) while en route to distant sites. However, prior work indicates that cancer cells are more resistant to brief pulses of high-level FSS in vitro relative to non-transformed epithelial cells. Herein, we identify a mechano-adaptive mechanism of FSS resistance in cancer cells. Our findings demonstrate that cancer cells activate RhoA in response to FSS, which protects them from FSS-induced plasma membrane damage. We show that cancer cells freshly isolated from mouse and human tumors are resistant to FSS, that formin and myosin II activity protects circulating tumor cells (CTCs) from destruction, and that short-term inhibition of myosin II delays metastasis in mouse models. Collectively, our data indicate that viable CTCs actively resist destruction by hemodynamic forces and are likely to be more mechanically robust than is commonly thought. : Moose et al. show that cancer cells exhibit a mechano-adaptive response to fluid shear stress through activation of the RhoA-actomyosin signaling axis. Utilizing in vivo models, they extend these findings to demonstrate that this axis maintains intravascular survival of circulating tumor cells (CTCs) that contributes to the development of metastasis. Keywords: fluid shear stress, circulating tumor cells, metastasis, RhoA, myosin II, formin

During metastasis cancer cells are exposed to potentially destructive hemodynamic forces including fluid shear stress (FSS) whileen routeto distant sites. However, prior work indicates that cancer cells are more resistant to brief pulses of high-level fluid shear stress (FSS)in vitrorelative to non-transformed epithelial cells. Herein we identify a mechanism of FSS resistance in cancer cells, and extend these findings to mouse models of circulating tumor cells (CTCs). We show that cancer cells acutely isolated from primary tumors are resistant to FSS. Our findings demonstrate that cancer cells activate the RhoA-myosin II axis in response to FSS, which protects them from FSS-induced plasma membrane damage. Moreover, we show that the myosin II activity is protective to CTCs in mouse models. Collectively our data indicate that viable CTCs actively resist destruction by hemodynamic forces and are likely to be more mechanically robust than is commonly thought.

The pathogenesis of intracranial aneurysms remains complex and multifactorial. While vascular, genetic, and epidemiological factors play a role, nascent aneurysm formation is believed to be induced by hemodynamic forces. Hemodynamic stresses and vascular insults lead to additional aneurysm and vessel remodeling. Advanced imaging techniques allow us to better define the roles of aneurysm and vessel morphology and hemodynamic parameters, such as wall shear stress, oscillatory shear index, and patterns of flow on aneurysm formation, growth, and rupture. While a complete understanding of the interplay between these hemodynamic variables remains elusive, the authors review the efforts that have been made over the past several decades in an attempt to elucidate the physical and biological interactions that govern aneurysm pathophysiology. Furthermore, the current clinical utility of hemodynamics in predicting aneurysm rupture is discussed.

Aims: Despite continuous efforts in improving the selection process, the rate of non-responders to cardiac resynchronization therapy (CRT) remains high. Recent studies on intraventricular blood flow suggested that the alignment of hemodynamic forces (HDFs) may be a reproducible biomarker of mechanical dyssynchrony. We aimed to explore the relationship between pacing-induced realignment of HDFs and positive response to CRT. Methods and results: We retrospectively analyzed 38 patients from the CRT database of our institution fulfilling the inclusion criteria for HDFs-related echocardiographic assessment early pre and post CRT implantation, with available mid-term follow-up (≥ 6 months) evaluation. Standard echocardiographic and deformation parameters early pre and post CRT implantation were integrated with the measurement of HFDs through novel methods based on speckle-tracking analysis. At midterm follow-up 71% of patients were classified as responders (reduction of Left Ventricular Systolic Volume Indexed ≥ 15%). Patients did not display significant changes between close evaluations pre and post-implant in terms of ejection fraction and strain metrics. A significant reduction of the ratio between the amplitudes of transversal and longitudinal force components was found. The variation of this ratio strongly correlates (R2 =0.60) with Left Ventricular (LV) end-systolic volume variation at mid-term follow up. Conclusion: Pacing-induced realignment of HDFs is associated with CRT efficacy at follow up. These preliminary results claim for dedicated prospective clinical studies testing the potential impact of HDFs study for patient selection and pacing optimization in CRT.

Intracranial aneurysm (IA) usually induced at a bifurcation site of intracranial arteries causes a lethal subarachnoid hemorrhage. Currently, IA is considered as a macrophage-mediated inflammatory disease triggered by a high wall shear stress (WSS) on endothelial cells. However, considered the fact that a high WSS can be observed at every bifurcation site, some other factors are required to develop IAs. We therefore aimed to clarify mechanisms underlying the initiation of IAs using a rat model. We found the transient outward bulging and excessive mechanical stretch at a prospective site of IA formation. Fibroblasts at the adventitia of IA walls were activated and produced (C-C motif) ligand 2 (CCL2) as well in endothelial cells loaded on high WSS at the earliest stage. Consistently, the mechanical stretch induced production of CCL2 in primary culture of fibroblasts and promoted migration of macrophages in a Transwell system. Our results suggest that distinct hemodynamic forces, mechanical stretch on fibroblasts and high WSS on endothelial cells, regulate macrophage-mediated IA formation.

