Turbulence significantly increases pressure and fluid shear stress in an aortic aneurysm model under resting and exercise flow conditions

The numerical models of abdominal aortic aneurysm (AAA) in use do not take into account the non-Newtonian behavior of blood and the development of local turbulence. This study examines the influence of pulsatile, turbulent, non-Newtonian flow on fluid shear stresses and pressure changes under rest and exercise conditions. We numerically analyzed pulsatile turbulent flow, using simulated physiological rest and exercise waveforms, in axisymmetric-rigid aortic aneurysm models (AAMs). Discretization of governing equations was achieved using a finite element scheme. Maximum turbulence-induced shear stress was found at the distal end of an AAM. In large AAMs (dilated to undilated diameter ratio = 3.33) at peak systolic flow velocity, fluid shear stress during exercise is 70.4% higher than at rest. Our study provides a numerical, noninvasive method for obtaining detailed data on the forces generated by pulsatile turbulent flow in AAAs that are difficult to study in humans and in physical models. Our data suggest that increased flow turbulence results in increased shear stress in aneurysms. While pressure readings are fairly uniform along the length of an aneurysm, the kinetic energy generated by turbulence impacting on the wall of the distal half of the aneurysm increases fluid and wall shear stress at this site. If the increased fluid shear stress results in further dilation and hence further turbulence, wall stress may be a mechanism for aneurysmal growth and eventual rupture.     

Wall shear stress and strain modulate experimental aneurysm cellularity

OBJECTIVE: Clinical evidence indicates that hemodynamic conditions influence abdominal aortic aneurysm (AAA) disease. We modified blood flow to evaluate the effects of wall shear stress (WSS) and relative wall strain (RWS) on aneurysm structure and cellularity. METHODS: Rodent AAAs were created with porcine pancreatic elastase infusion. In group 1 AAA WSS was increased with left femoral arteriovenous fistula creation, whereas in group 2 AAA WSS was decreased with left iliac artery ligation. Aortic flow, wall motion, and blood pressure were recorded in both groups. AAA diameter, endothelial and smooth muscle cellularity (CD31 and alpha-smooth muscle actin immunostaining), markers for cell proliferation (5-bromodeoxyuridine), endothelial and smooth muscle cell growth factor production (vascular endothelial growth factor-D and platelet-derived growth factor-beta, respectively), and apoptosis (deoxyuridine triphosphate nick end-labeled [TUNEL] stain) were compared between groups when the animals were killed. RESULTS: Arteriovenous fistula creation increased WSS (high-flow AAA) by 300% and RWS by 150%. Iliac ligation reduced WSS (low-flow AAA) by 60%. Neither procedure significantly altered systolic, diastolic, or mean aortic pressure. When the animals were killed 7 days after elastase infusion, low-flow AAAs were significantly larger than high-flow AAAs. High-flow AAAs also contained more endothelial cells and smooth muscle cells, and evidence of increased growth factor production, cell proliferation, and decreased apoptosis. No difference in type or severity of AAA inflammatory cell infiltrate was noted between groups. CONCLUSIONS: High flow conditions stimulate endothelial cell and smooth muscle cell proliferation in experimental aneurysms. Enhanced cellularity may stabilize aortic integrity, limiting aneurysm growth. Increased lower extremity activity may prevent or retard AAA disease through salutary effects on aortic remodeling mediated by endothelial cells and smooth muscle cells.     

