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A Computational Study of Dynamic Obstruction in Type B Aortic Dissection
Abstract
A serious complication in aortic dissection is dynamic obstruction of the true lumen (TL). Dynamic obstruction results in malperfusion, a blockage of blood flow to vital organs. Clinical data reveal that increases in central blood pressure promote dynamic obstruction. However, the mechanisms by which high pressures result in TL collapse are underexplored and poorly understood. We developed a computational model to investigate biomechanical and hemodynamical factors involved in dynamic obstruction. We hypothesize relatively small pressure gradient between TL and FL are sufficient to displace the flap and induce obstruction. An idealized fluid-structure interaction model of type B aortic dissection was created. Simulations were performed under mean cardiac output, while inducing dynamic changes in blood pressure by altering FL outflow resistance. As FL resistance increased, central aortic pressure increased from 95.7 to 115.3 mmHg. Concurrent with blood pressure increase, flap motion was observed, resulting in TL collapse, consistent with clinical findings. The maximum pressure gradient between TL and FL over the course of the dynamic obstruction was 4.5 mmHg, consistent with our hypothesis. Furthermore, the final stage of dynamic obstruction was very sudden in nature, occurring over a short time(< 1 second) in our simulation, consistent with the clinical understanding of this dramatic event. Simulations also revealed sudden drops in flow and pressure in the TL in response to the flap motion, consistent with first stages of malperfusion. To our knowledge, this study represents the first computational analysis of potential mechanisms driving dynamic obstruction in aortic dissection.
... [38][39][40][41][42][43][44][45] Informed by patient-specific inflow/outflow boundary conditions (BCs), referred to as flow BCs in this study, measured by either ultrasound or MRI, CFD simulations can provide a high-resolution assessment of hemodynamics inside FL of TBAD vessels reconstructed based on computed tomography (CT) angiography imaging. [46][47][48][49][50][51][52][53] Moreover, CFD can evaluate the pressure and shear stress that are difficult to measure in vivo. Notwithstanding these advantages, the reliability of CFD simulations primarily depends on the patient-specific flow BCs for all the inlet and outlet vessels, as illustrated in Figure 1B, which are often not accessible due to practical and ethical constraints. ...
Aortic dissection is a life-threatening event that is responsible for significant morbidity and mortality in individuals ranging in age from children to older adults. A better understanding of the complex hemodynamic environment inside the aorta enables clinicians to assess patient-specific risk of complications and administer timely interventions. In this study, we propose to develop and validate a new computational framework, warm-start physics-informed neural networks (WS-PINNs), to address the limitations of the current approaches in analyzing the hemodynamics inside the false lumen (FL) of type B aortic dissection vessels reconstructed from apolipoprotein null mice infused with AngII, thereby significantly reducing the amount of required measurement data and eliminating the dependency of predictions on the accuracy and availability of the inflow/outflow boundary conditions. Specifically, we demonstrate that the WS-PINN models allow us to focus on assessing the 3D flow field inside FL without modeling the true lumen and various branched vessels. Furthermore, we investigate the impact of the spatial and temporal resolutions of MRI data on the prediction accuracy of the PINN model, which can guide the data acquisition to reduce time and financial costs. Finally, we consider the use of transfer learning to provide faster results when looking at similar but new geometries. Our results indicate that the proposed framework can enhance the capacity of hemodynamic analysis in vessels with aortic dissections, with the promise of eventually leading to improved prognostic ability and understanding of the development of aneurysms.
Aortic dissection (AD) is one of the fatal and complex conditions. Since there is a lack of a specific treatment guideline for type-B AD, a better understanding of patient-specific hemodynamics and therapy outcomes can potentially control the progression of the disease and aid in the clinical decision-making process. In this work, a patient-specific geometry of type-B AD is reconstructed from computed tomography images, and a numerical simulation using personalised computational fluid dynamics (CFD) with three-element Windkessel model boundary condition at each outlet is implemented. According to the physiological response of beta-blockers to the reduction of left ventricular contractions, three case studies with different heart rates are created. Several hemodynamic features, including time-averaged wall shear stress (TAWSS), highly oscillatory, low magnitude shear (HOLMES), and flow pattern are investigated and compared between each case. Results show that decreasing TAWSS, which is caused by the reduction of the velocity gradient, prevents vessel wall at entry tear from rupture. Additionally, with the increase in HOLMES value at distal false lumen, calcification and plaque formation in the moderate and regular-heart rate cases are successfully controlled. This work demonstrates how CFD methods with non-invasive hemodynamic metrics can be developed to predict the hemodynamic changes before medication or other invasive operations. These consequences can be a powerful framework for clinicians and surgical communities to improve their diagnostic and pre-procedural planning.