Circulating tumor cells (CTCs) exist in a microenvironment quite different from the solid tumor tissue microenvironment. They are detached from matrix and exposed to the immune system and hemodynamic forces leading to the conclusion that life as a CTC is "nasty, brutish, and short." While there is much evidence to support this assertion, the mechanisms underlying this are much less clear. In this chapter we will specifically focus on biomechanical influences on CTCs in the circulation and examine in detail the question of whether CTCs are mechanically fragile, a commonly held idea that is lacking in direct evidence. We will review multiple lines of evidence indicating, perhaps counterintuitively, that viable cancer cells are mechanically robust in the face of exposures to physiologic shear stresses that would be encountered by CTCs during their passage through the circulation. Finally, we present emerging evidence that malignant epithelial cells, as opposed to their benign counterparts, possess specific mechanisms that enable them to endure these mechanical stresses.

We report here a rare complication in the form of kinking of flow diverter in a case of giant wide-necked supraclinoid internal carotid artery (ICA) aneurysm 48 hours after the procedure. This 28-year female presented with giant wide-necked right supraclinoid ICA aneurysm which was managed by flow diversion. On 2nd post-op day, patient developed weakness of left side with altered sensorium - angiography and CT showed kinking of flow diverter at the neck of the aneurysm with poor distal flow. Eventually, the patient developed right middle cerebral artery infarct for which decompressive hemicraniectomy was done. The likely cause of development of kink is because the aneurysm was wide-necked, the hemodynamic forces have resulted in inward buckling of the flow diverter at the aneurysm neck. This case shows that kinking of flow diverter can still happen 48 hours post-procedure.

Background An understanding of the natural history of unruptured intracranial aneurysms (IAs) has always played a critical role in presurgical or endovascular planning, to avoid possibly fatal events. Size, shape, morphology, and location are known risk factors for rupture of an aneurysm, but morphologic parameters alone may not be sufficient to perform proper rupture risk stratification. Methods We performed a systematic PubMed search and focused on hemodynamics forces that may influence aneurysmal initiation, growth, and rupture. Results We included 223 studies describing several hemodynamic parameters related to aneurysm natural history. In these studies, different modalities of aneurysm model creation have been used to evaluate flow and to comprehensively analyze the evolution of IAs. Controversy exists about the correlation between these parameters and initiation, growth, rupture risk, or stabilization of the aneurysmal sac. Recent findings have also shown the importance of flow patterns in this process and the relationship between unruptured IA geometry and hemodynamic parameters. Conclusions The role of hemodynamic forces in evaluation of the natural history of unruptured IAs presents is inherently complex and is still not completely understood. In this complex scenario, although several attempts have been described in the literature, a proper risk rupture stratification and treatment strategy selection based on hemodynamic forces has not yet been created. Further efforts should be made to accomplish this important goal. © 2017 Elsevier Inc.

Thromboembolic events are some of the major causes of death in the United States They must be carefully monitored in persons who are susceptible to thrombus formation due to hypercoagulability problems which may arise as a result of surgery or diseases such as sickle cell anemia thalassemia leukemia and diabetes Successful diagnosis and treatment of thrombosis pose a real challenge to the medical field and there exists an urgency to develop more sophisticated methods for countering this condition When thrombi detaches from the vessel wall patients are at great risk of stroke events and even death In an effort to gain a better understanding with regard to the thrombus to embolus transition we have performed simulations through CFD ACE computational engine in which we vary thrombus height shape location along the vessel wall blood pressure and blood viscosity Results of this simulation model suggest a higher likelihood for the thrombus to embolus transition as the thrombus height increases Results also show that a thrombus is more likely to become mobile in hypertensive patients but is less likely to become mobile in sickle cell diabetic and leukemic patients This we explain is due to higher blood viscosities in these patients which result in lowered wall shear stresses In addition we confirm the hypothesis that clot shape influences the occurrence of the thrombus to embolus transition as pressure on the clot is shown to be substantially greater in radially asymmetric thrombi Pressure profiles also suggest that prolonged exposure to high pressure as in hypertension increases the probability of initiation of the transition as the clot becomes fatigued and weakens resulting in the completion of the thrombus to embolus transition when the hemodynamic forces overcome the adhesive forces in the system Finally we propose a ldquo peel off rdquo type mechanism as an explanation of the process of transitioning from a thrombus to an embolus

Criteria for rupture prediction of Abdominal Aortic Aneurysm (AAA) are based only on the diameter of AAA. This method does not consider complex hemodynamic forces exerted on AAA wall. The methodology used in our study combines Computer-Aided Design (CAD) with Computational Fluid Dynamics (CFD). Three-dimensional vascular structures reconstructions were based on Computed Tomography (CT) images and CAD. CFD theory was used for mathematical modeling and simulations. In this way, dynamic behavior of blood flow in bounded three-dimensional space was described. Doppler Ultrasonography (US) was used for model results validation. All simulations were based on medical investigation of 4 patients (male older than 65years) with diagnosed AAA. Good correspondence between computed velocities in AAA and measured values with Doppler US (Patient 1 0.60m·s-1 versus 0.61m·s-1, Patient 2 0.80m·s-1 versus 0.80m·s-1, Patient 3 0.75m·s-1 versus 0.78m·s-1, Patient 4 0.50m·s-1 versus 0.49m·s-1) was noticed. The good agreement between measured and simulated velocities validates our methodology and the other data available from simulations (eg. von Misses stress) could be used to provide useful information about the possibility of AAA rupture.