Hemodynamic Changes Occurring during the Progressive Enlargement of Abdominal Aortic Aneurysms

The purpose of this study is to characterize the evolution of the hemodynamic forces acting on the arterial walls at progressive stages of enlargement of abdominal aortic aneurysms (AAA). The specific aims are twofold: first, to determine the magnitude of the wall shear stresses (WSS) and their spatial and temporal gradients at various stages of enlargement, and second, to identify the critical size at which the formation of regions of stasis and/or the transition to a turbulent state occur inside the AAA. A parametric in vitro study of the pulsatile blood flow was conducted in rigid models of AAA by systematically varying the hemodynamic conditions and the size of the aneurysm. The instantaneous flow characteristics inside the AAA models were measured along the cardiac cycle, using tomographic digital particle image velocimetry (TDPIV). The TDPIV measurements showed that even for the case of large dilatation ratios (internal diameter >4.5 mm), the flow inside the AAA remained fully attached to the walls during systole, but massively detached during diastole. A critical aneurysm aspect ratio (length-to-diameter ratio) was found, for which a transition to a turbulent state occurred. The formation of internal shear layers (internal jet) and slowly recirculating regions (stasis) generated large spatial gradients of WSS and regions of low and oscillating WSS. The formation of regions of flow stasis was observed even at very early stages in the aneurysm enlargement. These spatial and temporal variations in the hemodynamic forces, the formation of regions of stasis, and the transition to turbulence are postulated to play an important role in the etiology of the disease by activating endoluminar thrombus formation, lipid deposition, and certain inflammatory mechanisms. Presented at the Annual Meeting of the Southern California Vascular Surgical Society, Carlsbad, CA, April 11-13, 2003.     

In vivo analysis of mechanical wall stress and abdominal aortic aneurysm rupture risk

OBJECTIVE: The purpose of this study was to calculate abdominal aortic aneurysm (AAA) wall stresses in vivo for ruptured, symptomatic, and electively repaired AAAs with three-dimensional computer modeling techniques, computed tomographic scan data, and blood pressure and to compare wall stress with current clinical indices related to rupture risk. METHODS: CT scans were analyzed for 48 patients with AAAs: 18 AAAs that ruptured (n = 10) or were urgently repaired for symptoms (n = 8) and 30 AAAs large enough to merit elective repair within 12 weeks of the CT scan. Three-dimensional computer models of AAAs were reconstructed from CT scan data. The stress distribution on the AAA as a result of geometry and blood pressure was computationally determined with finite element analysis with a hyperelastic nonlinear model that depicted the mechanical behavior of the AAA wall. RESULTS: Peak wall stress (maximal stress on the AAA surface) was significantly different between groups (ruptured, 47.7 +/- 6 N/cm(2); emergent symptomatic, 47.5 +/- 4 N/cm(2); elective repair, 36.9 +/- 2 N/cm(2); P =.03), with no significant difference in blood pressure (P =.2) or AAA diameter (P =.1). Because of trends toward differences in diameter, comparison was made only with diameter-matched subjects. Even with identical mean diameters, ruptured/symptomatic AAAs had a significantly higher peak wall stress (46.8 +/- 4.5 N/cm(2) versus 38.1 +/- 1.3 N/cm(2); P =.05). Maximal wall stress predicted risk of rupture better than the LaPlace equation (20.7 +/- 5.7 N/cm(2) versus 18.8 +/- 2.9 N/cm(2); P =.2) or other proposed indices of rupture risk. The smallest ruptured AAA was 4.8 cm, but this aneurysm had a stress equivalent to the average electively repaired 6.3-cm AAA. CONCLUSION: Peak wall stresses calculated in vivo for AAAs near the time of rupture were significantly higher than peak stresses for electively repaired AAAs, even when matched for maximal diameter. Calculation of wall stress with computer modeling of three-dimensional AAA geometry appears to assess rupture risk more accurately than AAA diameter or other previously proposed clinical indices. Stress analysis is practical and feasible and may become an important clinical tool for evaluation of AAA rupture risk.     