Credible computational fluid dynamic (CFD) simulations of aortic dissection are challenging, because the defining parallel flow channels—the true and the false lumen—are separated from each other by a more or less mobile dissection membrane, which is made up of a delaminated portion of the elastic aortic wall. We present a comprehensive numerical framework for CFD simulations of aortic dissection, which captures the complex interplay between physiologic deformation, flow, pressures, and time-averaged wall shear stress (TAWSS) in a patient-specific model. Our numerical model includes (1) two-way fluid–structure interaction (FSI) to describe the dynamic deformation of the vessel wall and dissection flap; (2) prestress and (3) external tissue support of the structural domain to avoid unphysiologic dilation of the aortic wall and stretching of the dissection flap; (4) tethering of the aorta by intercostal and lumbar arteries to restrict translatory motion of the aorta; and a (5) independently defined elastic modulus for the dissection flap and the outer vessel wall to account for their different material properties. The patient-specific aortic geometry is derived from computed tomography angiography (CTA). Three-dimensional phase contrast magnetic resonance imaging (4D flow MRI) and the patient’s blood pressure are used to inform physiologically realistic, patient-specific boundary conditions. Our simulations closely capture the cyclical deformation of the dissection membrane, with flow simulations in good agreement with 4D flow MRI. We demonstrate that decreasing flap stiffness from \({E}_{\hbox{flap}}= 800\) to \({E}_{\hbox{flap}}= 20\) kPa (a) increases the displacement of the dissection flap from 1.4 to 13.4 mm, (b) decreases the surface area of TAWSS by a factor of 2.3, (c) decreases the mean pressure difference between true lumen and false lumen by a factor of 0.63, and (d) decreases the true lumen flow rate by up to 20% in the abdominal aorta. We conclude that the mobility of the dissection flap substantially influences local hemodynamics and therefore needs to be accounted for in patient-specific simulations of aortic dissection. Further research to accurately measure flap stiffness and its local variations could help advance future CFD applications.
Aortic dissection (AD) is a vascular condition with high morbidity and mortality rates. Computational fluid dynamics (CFD) can provide insight into the progression of AD and aid clinical decisions; however, oversimplified modelling assumptions and high computational cost compromise the accuracy of the information and impede clinical translation. To overcome these limitations, a patient-specific CFD multi-scale approach coupled to Windkessel boundary conditions and accounting for wall compliance was developed and used to study a patient with AD. A new moving boundary algorithm was implemented to capture wall displacement and a rich in vivo clinical dataset was used to tune model parameters and for validation. Comparisons between in silico and in vivo data showed that this approach successfully captures flow and pressure waves for the patient-specific AD and is able to predict the pressure in the false lumen (FL), a critical variable for the clinical management of the condition. Results showed regions of low and oscillatory wall shear stress which, together with higher diastolic pressures predicted in the FL, may indicate risk of expansion. This study, at the interface of engineering and medicine, demonstrates a relatively simple and computationally efficient approach to account for arterial deformation and wave propagation phenomena in a three-dimensional model of AD, representing a step forward in the use of CFD as a potential tool for AD management and clinical support.
Objective
Retrograde aortic type A dissection (RTAD) is a known complication in patients with aortic type B dissection. The purpose of this computational fluid dynamics (CFD) study was to identify haemodynamic risk factors for the occurrence of RTAD.
Methods
Computed tomographic angiography (CTA) images of 10 patients with type B dissections, who subsequently developed a RTAD, were retrospectively analysed together with patients constituting a control group (n = 10) where no further vascular events after the initial type B dissection occurred. CFD simulations were conducted based on 3D surface models of the aortic lumen derived from CTA datasets. For both groups, pressures, velocity magnitudes and wall shear stress (WSS) were compared at the site of the future RTAD entry tear and the surrounding aortic wall.
Results
WSS at the site of the future entry tear was significantly elevated compared with the surrounding wall (15.10 Pa vs. 5.15 Pa, p < .001) and was significantly higher in the RTAD group than in the control group (6.05 Pa, p < .002). Pressures and velocity magnitudes were not significantly elevated at the entry tear (3825.8 Pa, 0.63 m/s) compared with the aortic arch (3549.8 Pa, 0.50 m/s) or control group (3501.7 Pa, 0.62 m/s).