Incorporation of aortic arch vessels with fenestrated and branched stent grafts is the last frontier for total endovascular repair of complex aortic aneurysms. The arch poses significant challenges because of its curved and angulated anatomy, proximity to the aortic valve and coronary arteries, variable anatomy of the supra-aortic trunks, and significant hemodynamic forces. Since the first repairs done with branched and fenestrated endografts, there has been increasing clinical experience and improvements in device designs. Novel developments have focused on the development of off-the-shelf designs based on branch technology. Clinical investigations are under way by several stent manufacturers using stents intended to extend the landing to zone 0 (proximal arch) and zone 2 (distal arch). This chapter summarizes some of the device specifications and indications for use.

The arteriovenous fistula (AVF) is the preferred form of vascular access for maintenance hemodialysis, but it often fails to mature to become clinically usable, likely due to aberrant hemodynamic forces. A robust pipeline for serial assessment of hemodynamic parameters and subsequent lumen cross-sectional area changes has been developed and applied to a data set from contrast-free MRI of a dialysis patient's AVF collected over a period of months after AVF creation surgery. Black-blood MRI yielded images of AVF lumen geometry, while cine phase-contrast MRI provided volumetric flow rates at the in-flow and out-flow locations. Lumen geometry and flow rates were used as inputs for computational fluid dynamics (CFD) modeling to provide serial wall shear stress (WSS), WSS gradient, and oscillatory shear index (OSI) profiles. The serial AVF lumen geometries were co-registered at 1 mm intervals using respective lumen centerlines, with the anastomosis as an anatomical landmark. Lumen enlargement was limited at the vein region near the anastomosis and a downstream vein valve, potentially attributed to the physical inhibition of wall expansion at those sites. This work is the first serial and detail study of lumen and hemodynamic changes in human AVF using MRI and CFD. This novel protocol will be used for a multicenter prospective study to identify critical hemodynamic factors that contribute to AVF maturation failure.

Although vein bypass grafting is one of the primary options for the treatment of arterial occlusive disease and provides satisfactory results at an early stage of the treatment, the patency is limited to a few months in many patients. When the vein is implanted in the arterial system, it adapts to the high flow rate and high pressure of the arterial environment by changing the sizes of its layers, and this remodeling is believed to be a precursor of future graft failure. Hemodynamic forces, such as wall shear stress (WSS) and wall tension, have been recognized as major factors impacting vein graft remodeling. Although a wide range of experimental evidence relating hemodynamic forces to vein graft remodeling has been reported, a comprehensive mathematical model describing the relationship among WSS, wall tension, and the structural adaptation of each individual layer of the vein graft wall is lacking. The current manuscript presents a comprehensive and robust framework for treating the complex interaction between the WSS, wall tension, and the structural adaptation of each individual layer of the vein graft wall. We modeled the intimal and medial area and the radius of external elastic lamina, which in combination dictate luminal narrowing and the propensity for graft occlusion. Central to our model is a logistic relationship between independent and dependent variables to describe the initial increase and later decrease in the growth rate. The detailed understanding of the temporal changes in vein graft morphology that can be extracted from the current model is critical in identifying the dominant contributions to vein graft failure and the further development of strategies to improve their longevity.

Cerebral aneurysms are commonly named based on their relationship with adjacent vessels in either the anterior or posterior circulation. Although such an approach has long proved useful, this terminology does not take into account potential hemodynamic forces or aneurysm wall properties that are likely to be important for cerebral aneurysm formation, growth, rupture, and treatment. Dissecting, traumatic, false, infectious, and tumorous aneurysms were excluded from review. Only aneurysms in which preoperative imaging studies and operative findings were sufficient for classification were included. All 329 reviewed aneurysms could be divided into 2 groups: fusiform (n=16) and saccular (n=313). Fusiform aneurysms could be subdivided into 2 types: simple (no branch vessel; n=10) and complex (one or more side branches; n=6). Saccular aneurysms could be subdivided into 3 groups: those not associated with a branch vessel (n=31), those associated with a side-branch vessel (n=125), and those located at a bifurcation (n=157). Each of these categories of aneurysms could be classified further based on its association with a conducting, primary, secondary, tertiary, or side-branch vessel. Classification of cerebral aneurysms according to this scheme adequately described all reviewed aneurysms. Grouping aneurysms according to this approach focuses on similarities in angioarchitecture and potential rheologic properties that should prove useful for evaluation of aneurysm growth, rupture, and treatment.

Coronary atherosclerosis has long been recognized with high morbidity and mortality worldwide. The main cause of this group of diseases is thrombosis, resulting in insufficient oxygen perfusion by the blood to various organs in the body, thereby causing tissue necrosis. Dysfunction of vascular endothelial cell (ECs) is the major cause of atherosclerosis and thrombosis. Hemodynamic abnormalities are one of the many factors causing endothelial dysfunction. Shear stress and cyclic stretch are two major hemodynamic forces generated by pulsatile blood flow and pressure in the arterial vasculature. When hemodynamic abnormalities occur, endothelial dysfunction follows, this ultimately leads to atherosclerosis and thrombosis. Our objective, therefore, was to design and construct an unique hemodynamic equipment described herein. This hemodynamic device can concurrently produce shear stress and cyclic stretch to vascular ECs in vitro, and thus their morphological changes in response to simultaneous exposure to shear stress and cyclic stretch can be visualized in real-time via microscopy.