Wall stress distribution on three-dimensionally reconstructed models of human abdominal aortic aneurysm

PURPOSE: Abdominal aortic aneurysm (AAA) rupture is believed to occur when the mechanical stress acting on the wall exceeds the strength of the wall tissue. Therefore, knowledge of the stress distribution in an intact AAA wall could be useful in assessing its risk of rupture. We developed a methodology to noninvasively estimate the in vivo wall stress distribution for actual AAAs on a patient-to-patient basis. METHODS: Six patients with AAAs and one control patient with a nonaneurysmal aorta were the study subjects. Data from spiral computed tomography scans were used as a means of three-dimensionally reconstructing the in situ geometry of the intact AAAs and the control aorta. We used a nonlinear biomechanical model developed specifically for AAA wall tissue. By means of the finite element method, the stress distribution on the aortic wall of all subjects under systolic blood pressure was determined and studied. RESULTS: In all the AAA cases, the wall stress was complexly distributed, with distinct regions of high and low stress. Peak wall stress among AAA patients varied from 29 N/cm(2) to 45 N/cm(2) and was found on the posterior surface in all cases studied. The wall stress on the nonaneurysmal aorta in the control subject was relatively low and uniformly distributed, with a peak wall stress of 12 N/cm(2). AAA volume, rather than AAA diameter, was shown by means of statistical analysis to be a better indicator of high wall stresses and possibly rupture. CONCLUSION: The approach taken to estimate AAA wall stress distribution is completely noninvasive and does not require any additional involvement or expense by the AAA patient. We believe that this methodology may allow for the evaluation of an individual AAA's rupture risk on a more biophysically sound basis than the widely used 5-cm AAA diameter criterion.     

A comparative study of aortic wall stress using finite element analysis for ruptured and non-ruptured abdominal aortic aneurysms.

BACKGROUND: The decision to repair an asymptomatic abdominal aortic aneurysm (AAA) is currently based on diameter (> or =5.5 cm) alone. However, aneurysms less than 5.5 cm do rupture while some reach greater than 5.5 cm without rupturing. Hence the need to predict the risk of rupture on an individual patient basis is important. This study aims to calculate and compare wall stress in ruptured and non-ruptured AAA. METHODS: The 3D geometries of AAA were derived from CT scans of 27 patients (12 ruptured and 15 non-ruptured). AAA geometry, systolic blood pressure and literature derived material properties, were utilised to calculate wall stress for individual AAA using finite element analysis. RESULTS: Peak wall stress was significantly higher in the ruptured AAA (mean 1.02 MPa) than the non-ruptured AAA (mean 0.62 MPa). In patients with an identifiable site of rupture on CT scan, the area of peak wall stress correlated with rupture site. CONCLUSIONS: Peak wall stress can be calculated from routinely performed CT scans and may be a better predictor of risk of rupture than AAA diameter on an individual patient basis.     

Congenital abdominal aortic aneurysms in the young. Case report and review of the literature

Aneurysms of the aorta are rare in children and young adults. We report a case of a 19-year-old man with a saccular abdominal aortic aneurysm (AAA). No associated disorders were discovered in this patient. The aneurysm was resected and a Dacron aortic graft was implanted. Nine years after operation the patient was in good health without evidence of other aneurysms. Thirty-two cases of probable congenital abdominal aortic aneurysms were collected from the literature. In 19 cases, the cause of aneurysm was not ascertained. We identified two groups of patients with probably congenital AAAs: type I congenital AAA, in which there is a generalized disorder of the arterial tissue and usually aneurysms are present in other areas and type II congenital AAA, in which there is a localized defect of the abdominal aorta, without aneurysms in other areas. We speculate that a congenital defect localized to the wall of the abdominal aorta was the cause of the aneurysm in this patient (type II congenital AAA).     

Patient-specific hemodynamic analysis of small internal carotid artery-ophthalmic artery aneurysms