Conclusions
Increased WSS accompanies the occurrence of RTAD. The results merit the design for a prospective study to confirm whether WSS is a risk factor for the occurrence of RTAD.
Although considered by many as the gold standard clinical measure of arterial stiffness, carotid-to-femoral pulse wave velocity (cf-PWV) averages material and geometric properties over a large portion of the central arterial tree. Given that such properties may evolve differentially as a function of region in cases of hypertension and aging, among other conditions, there is a need to evaluate the potential utility of cf-PWV as an early diagnostic of progressive vascular stiffening. In this paper, we introduce a data-driven fluid-solid-interaction computational model of the human aorta to simulate effects of aging-related changes in regional wall properties (e.g., biaxial material stiffness and wall thickness) and conduit geometry (e.g., vessel caliber, length, and tortuosity) on several metrics of arterial stiffness, including distensibility, augmented pulse pressure, and cyclic changes in stored elastic energy. Using the best available biomechanical data, our results for PWV compare well to findings reported for large population studies while rendering a higher resolution description of evolving local and global metrics of aortic stiffening. Our results reveal similar spatio-temporal trends between stiffness and its surrogate metrics, except PWV, thus indicating a complex dependency of the latter on geometry. Lastly, our analysis highlights the importance of the tethering exerted by external tissues, which was iteratively estimated until hemodynamic simulations recovered typical values of tissue properties, pulse pressure, and PWV for each age group.
Aortic dissection causes splitting of the aortic wall layers, allowing blood to enter a ‘false lumen’ (FL). For type B dissection, a significant predictor of patient outcomes is patency or thrombosis of the FL. Yet, no methods are currently available to assess the chances of FL thrombosis. In this study, we present a new computational model that is capable of predicting thrombus formation, growth and its effects on blood flow under physiological conditions. Predictions of thrombus formation and growth are based on fluid shear rate, residence time and platelet distribution, which are evaluated through convection–diffusion–reaction transport equations. The model is applied to a patient-specific type B dissection for which multiple follow-up scans are available. The predicted thrombus formation and growth patterns are in good qualitative agreement with clinical data, demonstrating the potential applicability of the model in predicting FL thrombosis for individual patients. Our results show that the extent and location of thrombosis are strongly influenced by aortic dissection geometry that may change over time. The high computational efficiency of our model makes it feasible for clinical applications. By predicting which aortic dissection patient is more likely to develop FL thrombosis, the model has great potential to be used as part of a clinical decision-making tool to assess the need for early endovascular intervention for individual dissection patients.
OBJECTIVE/BACKGROUND:
Several risk factors have been identified in type B aortic dissection (TBAD), namely tear size, location, patency and number, and false lumen (FL) location. However, the individual impact of each of these factors is poorly understood. The impact of these factors was investigated using computational fluid dynamics (CFD).
METHODS:
Fourteen idealized models of chronic TBAD were created of different shapes (straight vs. curved vessels), different number of proximal and distal tears, tear size (4, 10, and 20 mm diameter) and shape (circular or elliptical), FL location (inner or outer arch), treated (stented), and untreated. All models had identical length, relative size of true lumen (TL) and FL, and inlet (flow) and outlet (pressure) boundary conditions. Using validated CFD tools, inlet mean pressure (MP), pulse pressure (PP), TL and FL pressures, velocities, and flows were computed for each model.
RESULTS:
AD increased PP and MP relative to undissected aorta. Curvature did not change pressure and flow ratio between TL and FL. Inner curvature FL showed slightly larger pressures and tear velocities. Larger tears decreased hemodynamic differences between TL and FL. The combination of proximal and distal tear size determines the overall hemodynamics: larger proximal tears increased FL PP by up to 76%. Conversely, larger distal tears decreased FL PP and MP. Large proximal and distal tears decreased tear velocity (by up to 65%) and increased FL flow (up to 12 times). Proximal tear stenting resulted in a 54% reduction of PP. Conversely, distal occlusion tear increased FL PP and MP by 144% and 7%, respectively.
CONCLUSION:
Unfavorable hemodynamic conditions such as larger FL pressure occur when distal tear is small or absent, proximal tears are large, and FL is at the inner curvature, in agreement with previous clinical studies. CFD analysis is a powerful tool to understand the interplay between anatomy and hemodynamics in TBAD.