Coronary plaque disruption with superimposed thrombosis is the underlying pathology in the acute coronary syndromes and sudden death. Coronary plaques are constantly stressed by a variety of mechanical and hemodynamic forces that may precipitate or 'trigger' disruption of vulnerable or, at extreme conditions, even stable plaques. This paper reviews the exciting new evidence on the hemodynamic factors that may play a role in this process and provides the rationale for the introduction of the concept of the vulnerable coronary segment in the study of acute coronary syndromes.

While hemodynamic forces and intraluminal thrombus (ILT) are believed to play important roles on abdominal aortic aneurysm (AAA), it has been suggested that hemodynamic forces and ILT also interact with each other, making it a complex problem. There is, however, a pressing need to understand relationships among three factors: hemodynamics, ILT accumulation, and AAA expansion for AAA prognosis. Hence this study used longitudinal computer tomography scans from 14 patients and analyzed the relationship between them. Hemodynamic forces, represented by wall shear stress (WSS), were obtained from computational fluid dynamics; ILT accumulation was described by ILT thickness distribution changes between consecutives scans, and ILT accumulation and AAA expansion rates were estimated from changes in ILT and AAA volume. Results showed that, while low WSS was observed at regions where ILT accumulated, the rate at which ILT accumulated occurred at the same rate as the aneurysm expansion. Comparison between AAAs with and without thrombus showed that aneurysm with ILT recorded lower values of WSS and higher values of AAA expansion than those without thrombus. Findings suggest that low WSS may promote ILT accumulation and submit the idea that by increasing WSS levels ILT accumulation may be prevented.

Unruptured intracranial aneurysms are frequently and incidentally discovered with noninvasive imaging and the decision for preventive treatment is supported by epidemiologic and statistics data, lacking personalized argumentation about individual aneurysm behavior and inflammatory status of its wall. After a review of hemodynamic forces leading to aneurysm genesis and interaction with inflammation onset within aneurysmal wall, we will successively detail routine imaging methods for the aneurysmal wall and their respective contribution. Then, we will draw up the inventory of different experimental imaging and in vitro methods for future investigation of the aneurysmal wall. We emphasize the need for cooperation with various specialties: histopathology, genetics, and immunology in order to understand the natural history of the aneurysmal sac leading most often to stability but elsewhere to aneurysmal growth, thrombosis or rupture. A description of a research protocol devoted to aneurysmal wall inflammation and recently accepted in our university is introduced.

Background Adverse cardiac remodeling is a key component of the failing heart. Increased diastolic wall stress plays a pivotal role in the development and progression of adverse cardiac remodeling. The forces generated by the left ventricular (LV) myocardium initiate blood flow, while the moving blood itself also exerts a force on the ventricular wall and heart valves. Abnormal hemodynamic forces may contribute to increased diastolic wall stress. We calculated LV hemodynamic forces from the moving blood, and hypothesized that these forces are mostly directed along the “mitral valve (MV) to apex axis” in the healthy LV, while the distribution is altered in myopathic LVs.

This review is based on recently published data from our laboratory. We investigated the relationship between local hemodynamic forces and intimal and medial remodeling in the proximal and distal segments of the arterial walls of rats in relation to severe infradiaphragmatic stenosis of the aorta. Our findings support the plausible hypothesis that aorta remodeling induced by stretch as a consequence of hypertension in contrast to aorta remodeling induced by turbulent flow/low wall shear stress are distinctly different biological phenomena mediated through different mechanisms.

Atherosclerosis complicated by plaque rupture or disruption and thrombosis is primarily responsible for the development of acute coronary syndromes. Plaques with a large extracellular lipid-rich core, thin fibrous cap due to reduced collagen content and smooth muscle density, and increased numbers of activated macrophages and mast cells, appear to be vulnerable to rupture. Plaque disruption tends to occur at points at which the plaque surface is weakest and most vulnerable, which coincide with points at which stresses, resulting from biomechanical and hemodynamic forces acting on plaques, are concentrated. Reduced matrix synthesis as well as increased matrix degradation predisposes vulnerable plaques to rupture in response to extrinsic mechanical or hemodynamic stresses. Modification of endothelial dysfunction and reduction of vulnerability to plaque rupture and thrombosis may lead to plaque stabilization. The broad concept of plaque stabilization, although attractive, has not yet been rigorously validated in humans. This article reviews the mechanism of atherosclerosis development and the pathophysiology of acute coronary syndromes in order to provide a molecular and cellular basis for understanding how plaque passivation might be accomplished in clinical medicine.