BackgroundProphylactic treatment of unruptured small brain aneurysms is still controversial due to the low risk of rupture. Distinguishing which small aneurysms are at risk for rupture has become important for treatment. Previous studies have indicated a variety of hemodynamic properties that may influence aneurysm rupture. This study uses hemodynamic principles to evaluate these in the context of ruptured and unruptured small aneurysms in a single location.MethodsEight small internal carotid artery-ophthalmic artery (ICA-Oph) aneurysms (<10 mm) were selected from the University of California, Los Angeles, database. We analyzed rupture-related hemodynamic characteristics including flow patterns, wall shear stress (WSS), and flow impingement using previously developed patient-specific computational fluid dynamics software.ResultsMost ruptured aneurysms had complicated flow patterns in the aneurysm domes, but all of the unruptured cases showed a simple vortex. A reduction in flow velocity between the parent artery and the aneurysm sac was found in all the cases. Inside the aneurysms, the highest flow velocities were found either at the apex or neck. We also observed a trend of higher and more inhomogeneous WSS distribution within ruptured aneurysms (10.66 ± 5.99 Pa) in comparison with the unruptured ones (6.31 ± 6.47 Pa) (P < .01).ConclusionA comparison of hemodynamic properties between ruptured and unruptured small ICA-Oph aneurysms found that some hemodynamic properties vary between small aneurysms although they are similar in size and share the same anatomical location. In particular, WSS may be a useful hemodynamic factor for studying small aneurysm rupture.     

Simple geometric characteristics fail to reliably predict abdominal aortic aneurysm wall stresses

PURPOSE: The treatment of patients with abdominal aortic aneurysms (AAAs) is typically based on the potential for rupture. Current rupture assessments are in turn based on statistics from aggregate populations and are incapable of providing precise risk estimates for individual AAAs. Significant benefit could be realized if rupture potential for individual AAAs could be reliably determined on the basis of simple geometric characteristics or the results of symmetric thin-shell analysis. This study seeks to determine whether it is possible to estimate wall stresses by use of these simple measures. METHODS: Linear finite element analysis was used to estimate the distribution of von Mises stresses in a series of homogeneous, isotropic, three-dimensional AAA models subject to static loading and assumed to have zero residual stresses. The magnitude of the peak stress was tabulated for each model along with the following characteristics: aneurysm volume; maximum diameter; maximum radius; maximal wall distention; aspect ratio (ratio of greatest anteroposterior diameter to transverse diameter); local radii of curvature (in both longitudinal and circumferential directions); and maximum symmetric thin-shell stress estimates (on the basis of the meridional contour). The relationship between peak stress and each of the characteristics was assessed by use of Spearman rank correlation coefficients, with values less than 0.95 interpreted as signifying unreliable associations. RESULTS: Peak stresses in the individual models ranged from 1.79 x 10(6) dyne/cm2 to 15.1 x 10(6) dyne/cm2. The circumferential and longitudinal radii of curvature were frequently able to predict the locations of high stress, but were unreliable in predicting the magnitude of peak stress. The aspect ratio showed the strongest correlation with peak wall stress (r = 0.88, 95% CI, 0.68-0.96), whereas the other characteristics showed even less correlation. Symmetric thin shell analysis accurately predicted stresses in axially symmetric models, but it was incapable of predicting either the location or magnitude of peak stress in asymmetric models. CONCLUSIONS: Simple geometric criteria and symmetric thin shell analyses are unreliable in predicting AAA stresses. Future attempts to estimate wall stress and assess risk of rupture for individual AAAs may require detailed three-dimensional modeling.     

Size and location of thrombus in intact and ruptured abdominal aortic aneurysms

PURPOSE: This study compared the volume and morphology of intraluminal thrombus (ILT) in intact and ruptured abdominal aortic aneurysms (AAAs). METHODS: ILT volume in 67 intact AAAs and in 31 ruptured AAAs was assessed by using computed tomography (CT) angiography to measure the major and minor diameter of the outer wall and lumen of AAA as outlined by contrast at multiple sites. ILT thrombus morphology was recorded by AutoCAD 2000 software. Four equidistant images traced from the CT scan were recorded along the length of AAA. Thrombus volume was categorized as anterior-eccentric if the calculated area of thrombus was greater anteriorly, posterior-eccentric if greater posteriorly, eccentric-equal if the difference between the anterior and posterior thrombus was 相似文献   

Biomechanical properties of ruptured versus electively repaired abdominal aortic aneurysm wall tissue