This work presents a mathematical model of the metabolic feedback and adrenergic feedforward control of coronary blood flow that occur during variations in the cardiac workload. It is based on the physiological observations that coronary blood flow closely follows myocardial oxygen demand, that myocardial oxygen debts are repaid, and that control oscillations occur when the system is perturbed, and so is phenomenological in nature. Using clinical data, we demonstrate that the model can provide patient-specific estimates of coronary blood flow changes between rest and exercise, requiring only the patient's heart rate and peak aortic pressure as input. The model can be used in zero-dimensional lumped parameter network studies, or as a boundary condition for three-dimensional multidomain Navier-Stokes blood flow simulations. For the first time, this model provides feedback control of the coronary vascular resistance which can be used to enhance the physiological accuracy of any haemodynamic simulation which includes both a heart model and coronary arteries. This has particular relevance to patient-specific simulation for which heart-rate and aortic pressure recordings are available. In addition to providing a simulation tool, under our assumptions, the derivation of our model shows that β-feedforward control of the coronary microvascular resistance is a mathematical necessity, and that the metabolic feedback control must be dependent upon two error signals: the historical myocardial oxygen debt, and the instantaneous myocardial oxygen deficit.
Aortic dissection is a disease whereby an injury in the wall of the aorta leads to the creation of a true lumen and a false lumen separated by an intimal flap which may contain multiple communicating tears between the lumina. It has a high associated morbidity and mortality, but at present, the timing of surgical intervention for stable type B dissections remains an area of debate. Detailed knowledge of hemodynamics may yield greater insight into the long-term outcomes for dissection patients by providing a greater understanding of pressures, wall shear stress and velocities in and around the dissection. In this paper, we aim to gather further insight into the complex hemodynamics in aortic dissection using medical imaging and computational fluid dynamics modelling. Towards this end, several computer models of the aorta of a patient presenting with an acute Stanford type B dissection were created whereby morphometric parameters related to the dissection septum were altered, such as removal of the septum, and the variation of the number of connecting tears between the lumina. Patient-specific flow data acquired using 2D PC- MRI in the ascending aorta were used to set the inflow boundary condition. Coupled zero-dimensional (Windkessel) models representing the distal vasculature were used to define the outlet boundary conditions and tuned to match 2D PC-MRI flow data acquired in the descending aorta. Hemodynamics in the dissected aorta were compared to those in an equivalent ‘healthy aorta’, created by virtually removing the intimal flap (septum). Local regions of increased velocity, pressure, wall shear stress and alterations in flow distribution were noted, particularly in the narrow true lumen and around the primary entry tear. The computed flow patterns compared favourably with those obtained using 4D PC-MRI. A lumped-parameter heart model was subsequently used to show that in this case there was an estimated 14 % increase in left ventricular stroke work with the onset of dissection. Finally, the effect of secondary connecting tears (i.e. those excluding the primary entry and exit tears) was also studied, revealing significant hemodynamic changes when no secondary tears are included in the model, particularly in the true lumen where increases in flow over  and drops in peak pressure of 18 % were observed.
Background:
The management and prognosis of aortic dissection (AD) is often challenging and the use of personalised computational models is being explored as a tool to improve clinical outcome. Including vessel wall motion in such simulations can provide more realistic and potentially accurate results, but requires significant additional computational resources, as well as expertise. With clinical translation as the final aim, trade-offs between complexity, speed and accuracy are inevitable. The present study explores whether modelling wall motion is worth the additional expense in the case of AD, by carrying out fluid-structure interaction (FSI) simulations based on a sample patient case.
Methods:
Patient-specific anatomical details were extracted from computed tomography images to provide the fluid domain, from which the vessel wall was extrapolated. Two-way fluid-structure interaction simulations were performed, with coupled Windkessel boundary conditions and hyperelastic wall properties. The blood was modelled using the Carreau-Yasuda viscosity model and turbulence was accounted for via a shear stress transport model. A simulation without wall motion (rigid wall) was carried out for comparison purposes.
Results:
The displacement of the vessel wall was comparable to reports from imaging studies in terms of intimal flap motion and contraction of the true lumen. Analysis of the haemodynamics around the proximal and distal false lumen in the FSI model showed complex flow structures caused by the expansion and contraction of the vessel wall. These flow patterns led to significantly different predictions of wall shear stress, particularly its oscillatory component, which were not captured by the rigid wall model.