Coronary atherosclerosis complicated by plaque rupture or disruption and thrombosis is primarily responsible for the development of acute coronary syndromes. Plaques with a large extracellular lipid-rich core, a thin fibrous cap due to reduced collagen content and smooth muscle density, and increased numbers of activated macrophages and mast cells appear to be vulnerable to rupture. Plaque disruption tends to occur at points at which the plaque surface is weakest and most vulnerable, which coincide with points at which stresses resulting from biomechanical and hemodynamic forces acting on plaques are concentrated. Reduced matrix synthesis as well as increased matrix degradation predisposes vulnerable plaques to rupture in response to extrinsic mechanical or hemodynamic stresses. Modification of endothelial dysfunction and reduction of vulnerability to plaque rupture and thrombosis may lead to plaque stabilization. These concepts have significant clinical implications that are just beginning to be explored and incorporated into clinical practice. This article reviews the mechanism of coronary atherosclerosis development and the pathophysiology of acute coronary syndromes to provide a framework for understanding how plaque passivation might be accomplished in clinical medicine.

Vascular adaptation following local injury occurs through a combination of intimal hyperplasia and wall (inward/outward) remodeling. Over the past two decades, researchers have applied a wide variety of approaches to investigate neointimal hyperplasia and vascular remodeling in an effort to identify novel therapeutic strategies. However, despite incremental progress over these decades, specific cause/effect links between hemodynamic factors, inflammatory biochemical mediators, cellular effectors, and vascular occlusive phenotype remain lacking.

Background and Purpose— Flow-induced hemodynamic forces are critical in extra- and intracranial arterial caliber regulation and have been proposed to mediate intracranial aneurysm (IA) formation and rupture. We hypothesized that vascular structural control may be impaired in patients harboring brain aneurysms and sought to examine any differences in extradural internal carotid artery (ICA) caliber profiles. Methods— Ninety-six catheter 2-dimensional angiograms were divided into 3 subgroups: (1) ICA leading to IA (n=38), (2) matched contralateral ICA (n=25), and (3) ICA from nonaneurysmal controls (n=33). ICA diameter was measured proximally beyond the bulb ( D Prox ) and distally at the extradural point of maximal dilation ( D MaxDist ), yielding maximal distal-to-proximal ratio ( R Mdp ). Results— Unlike non-IA controls that tapered smoothly, ICAs leading to IA consistently demonstrated focal sites of abnormal dilation in the distal cervical or petrous extradural segments. R Mdp was greater in ICAs leading to IA compared with non-IA controls (1.17±0.1 versus 1.0±0.08; P R Mdp to be higher in ICAs leading to IA than the corresponding contralateral ICAs (1.19±0.1 versus 1.07±0.11; P =0.001); R Mdp from contralateral ICAs was greater than non-IA controls ( P =0.005). Among ICAs leading to IA, women showed higher R Mdp (1.11±0.12 versus 1.05±0.11; P =0.02) with no relationship to intradural IA location. Conclusions— Measurements of the extradural ICA in patients harboring intradural IA suggest an association with a remote upstream abnormal vascular caliber control consistent with a diffuse flow–mediated structural dysregulation showing laterality and sex dependence.

Once an arteriovenous fistula is established, the blood vessels are subjected to marked changes in hemodynamic forces that trigger remodeling to re-establish baseline parameters of sheer and hoop stress. These homeostatic processes culminate in two requirements that define an adequate and enduring access. First, blood flow must increase to provide amounts that will provide adequate delivery of blood to the artificial kidney. Second, the vessel wall must undergo changes that will allow it to withstand repeated cannulation. Hence, a fistula is mature when it can do what it sets out to do (flow readiness) despite what is being done to it (cannulation readiness). Although flow has been measured with Doppler, high-frequency ultrasound is needed to measure vessel wall thickness to determine hoop stress. Beyond the wall of the vessel, the concept of cannulation readiness depends on the skill and expertise of the cannulator.

The bicuspid aortic valve (BAV) is the most common congenital valvular defect and a major risk factor for secondary calcific aortic valve disease. While hemodynamics is presumed to be a potential contributor to this complication, the validation of this theory has been hampered by the limited knowledge of the mechanical stress abnormalities experienced by BAV leaflets and their dependence on the heterogeneous BAV fusion patterns. The objective of this study was to compare computationally the regional and temporal fluid wall shear stress (WSS) and structural deformation characteristics in tricuspid aortic valve (TAV), type-0, and type-I BAV leaflets. Arbitrary Lagrangian-Eulerian fluid-structure interaction models were designed to simulate the flow and leaflet dynamics in idealized TAV, type-0, and type-I BAV geometries subjected to physiologic transvalvular pressure. The regional leaflet mechanics was quantified in terms of temporal shear magnitude (TSM), oscillatory shear index (OSI), temporal shear gradient (TSG), and stretch. The simulations identified regions of WSS overloads and increased WSS bidirectionality (174% increase in temporal shear magnitude, 0.10 increase in OSI on type-0 leaflets) in BAV leaflets relative to TAV leaflets. BAV leaflets also experienced larger radial deformations than TAV leaflets (4% increase in type-0 BAV leaflets). Type-I BAV leaflets exhibited contrasted WSS environments marked by WSS overloads on the non-coronary leaflet and sub-physiologic WSS levels on the fused leaflet. This study provides important insights into the mechanical characteristics of BAV leaflets, which may further our understanding of the role played by hemodynamic forces in BAV disease. Copyright © 2016 John Wiley & Sons, Ltd.