OBJECTIVE: The purpose of this study was to evaluate and compare the biomechanical properties of abdominal aortic aneurysm (AAA) wall tissue from patients who experienced AAA rupture with that of those who received elective repair. METHODS: Rectangular, circumferentially oriented AAA wall specimens (approximately 2.5 cm x 7 mm) were obtained fresh from the operating room from patients undergoing surgical repair. The width and thickness were measured for each specimen by using a laser micrometer before testing to failure with a uniaxial tensile testing system. The force and deformation applied to each specimen were measured continuously during testing, and the data were converted to stress and stretch ratio. The tensile strength was taken as the peak stress obtained before specimen failure, and the distensibility was taken as the stretch ratio at failure. The maximum tangential modulus and average modulus were also computed according to the peak and average slope of the stress-stretch ratio curve. RESULTS: Twenty-six specimens were obtained from 16 patients (aged 73 +/- 3 years [mean +/- SEM]) undergoing elective repair of their AAA (diameter, 7.0 +/- 0.5 cm). Thirteen specimens were resected from nine patients (aged 73 +/- 3 years; P = not significant in comparison to the electively repaired AAAs) during repair of their ruptured AAA (diameter, 7.8 +/- 0.6 cm; P = not significant). A significant difference was noted in wall thickness between ruptured and elective AAAs: 3.6 +/- 0.3 mm vs 2.5 +/- 0.1 mm, respectively (P < .001). The tensile strength of the ruptured tissue was found to be lower than that for the electively repaired tissue (54 +/- 6 N/cm2 vs 82 +/- 9.0 N/cm2; P = .04). Considering all specimens, no significant correlation was noted between tensile strength and diameter (R = -0.10; P = .55). Tensile strength, however, had a significant negative correlation with wall thickness (R = -0.42; P < .05) and a significant positive correlation with the tissue maximum tangential modulus (R = 0.76; P < .05). CONCLUSIONS: Our data suggest that AAA rupture is associated with aortic wall weakening, but not with wall stiffening. A widely accepted indicator for risk of aneurysm rupture is the maximum transverse diameter. Our results suggest that AAA wall strength, in large aneurysms, is not related to the maximum transverse diameter. Rather, wall thickness or stiffness may be a better predictor of rupture for large AAAs.     

Can Local Secretion of Prostaglandin E2, Thromboxane B2, and Interleukin-6 Play a Role in Ruptured Abdominal Aortic Aneurysm?

Background Our laboratory has previously shown that the levels of secreted prostaglandin E₂ (PGE₂), Thromboxane B₂ (TxB₂), and interleukin-6 (IL-6) by aortic explant cultures were high in patients with ruptured abdominal aortic aneurysm (AAA). In the present study, we sought to examine the secretory levels of these inflammatory mediators in aortic explant cultured from a group of AAAs rupturing at a certain size and a group that did not rupture at that size. It was thought that such a comparison might reveal the contribution of those inflammatory mediators to the risk of AAA rupture. Materials and methods All subjects had abdominal computed tomography (CT) scans to determine the size of the aneurysm, and surgical aortic tissue was collected from both nonruptured AAAs (18 with a mean size of 6 + 0.5 cm [range: 5–7 cm] and 12 with a mean size of 8 + 0.1 cm [range: 7.01–10 cm]) and ruptured AAAs (10 with a mean size of 5.8 + 0.3 cm [range: 5–7 cm] and 10 with a mean size of 7.8 + 0.1 cm [range: 7.01–10 cm]). Aortic explant cultures from different sizes of aneurysms were immediately established and the culture media were collected 72 h later. Results The levels of PGE₂, TxB₂, and IL-6 secreted in the cultured medium were quantified by specific enzyme-linked immunosorbent assays (ELISA). The secretary levels of PGE₂, TxB₂, and IL-6 were significantly higher in ruptured AAAs than in nonruptured AAAs of similar diameter. However, there was no correlation between these three inflammatory mediators and the size of AAA. Conclusions This study shows that these inflammatory mediators may play a role in the progression toward rupture but may not be responsible for the expansion of AAA.     