Conclusions:
Through comparison with imaging data, the results of the present study indicate that the fluid-structure interaction methodology employed herein is appropriate for simulations of aortic dissection. Regions of high wall shear stress were not significantly altered by the wall motion, however, certain collocated regions of low and oscillatory wall shear stress which may be critical for disease progression were only identified in the FSI simulation. We conclude that, if patient-tailored simulations of aortic dissection are to be used as an interventional planning tool, then the additional complexity, expertise and computational expense required to model wall motion is indeed justified.
Short-term fluctuations in arterial pressures arising from normal physiological function are buffered by a negative feedback system known as the arterial baroreflex. Initiated by altered biomechanical stretch in the vessel wall, the baroreflex coordinates a systemic response that alters heart rate, cardiac contractility and peripheral vessel vasoconstriction. In this work, a coupled 3D–0D formulation for the short-term pressure regulation of the systemic circulation is presented. Including the baroreflex feedback mechanisms, a patient-specific model of the large arteries is subjected to a simulated head up tilt test. Comparative simulations with and without baroreflex control highlight the critical role that the baroreflex has in regulating variations in pressures within the systemic circulation.
The principle functions of arterial smooth muscle cells include contraction, relaxation, and growth. Calcium signaling mechanisms govern the main functions of arterial smooth muscle and trigger specific responses.1–3 Cytosolic calcium concentrations and calcium signals are finely tuned by intracellular sources such as the sarcoplasmic reticulum, calcium-binding proteins, and plasma membrane calcium permeable channels. In hypertension, these mechanisms are substantially modified, promoting a hypercontractile state and arterial wall remodeling. In this review, we will discuss various elements that are central to intracellular calcium handling and signaling in arterial smooth muscle cells. Emphasis will be given to most recent discoveries of components that link intracellular calcium stores to plasma membrane calcium entry channels. In addition, we will propose a novel paradigm, suggesting that in hypertension, alarm signals generated by chronic innate immune system activation and transduced by pattern recognition receptors modulate calcium signaling mechanisms in arterial smooth muscle, promoting vascular dysfunction. Finally, new research directions in the context of calcium signaling in hypertension will be addressed.
Arterial smooth muscle contraction is regulated by receptor or mechanical activation of the contractile proteins actin and myosin.4 Changes in the membrane potential can also initiate contraction. The phosphorylation state of the light chain of myosin determines the contractile activity of arterial smooth muscle. Specifically, for contraction to occur, myosin light chain (MLC) kinase must phosphorylate Ser 19 of the 20-kDa regulatory MLC, enabling the interaction between myosin and actin.5,6 The cycling of the myosin cross-bridges with actin is promoted by energy released from ATP by myosin ATPase activity.7,8 In some arteries, MLC is in a phosphorylated state in the absence of any external stimuli (ie, vascular smooth muscle tone).
An increase in cytosolic calcium concentration is the trigger for vascular contraction.9 Hypertensive patients and …
Advances in numerical methods and three-dimensional imaging techniques have enabled the quantification of cardiovascular mechanics in subject-specific anatomic and physiologic models. Patient-specific models are being used to guide cell culture and animal experiments and test hypotheses related to the role of biomechanical factors in vascular diseases. Furthermore, biomechanical models based on noninvasive medical imaging could provide invaluable data on the in vivo service environment where cardiovascular devices are employed and on the effect of the devices on physiologic function. Finally, patient-specific modeling has enabled an entirely new application of cardiovascular mechanics, namely predicting outcomes of alternate therapeutic interventions for individual patients. We review methods to create anatomic and physiologic models, obtain properties, assign boundary conditions, and solve the equations governing blood flow and vessel wall dynamics. Applications of patient-specific models of cardiovascular mechanics are presented, followed by a discussion of the challenges and opportunities that lie ahead.
Arterial hypertension together with proteinuria is one of the most important factors associated with the progression of both diabetic and nondiabetic chronic kidney disease. In this review, the role of hypertension and proteinuria in renal disease progression, the BP target that should be achieved to slow the progression of renal damage, and the influence of baseline and current proteinuria on the renoprotective effects of antihypertensive therapy are discussed thoroughly. The interaction between the renoprotective effects of specific antihypertensive agents--mostly angiotensin-converting enzyme inhibitors and angiotensin receptor blockers--and the level of achieved BP also are evaluated. The body of evidence provided by several studies emphasizes the importance of both lowering BP and inhibiting the renin-angiotensin system as specific goals for renal and cardiovascular protection in chronic kidney disease.