We hypothesized that the direction of global left ventricular (LV) hemodynamic forces during diastolic filling are concordant with the main flow axes in normal LVs, but that this pattern would be altered in dilated and dysfunctional LVs. Therefore, we aimed to assess the LV hemodynamic filling forces in a group of healthy subjects and compare them to the results from a group of patients with dilated cardiomyopathy (DCM). Ten healthy subjects and 10 DCM patients were enrolled. Morphological short‐ (SAx) and long‐axis (LAx) images and 4D flow MRI data were acquired at 1.5T. The LV pressure gradients were computed from the 4D flow data using the Navier–Stokes equations. By integrating the pressure gradients over the LV volume at each time frame, the magnitude and direction of the global hemodynamic force was calculated over the cardiac cycle. The hemodynamic forces acting in the SAx‐ and LAx‐directions were used to calculate the “SAx‐max/LAx‐max”‐ratio for the early (E‐wave) and late (A‐wave) diastolic filling. In the LAx‐plane, the temporal progression of the hemodynamic force followed a consistent pattern in the healthy subjects. The “SAx‐max/LAx‐max”‐ratio was significantly larger at both E‐wave (0.53 ± 0.15 vs. 0.23 ± 0.12, P

The aim of the present work is to quantitatively assess the three-dimensional distributions of the displacements experienced during the cardiac cycle by the luminal boundary of abdominal aortic aneurysm (AAA) and to correlate them with the local bulk hemodynamics. Ten patients were acquired by means of time resolved computed tomography, and each patient-specific vascular morphology was reconstructed for all available time frames. The AAA lumen boundary motion was tracked, and the lumen boundary displacements (LBD) computed for each time frame. The intra-aneurysm hemodynamic quantities, specifically wall shear stress (WSS), were evaluated with computational fluid dynamics simulations. Co-localization of LBD and WSS distributions was evaluated by means of Pearson correlation coefficient. A clear anisotropic distribution of LBD was evidenced in both space and time; a combination of AAA lumen boundary inward- and outward-directed motions was assessed. A co-localization between largest outward LBD and high WSS was demonstrated supporting the hypothesis of a mechanistic relationship between anisotropic displacement and hemodynamic forces related to the impingement of the blood on the lumen boundary. The presence of anisotropic displacement of the AAA lumen boundary and their link to hemodynamic forces have been assessed, highlighting a new possible role for hemodynamics in the study of AAA progression.

Intracranial aneurysms and artery stenosis are vascular diseases with different pathophysiological characteristics. However, although unusual, aneurysms may coexist in up to 5% of patients with stenotic plaque, according to a previous study. Another study showed that incidental detection of cerebral aneurysm in the same cerebral circulation as the stenotic plaque was less than 2%. Patients with concomitant carotid artery stenosis and unruptured intracranial aneurysms pose a difficult management decision for the physician. Case reports showed patients who died due to aneurysm rupture months after endarterectomy but before aneurysm clipping, while others did not show any change in the aneurysm after plaque removal, having optimum outcome after aneurysm coiling. The purpose of this study is to investigate the intraaneurysmal hemodynamic changes before and after treatment of stenotic plaque. Idealized models were constructed with different stenotic grade, distance and relative position to the aneurysm. Digital removal of the stenotic plaque was performed in the reconstructed model of a patient with both pathologies. Computational fluid dynamic simulations were performed using a finite element method approach. Blood velocity field and hemodynamic forces were recorded and analyzed. Changes in the flow patterns and wall shear stress values and distributions were observed in both ideal and image-based models. Detailed investigation of wall shear stress distributions in patients with both pathologies is required to make the best management decision.

Between half and two thirds of human mortality in developed countries can be attributed to vascular diseases. Financial losses, human sufferings are increasing with aging of the population. Vascular diseases develop when some or many vessels in the body are unable to fulfill their functions. The main function of blood vessels is essentially a mechanical one: to conduct blood. Vessels are functioning in a unique in the body mechanical environment: they are continuously subjected to hemodynamic forces: to shear stress of flowing blood and to distending forces of pressure of the blood in the lumen. Vessels are so much adapted to these hemodynamic forces that it is impossible to understand their physiology, pharmacology and pathology without taking into consideration the unavoidable biomechanical steps in the complicated pathways of cellular and systemic physiological vascular feed-back control loops, to understand vascular drug action and pathomechanism of vascular disease (Lee 2000). Biomechanics is thus at the very core of all vascular sciences. That is reflected in the high number of papers published in the area. 35 000 papers listed in the Ovid Medline between 1948 and 2010 included knowledge on vascular mechanics in its narrower sense (excluding papers dealing only with physiological and pharmacological means of vascular smooth muscle control). Deteriorating Windkessel function of the aged, of the chronic hypertensive, even after effective treatment of mean arterial pressure, geometric, biomechanical consequences of atheroscerotic focal remodeling of large arteries, contractile and elastic remodeling of resistance arteries with aging, with hypertension and with diabetes, remodeling of venous networks and the venous wall in chronic venous disease, inevitably draws the attention of clinicians and of pathologists to biomechanical questions. Recent developments in vascular mechanics, backed with many methodical improvements in the field (Berczi 2005, Cox 1974, Duling 1981, Huotari 2010, Mersich 2005, Nadasy 2001, Shimazu 1986, See Fig. 1.), integration of these results into the context of reliable older knowledge makes now a systemic overview of the most important aspects of vascular mechanics possible. We will see that an almost axiomatic approach to a phenomenological description of vascular biomechanics is now in sight. Methodical advancement in the field of cellular physiology, histochemistry and biochemistry (Discher 2009) identified many if not all extraand intracellular fiber types and molecules contributing to the biomechanics of the vascular wall. Mechanical factors in intraand extracellular fiber protein expression control are just being identified. The emerging debate whether mechanics or biochemistry controls vascular