Effects of arterial geometry on aneurysm growth: three-dimensional computational fluid dynamics study

OBJECT: Few researchers have quantified the role of arterial geometry in the pathogenesis of saccular cerebral aneurysms. The authors investigated the effects of parent artery geometry on aneurysm hemodynamics and assessed the implications relative to aneurysm growth and treatment effectiveness. METHODS: The hemodynamics of three-dimensional saccular aneurysms arising from the lateral wall of arteries with varying arterial curves (starting with a straight vessel model) and neck sizes were studied using a computational fluid dynamics analysis. The effects of these geometric parameters on hemodynamic parameters, including flow velocity, aneurysm wall shear stress (WSS), and area of elevated WSS during the cardiac cycle (time-dependent impact zone), were quantified. Unlike simulations involving aneurysms located on straight arteries, blood flow inertia (centrifugal effects) rather than viscous diffusion was the predominant force driving blood into aneurysm sacs on curved arteries. As the degree of arterial curvature increased, flow impingement on the distal side of the neck intensified, leading to elevations in the WSS and enlargement of the impact zone at the distal side of the aneurysm neck. CONCLUSIONS: Based on these simulations the authors postulate that lateral saccular aneurysms located on more curved arteries are subjected to higher hemodynamic stresses. Saccular aneurysms with wider necks have larger impact zones. The large impact zone at the distal side of the aneurysm neck correlates well with other findings, implicating this zone as the most likely site of aneurysm growth or regrowth of treated lesions. To protect against high hemodynamic stresses, protection of the distal side of the aneurysm neck from flow impingement is critical.     

Aortic aneurysms secrete interleukin-6 into the circulation

OBJECTIVE: Circulating plasma interleukin-6 (IL-6) concentrations are elevated in patients with abdominal aortic aneurysms (AAAs) compared with controls. In vitro studies suggest that the aneurysm is the source of the IL-6. Because IL-6 is an independent risk factor for cardiovascular mortality, elevation of this cytokine may be significant in these patients, who represent a group at increased risk from cardiovascular death. The aim of this study was to directly measure in vivo aortic IL-6 concentrations, testing the hypothesis that aneurysms secrete IL-6 into the circulation. METHODS: Before endovascular aneurysm repair took place, blood was sampled from the entire length of the aorta in 27 patients with AAA and nine with thoracic aneurysms (TAs). A control group consisted of 15 patients without aneurysms undergoing angiography. Plasma IL-6 was determined using enzyme-linked immunosorbent assay, and high-sensitivity C-reactive protein (hs-CRP) was measured turbidimetrically. Aneurysm surface area was calculated from axial computed tomography scans. RESULTS: Mean IL-6 concentrations (pg/mL) were higher in the TA and AAA groups compared with controls (10.4 +/- 3.7 and 4.9 +/- 0.5 vs 2.7 +/- 0.5, P = .002). There was a significant difference in plasma IL-6 concentration corresponding to aneurysm position in the AAA (P = .002) and TA (P = .008) groups, with both patterns conforming to a linear trend. This pattern was not observed in the control group, in which no significant difference in IL-6 concentrations was found throughout the aorta. Peak IL-6 occurred earlier in TAs compared with AAAs (descending aorta vs iliac artery) corresponding to aneurysm position (P = .0007). Linear regression revealed a positive correlation between aneurysm surface area and mean plasma IL-6 (Spearman's correlation, P = .003). The mean surface areas of the TAs, at 0.07 m2 (interquartile range [IQR], 0.06 to 0.09), were higher than those of the AAAs at 0.03 m2 (IQR, 0.02 to 0.04; P = .002). High-sensitivity CRP was within normal limits, and no significant differences were found between the AAA group and the controls. CONCLUSIONS: Circulating IL-6 is elevated within the aorta in patients with aneurysms and corresponds to aneurysm position. Furthermore, aneurysm surface area and mean plasma IL-6 are correlated. In the absence of any evidence of systemic inflammation in the form of elevated hs-CRP, these data support the hypothesis that aneurysms secrete IL-6 into the circulation. This may contribute to the high cardiovascular mortality observed in patients with aneurysms.     