The behavior of blood cells and vessel compliance significantly influence hemodynamic parameters, which are closely related to the development of aortic dissection. Here the two-phase non-Newtonian model and the fluid-structure interaction (FSI) method are coupled to simulate blood flow in a patient-specific dissected aorta. Moreover, three-element Windkessel model is applied to reproduce physiological pressure waves. Important hemodynamic indicators, such as the spatial distribution of red blood cells (RBCs) and vessel wall displacement, which greatly influence the hemodynamic characteristics are analyzed. Results show that the proximal false lumen near the entry tear appears to be a vortex zone with a relatively lower volume fraction of RBCs, a low time-averaged wall shear stress (TAWSS) and a high oscillatory shear index (OSI), providing a suitable physical environment for the formation of atherosclerosis. The highest TAWSS is located in the narrow area of the distal true lumen which might cause further dilation. TAWSS distributions in the FSI model and the rigid wall model show similar trend, while there is a significant difference for the OSI distributions. We suggest that an integrated model is essential to simulate blood flow in a more realistic physiological environment with the ultimate aim of guiding clinical treatment.
Aortic dissection (AD) is a complex and highly patient-specific vascular condition difficult to treat. Computational fluid dynamics (CFD) can aid the medical management of this pathology, yet its modelling and simulation are challenging. One aspect usually disregarded when modelling AD is the motion of the vessel wall, which has been shown to significantly impact simulation results. Fluid-structure interaction (FSI) methods are difficult to implement and are subject to assumptions regarding the mechanical properties of the vessel wall, which cannot be retrieved non-invasively. This paper presents a simplified 'moving-boundary method' (MBM) to account for the motion of the vessel wall in type-B AD CFD simulations, which can be tuned with non-invasive clinical images (e.g. 2D cine-MRI). The method is firstly validated against the 1D solution of flow through an elastic straight tube; it is then applied to a type-B AD case study and the results are compared to a state-of-the-art, full FSI simulation. Results show that the proposed method can capture the main effects due to the wall motion on the flow field: the average relative difference between flow and pressure waves obtained with the FSI and MBM simulations was less than 1.8% and 1.3%, respectively and the wall shear stress indices were found to have a similar distribution. Moreover, compared to FSI, MBM has the advantage to be less computationally expensive (requiring half of the time of an FSI simulation) and easier to implement, which are important requirements for clinical translation.
We review current knowledge regarding the natural transition of aortic dissection from acute to chronic stages. As this is not well understood, we also bring to bear new data from our institution. Type A dissection rarely transitions naturally into the chronic state; consequently, information is limited. Type B dissections are routinely treated medically and indeed undergo substantial changes during their temporal course. General patterns include: 1) the aorta dilates and, absent surgical intervention, aortic enlargement may cause mortality; 2) continued false lumen patency, particularly with an only partially thrombosed false lumen, increases aortic growth, whereas calcium-channel blockers affect aortic dilation favorably; 3) aortic dilation manifests a temporal dynamic, with early rapid growth and deceleration during transition; 4) the intimal flap dynamically changes over time via thickening, straightening, and loss of mobility; and 5) temporal remodeling, on the cellular level, initially shows a high grade of wall destruction; subsequently, significant fibrosis ensues.
Systemic hypertension is a risk factor for many diseases affecting the heart, brain, and kidneys. It has long been thought that hypertension leads to a thickening and stiffening of central arteries (i.e., stiffness is a consequence) while more recent evidence suggests that stiffening precedes hypertension (i.e., stiffness is a cause). We submit, however, that consideration of the wall biomechanics and hemodynamics reveals an insidious positive feedback loop that may render it irrelevant whether hypertension causes or is caused by central arterial stiffening. A progressive worsening can ensue in either case, thus any onset of stiffening merits early intervention.