BACKGROUND AND PURPOSE: Cerebral aneurysms are preferentially located at arterial curvatures and bifurcations that are exposed to major hemodynamic forces, increasingly implicated in the life cycle of aneurysms. By observing the natural history of aneurysm formation from its preaneurysm state, we aimed to examine the hemodynamic microenvironment related to aneurysm initiation at certain arterial segments later developing an aneurysm. MATERIALS AND METHODS: The 3 patients included in the study underwent cerebral angiography with 3D reconstruction before a true aneurysm developed. The arterial geometries obtained from the 3D-DSA models were used for flow simulation by using finite-volume modeling. The WSS and SWSSG at the site of the future aneurysm and the flow characteristics of the developed aneurysms were analyzed. RESULTS: The analyzed regions of interest demonstrated significantly increased WSS, accompanied by an increased positive SWSSG in the adjacent proximal region. The WSS reached values of >5 times the temporal average values of the parent vessel, whereas the SWSSG approximated or exceeded peaks of 40 Pa/mm in all 3 cases. All patients developed an aneurysm within 2 years, 1 of which ruptured. CONCLUSIONS: The results of this hemodynamic study, in accordance with the clinical follow-up, suggest that the combination of high WSS and high positive SWSSG focused on a small segment of the arterial wall may have a role in the initiation process of aneurysm formation.

Submitted by Guilherme Lemeszenski (guilherme@nead.unesp.br) on 2013-08-22T18:43:28Z No. of bitstreams: 1 S1677-54492010000200009.pdf: 342467 bytes, checksum: 0c110f43128cf44aef6833fe22a0ca71 (MD5) Made available in DSpace on 2013-08-22T18:43:28Z (GMT). No. of bitstreams: 1 S1677-54492010000200009.pdf: 342467 bytes, checksum: 0c110f43128cf44aef6833fe22a0ca71 (MD5) Previous issue date: 2010-06-01 Made available in DSpace on 2013-09-30T18:16:34Z (GMT). No. of bitstreams: 2 S1677-54492010000200009.pdf: 342467 bytes, checksum: 0c110f43128cf44aef6833fe22a0ca71 (MD5) S1677-54492010000200009.pdf.txt: 50919 bytes, checksum: dfdd3d72ff1f5a410aa096be759dcb5e (MD5) Previous issue date: 2010-06-01 Submitted by Vitor Silverio Rodrigues (vitorsrodrigues@reitoria.unesp.br) on 2014-05-20T13:32:48Z No. of bitstreams: 2 S1677-54492010000200009.pdf: 342467 bytes, checksum: 0c110f43128cf44aef6833fe22a0ca71 (MD5) S1677-54492010000200009.pdf.txt: 50919 bytes, checksum: dfdd3d72ff1f5a410aa096be759dcb5e (MD5) Made available in DSpace on 2014-05-20T13:32:48Z (GMT). No. of bitstreams: 2 S1677-54492010000200009.pdf: 342467 bytes, checksum: 0c110f43128cf44aef6833fe22a0ca71 (MD5) S1677-54492010000200009.pdf.txt: 50919 bytes, checksum: dfdd3d72ff1f5a410aa096be759dcb5e (MD5) Previous issue date: 2010-06-01 A migração da endoprótese é complicação do tratamento endovascular definida como deslocamento da ancoragem inicial. Para avaliação da migração, verifica-se a posição da endoprótese em relação a determinada região anatômica. Considerando o aneurisma da aorta abdominal infrarrenal, a área proximal de referência consiste na origem da artéria renal mais baixa e, na região distal, situa-se nas artérias ilíacas internas. Os pacientes deverão ser monitorizados por longos períodos, a fim de serem identificadas migrações, visto que estas ocorrem normalmente após 2 anos de implante. Para evitar migrações, forças mecânicas que propiciam fixação, determinadas por características dos dispositivos e incorporação da endoprótese, devem predominar sobre forças gravitacionais e hemodinâmicas que tendem a arrastar a prótese no sentido caudal. Angulação, extensão e diâmetro do colo, além da medida transversa do saco aneurismático, são importantes aspectos morfológicos do aneurisma relacionados à migração. Com relação à técnica, não se recomenda implante de endopróteses com sobredimensionamento excessivo (> 30%), por provocar dilatação do colo do aneurisma, além de dobras e vazamentos proximais que também contribuem para a migração. Por outro lado, endopróteses com mecanismos adicionais de fixação (ganchos, farpas e fixação suprarrenal) parecem apresentar menos migrações. O processo de incorporação das endopróteses ocorre parcialmente e parece não ser suficiente para impedir migrações tardias. Nesse sentido, estudos experimentais com endopróteses de maior porosidade e uso de substâncias que permitam maior fibroplasia e aderência da prótese à artéria vêm sendo realizados e parecem ser promissores. Esses aspectos serão discutidos nesta revisão. Migration of the endoprosthesis is defined as the misplacement of its initial fixation. To assess the migration, the position of the endoprosthesis regarding a certain anatomic region is verified. Considering the aneurysm of the infrarenal abdominal aorta, the proximal area of reference is the origin of the lowest renal artery and, at the distal region, it is located next to the internal iliac arteries. Patients should be monitored for long periods so that migrations can be identified; these migrations usually occur 2 years after the implantation. To avoid migrations, mechanical forces that enable fixation and that are determined by the characteristics of the devices and by the incorporation of the endoprosthesis should predominate over gravitational and hemodynamic forces, which tend to drag the prosthesis toward to caudal direction. Angulation, extension, and diameter of the neck, and transversal measure of the aneurysmatic sac are important morphological aspects related to migration. In relation to the technique, endoprosthesis implantation with excessive oversizing (> 30%) is not recommended because it leads to aortic neck dilatation, folds and proximal leakage that also contribute to migration. on the other hand, endoprosthesis with additional fixation devices (hooks, barbs and suprarenal fixation) seem to be less associated with migration. The process of endoprosthesis incorporation is partial and does not seem to be enough to prevent later migrations. In this sense, experimental studies with endoprosthesis of higher porosity, as well as the use of substances that allow higher fibroplasia and adherence of the prosthesis to the artery, have been conducted and are promising. Such aspects are discussed in the present review of the literature. Faculdade de Medicina de Marília UNESP FMB Departamento de Cirurgia e Ortopedia UNESP FMB Departamento de Cirurgia e Ortopedia