Aortic aneurysms in children and young adults with tuberous sclerosis: report of two cases and review of the literature

Abdominal aortic aneurysms (AAAs) in children and young adults are rare; some have been observed in patients with tuberous sclerosis (TS). We report two cases and review the literature. A 9-year-old girl with TS was diagnosed with a 3-cm calcified AAA, and a 41-year-old man with TS was diagnosed with a 7.5-cm thoracic aortic aneurysm (TAA). Both patients underwent open repair with a tube polyester graft without complication. They are both doing well at 7 and 8 years after surgery. Pathologic evaluation revealed medial atrophy and focal medial disruption in the aortic wall in both patients. With our two cases, 15 patients with TS and aneurysms have been reported; 12 had AAA, and four had TAA (one patient had both). Three AAAs and two TAAs ruptured. Six patients died because of aneurysmal disease. There is an association between TS and aortic aneurysms. Patients should be screened for aortic aneurysms at the time TS is diagnosed and annually thereafter. Because of the high risk of rupture, early elective repair is suggested. New aortic aneurysms after repair may also develop.     

Hemodynamic changes in a middle cerebral artery aneurysm at follow-up times before and after its rupture: a case report and a review of the literature

Hemodynamic parameters play a significant role in the development of cerebral aneurysms. Parameters such as wall shear stress (WSS) or velocity could change in time and may contribute to aneurysm growth and rupture. However, the hemodynamic changes at the rupture location remain unclear because it is difficult to obtain data prior to rupture. We analyzed a case of a ruptured middle cerebral artery (MCA) aneurysm for which we acquired imaging data at three time points, including at rupture. A patient with an observed MCA aneurysm was admitted to the emergency department with clinical symptoms of a subarachnoid hemorrhage. During three-dimensional (3D) digital subtraction angiography (DSA), the aneurysm ruptured again. Imaging data from two visits before rupture and this 3D DSA images at the moment of rupture were acquired, and computational fluid dynamic (CFD) simulations were performed. Results were used to describe the time-dependent changes of the hemodynamic variables associated with rupture. Time-dependent hemodynamic changes at the rupture location were characterized by decreased WSS and flow velocity magnitude. The impingement jet in the dome changed its position in time and the impingement area at follow-up moved near the rupture location. The results suggest that the increased WSS on the dome and increased low wall shear stress area (LSA) and decreased WSS on the daughter bleb with slower flow and slow vortex may be associated with rupture. CFD performed during the follow-up period may be part of diagnostic tools used to determine the risk of aneurysm rupture.     

Prediction of Hemolysis in Turbulent Shear Orifice Flow

Abstract
This study proposes a method of predicting hemolysis induced by turbulent shear stress (Reynolds stress) in a simplified orifice pipe flow. In developing centrifugal blood pumps, there has been a serious problem with hemolysis at the impeller or casing edge; because of flow separation and turbulence in these regions. In the present study, hemolysis caused by turbulent shear stress must occur at high shear stress levels in regions near the edge of an orifice pipe flow. We have computed turbulent shear flow using the low-Reynolds number k - ε model. We found that the computed turbulent shear stress near the edge was several hundreds times that of the laminar shear stress (molecular shear stress). The peak turbulent shear stress is much greater than that obtained in conventional hemolysis testing using a viscometer apparatus. Thus, these high turbulent shear stresses should not be ignored in estimating hemolysis in this blood flow. Using an integrated power by shear force, it is optimimal to determine the threshold of the turbulent shear stress by comparing computed stress levels with those of hemolysis experiments of pipe orifice blood flow.     