Study objectives: To determine the incidence and mortality as well as to analyze the clinical and pathologic changes of aortic dissection. Design and setting: A population-based longitudinal study over 27 years on a study population of 106,500, including 66 hospitalized and 18 nonhospitalized consecutively observed patients. Measures: Analysis of data from the medical, surgical, and autopsy records of patients with aortic dissection, Results: Altogether, 86 cases of aortic dissection were found in 84 patients, corresponding to a 2.9/100,000/yr incidence. Sixty-six of the 84 patients (79%) were admitted to the hospital, and 18 patients (21%) died before admission. Their ages ranged from 36 to 97 years, with a mean of 65.7 years. The male/female ratio was 1.55 to 1. A total of 22.7% of the hospitalized patients died within the first 6 h, 33.3% within 12 h, 50% within 24 h, and 88.2% within the first 2 days after admission. Six patients were operated on, with a perioperative mortality of two of six patients and a 5-year survival of two of six patients. All patients who were not operated on died. Pain was the most frequent initial symptom. Every patient had some kind of cardiovascular and respiratory sign. Neurologic symptoms occurred in 28 of 66 patients (42%). Five patients presented with clinical pictures of acute abdomen and two with acute renal failure, Trunk arteries were affected in 33 of the 80 autopsied cases (41%), and rupture of aorta was seen in 69 cases (86%). In five cases, spontaneous healing of dissection was also found. The ratio of proximal/distal dissections was 5.1 to 1. All 18 prehospital cases were acute. Fifty-nine cases (89.4%) were acute at admission, and 7 cases (10.6%) were chronic dissections. Hypertension and advanced age were the major predisposing factors. Conclusion: Aortic dissection was the initial clinical impression in only 13 of the 84 patients (15%), Thus, 85% of the patients did not receive immediate appropriate medical treatment, For this reason, these late-recognized and/or unrecognized cases may be regarded as an untreated or symtomatically treated group, whose course may resemble the natural course of aortic dissection.
Acute type B aortic dissection (ABAD) can lead to visceral malperfusion, a potentially life-threatening complication. The purpose of this study was to investigate the presentation, management, and outcomes of ABAD patients with visceral ischemia who are enrolled in the International Registry of Acute Aortic Dissection.
Patients with ABAD enrolled in the registry between 1996 and 2013 were identified and stratified based on presence of visceral ischemia at admission. Demographics, medical history, imaging results, management, and outcomes were compared for patients with versus without visceral ischemia.
A total of 1456 ABAD patients were identified, of which 104 (7.1%) presented with visceral ischemia. Preoperative limb ischemia (28% vs 7%, P < .001) and acute renal failure (41% vs 14%, P < .001) were more common among patients with visceral ischemia. Endovascular treatment and surgery were offered to 49% and 30% of the visceral ischemia cohort, respectively; remaining patients were managed conservatively. The in-hospital mortality was 30.8% for patients with visceral ischemia and 9.1% for those without visceral ischemia (odds ratio [OR] 4.44; 95% confidence interval [CI], 2.8-7.0, P < .0001). Mortality rates were similar after surgical and endovascular management of visceral ischemia (25.8% and 25.5%, respectively, P = not significant). Among the visceral ischemia group, medical management was a predictor of mortality in multivariate analysis (OR, 5.91; 95% CI, 1.2-31.0; P = .036).
Patients with ABAD complicated by visceral ischemia have a high risk of mortality. We observed similar outcomes for patients treated by endovascular management versus surgery, whereas medical management was an independent predictor of mortality. Early diagnosis and intervention for visceral ischemia seems to be crucial.
Copyright © 2014 The American Association for Thoracic Surgery. Published by Elsevier Inc. All rights reserved.
Aortic dissection is the most devastating complication of thoracic aortic disease. In the more than 250 years since thoracic aortic dissection was first described, much has been learned about diseases of the thoracic aorta. In this review, we describe normal thoracic aortic size; risk factors for dissection, including genetic and inflammatory conditions; the underpinnings of genetic diseases associated with aneurysm and dissection, including Marfan syndrome and the role of transforming growth factor beta signaling; data on the role for medical therapies in aneurysmal disease, including beta-blockers, angiotensin receptor blockers, and angiotensin-converting enzyme inhibitors; prophylactic surgery for aneurysm; surgical techniques for the aortic root; and surgical and endovascular management of aneurysm and dissection for different aortic segments.
Uncomplicated acute type B aortic dissections are usually treated medically, but they can become acutely complicated by rapid expansion, rupture and malperfusion syndromes and in the longer term by chronic dilatation and aortic aneurysm formation. The objective of this study is to use computational fluid dynamics reconstructions of type B aortic dissections to compare geometric and haemodynamic factors between the cases selected for medical treatment and the cases selected for thoracic endovascular aortic repair (TEVAR), and to examine whether any of these factors are associated with the outcome of the medically treated group. This study includes eight type B dissection cases, with four in each group. Aortic flow analyses were carried out based on patient-specific anatomy at initial presentation before treatment. Comparisons between the two groups show that the false lumen to true lumen volume ratio is considerably higher in patients selected for TEVAR. Results from the four medically treated cases indicate that the size of the primary entry tear is the key determinant of the false lumen flow rate, which may influence the long-term outcome of medically treated patients. Potential relations between flow related parameters based on initial anatomy and subsequent anatomical changes in the medically treatment group were examined. Our initial findings based on the limited cases are that high relative residence time is a strong predictor of subsequent false lumen thrombosis, whereas pressure difference between the true and false lumen as well as the location of the largest pressure difference may be associated with the likelihood of subsequent aortic expansion.