Eczematous dermatitis was found in two port wine stain (PWS) lesions in two different individuals following variable pulsed 532-nm laser therapy. Both of the individuals described in this report had received low-dose superficial X-ray several years prior to the development of the eczematous dermatitis. The eczematous dermatitis in the PWS lesions was characterized by oozing, crusting, and pruritus, which showed a tendency to expand to other sites when exacerbated. Treatment with topical corticosteroid ointments produced some temporary improvement, but the dermatitis in both cases recurred when the topical medications were stopped. The mechanism of action for the development of an eczematous dermatitis in a PWS remains unclear, but may be related to multiple factors including abnormal hemodynamic forces resulting from the malformed vessels, an abnormal production of cytokines, local pathophysiological and immunological changes resulting from either the X-ray therapy or the laser therapy, and atopic constitution inherent in these individuals. These hypotheses and ideas need further study for additional insight into this rare, but reported adverse event.

The first commercially available stent grafts were unable to withstand the hemodynamic forces of the vascular environment. The past 15 years have seen a gradual improvement in long-term stent graft performance as designs evolved through the elimination of features associated with late failure and the replication of features associated with durable success. Clinical experience provides the following principles on which to base device design and implantation techniques. Few patients have an adequate length of non-dilated aorta distal to the aneurysm to allow implantation of an aorto-aortic stent graft; bifurcated stent grafts are usually required for AAA repair. Friction, column strength and tissue ingrowth do not prevent migration of the stent graft from its attachment within the neck into the aneurysm; some form of active fixation is required, usually in the form of barbs. Any movement between the apex of a stent and the overlying graft material will erode the fabric; stents and grafts need to move as a single unit. Nitinol is versatile, but fragile; Nitinol components must be polished to eliminate all surface irregularities and they cannot be subjected to compression loading, or excessive pulsatile movement. The neck of an aneurysm is unstable; it will dilate unless protected by a securely fixed, non-compliant stent graft. The aneurysm does not heal; freedom from risk of rupture depends on durable depressurization of the sac. The sole objective of image-based follow-up is the early detection, and catheter-based correction, of device failure. Once any given design has been in use long enough to identify its failure modes, the frequency of follow-up studies can be adjusted accordingly. However, it takes a long time to identify all the potential forms of late failure, and pre-clinical testing remains an imprecise science. New, or recently modified, devices cannot necessarily be assumed to be as durable as their predecessors.

Although local hemodynamic forces are widely believed to play a role in aneurysm pathogenesis, the hemodynamic mechanisms have not been confirmed in a prospective manner. Ideally, one would identify the patient-specific vessel that is prone to aneurysm formation and follow it longitudinally to investigate the associated aneurysm formation factors or mechanisms. However, such studies are not practical in humans, and so the knowledge to predict aneurysm formation at a specific location, a priori, is not available.Copyright © 2009 by ASME

Hemodynamics is important in the formation, growth and rupture of the cerebral aneurysm. The treatments in the patients with aneurysm are closely related to the hemodynamic behaviors. However, clinical image studies and observations can’t provide enough information needed during the surgery such as the hemodynamic forces that exert on the wall of the aneurysm. Therefore the goal of this research is to simulate the vascular flow field in patients with cerebral aneurysm, and guide clinicians to choose the best treatment method for aneurysm.