Rupture of a giant carotid aneurysm after extracranial-to-intracranial bypass surgery

We report a case of a fatal rupture of a previously unruptured giant aneurysm of the bifurcation of the internal carotid artery (ICA), which occurred after an extracranial-intracranial (EC-IC) bypass and the partial occlusion of the ICA. Interim angiography showed retrograde filling of the proximal middle cerebral artery to the aneurysm. There have been four previously reported cases of giant aneurysms rupturing after treatment with an EC-IC bypass and carotid ligation, and it appears likely that a change in pressure/flow dynamics produced by the bypass may have been the cause. The technique of carotid ligation with an EC-IC bypass is used frequently to treat unclippable intracranial aneurysms, and the resulting hemodynamic changes need to be considered carefully to prevent this type of complication. To minimize hemodynamic stress on the aneurysm, we suggest that 1) the bypass caliber should be as small as possible consistent with sufficient cerebral blood flow after ICA occlusion, and 2) complete ICA occlusion should be performed as soon as possible after the bypass.     

Suitability for endovascular aneurysm repair in an unselected population

BACKGROUND: Tertiary referral centres report that up to 60 per cent of patients may be suitable for endovascular repair of abdominal aortic aneurysm (EVAR). The aim of this study was to determine the percentage of abdominal aortic aneurysms (AAAs) presenting to a county-wide vascular service that were suitable for EVAR, and to examine the outcome of subsequent AAA repair in relation to aneurysm morphology. PATIENTS AND METHODS: All patients being assessed for AAA repair between January 1998 and December 1999 underwent spiral computed tomography angiography to determine aneurysm morphology and suitability for EVAR. Subsequent outcome for all patients in the study was recorded in a prospective vascular database. RESULTS: A total of 115 patients was assessed. Sixty-three aneurysms (55 per cent) had one or more absolute contraindications to EVAR, a further 13 (11 per cent) had at least one relative contraindication, and 39 (34 per cent) had no contraindication. Of patients with no absolute contraindication to EVAR, ten underwent successful EVAR, five did not meet recognized criteria for surgery, one awaits EVAR, four remain under observation, one awaits open repair, and 31 underwent open repair without death. CONCLUSION: Only 30 per cent of unselected AAAs presenting to a vascular service are entirely suitable for EVAR; most of these patients can safely undergo open AAA repair. These data suggest that increased use of EVAR is only possible by deploying devices in suboptimal morphology, and in treating patients who would not normally be considered for open AAA repair.     

Epidemiology and Outcome of Aortic Aneurysms in Hong Kong

Abstract The objective of this study was to determine epidemiology and mortality statistics for abdominal aortic aneurysms (AAAs) in Hong Kong. Data from three sources were obtained and analyzed: (1) Hong Kong Hospital Authority discharge statistics for 1999 and 2000; (2) a survey on aortic aneurysms in public hospitals conducted by the Working Group of Vascular Surgery; and (3) the Department of Surgery, University of Hong Kong Medical Center aortic aneurysm database. The disease pattern, distribution, and operative mortality were determined. The annual incidence of AAA in Hong Kong is 13.7 per 100,000 population and 105 per 100,000 for those aged 65 and above. About 10% of the AAAs that presented were ruptured. The mean age of the AAA patients was 74 years, with 84% of them over age 65. The operative repair rate for AAAs was low, being only 8% for intact aneurysms and 54% for ruptured ones. Overall, 45% of all aneurysm repairs were performed for a ruptured AAA. There is diverse practice between major vascular centers and smaller regional hospitals. The territory-wide operative mortality rates for intact and ruptured aneurysms were 10% (range 4–24%) and 70% (range 38––100%), respectively. There was no gender bias in the rupture and operative rates. The overall mortality was 17% for intact AAAs and 78% for ruptured AAAs. The average length of hospital stay was 19 days for elective AAA surgery and 13 days for ruptured AAAs. The number of operations in high-volume centers is increasing with a concomitant decrease in operative mortality. There are no definitive data to indicate that the incidence of AAAs is rising, but a trend toward an increasing number of operations in referral centers is noted. The low repair rates for intact AAAs and the high proportion of repairs for ruptured aneurysms suggest that AAAs are undertreated in Hong Kong.