It was found that bypass graft alone could achieve great effects in treating aortic dissection. In order to investigate the mechanical mechanism and the haemodynamic validity of the bypassing treatment for DeBakey III aortic dissection, patient-specific models of DeBakey III aortic dissection treated with different bypassing strategies were constructed. One of the bypassing strategies is bypassing between ascending aorta and abdominal aorta, and the other is bypassing between left subclavian artery and abdominal aorta. Numerical simulations under physiological flow conditions based on fluid-structure interaction were performed using finite element method. The results show that blood flow velocity, pressure and vessel wall displacement of false lumen are all reduced after bypassing. This phenomenon indicates that bypassing is an effective surgery for the treatment of DeBakey III aortic dissection. The effectiveness to cure through lumen is better when bypassing between left subclavian artery and abdominal aorta, while the effectiveness to cure blind lumen is better when bypassing between ascending aorta and abdominal aorta.
Conservative medical treatment is commonly first recommended for patients with uncomplicated Type-B aortic dissection (AD). However, if dissection-related complications occur, endovascular repair or open surgery is performed. Here we establish computational models of AD based on radiological three-dimensional images of a patient at initial presentation and after 4-years of best medical treatment (BMT). Computational fluid dynamics analyses are performed to quantitatively investigate the hemodynamic features of AD. Entry and re-entries (functioning as entries and outlets) are identified in the initial and follow-up models, and obvious variations of the inter-luminal flow exchange are revealed. Computational studies indicate that the reduction of blood pressure in BMT patients lowers pressure and wall shear stress in the thoracic aorta in general, and flattens the pressure distribution on the outer wall of the dissection, potentially reducing the progressive enlargement of the false lumen. Finally, scenario studies of endovascular aortic repair are conducted. The results indicate that, for patients with multiple tears, stent-grafts occluding all re-entries would be required to effectively reduce inter-luminal blood communication and thus induce thrombosis in the false lumen. This implicates that computational flow analyses may identify entries and relevant re-entries between true and false lumen and potentially assist in stent-graft planning.
Type B aortic dissection can be acutely complicated by rapid expansion, rupture, and malperfusion syndromes. Short-term adverse outcomes are associated with failure of the false lumen to thrombose. The reasons behind false lumen patency are poorly understood, and the objective of this pilot study was to use computational fluid dynamics reconstructions of aortic dissection cases to analyze the effect of aortic and primary tear morphology on flow characteristics and clinical outcomes in patients with acute type B dissections.
Three-dimensional patient-specific aortic dissection geometry was reconstructed from computed tomography scans of four patients presenting with acute type B aortic dissection and a further patient with sequential follow-up scans. The cases were selected based on their clinical presentation. Two were complicated by acute malperfusion that required emergency intervention. Three patients were uncomplicated and were managed conservatively. The patient-specific aortic models were used in computational simulations to assess the effect of aortic tear morphology on various parameters including flow, velocity, shear stress, and turbulence.
Pulsatile flow simulation results showed that flow rate into the false lumen was dependent on both the size and position of the primary tear. Linear regression analysis demonstrated a significant relationship between percentage flow entering the false lumen and the size of the primary entry tear and an inverse relationship between false lumen flow and the site of the entry tear. Subjects complicated by malperfusion had larger-dimension entry tears than the uncomplicated cases (93% and 82% compared with 32% and 55%, respectively). Blood flow, wall shear stress, and turbulence levels varied significantly between subjects depending on aortic geometry. Highest wall shear stress (>7 Pa) was located at the tear edge, and progression of false lumen thrombosis was associated with prolonged particle residence times.
Results obtained from this preliminary work suggest that aortic morphology and primary entry tear size and position exert significant effects on flow and other hemodynamic parameters in the dissected aorta in this preliminary work. Blood flow into the false lumen increases with increasing tear size and proximal location. Morphologic analysis coupled with computational fluid dynamic modeling may be useful in predicting acute type B dissection behavior allowing for selection of proper treatment modalities, and further confirmatory studies are warranted.
This paper is concerned with the mathematical structure of the immersed
boundary (IB) method, which is intended for the computer simulation of
fluid–structure interaction, especially in biological fluid dynamics. The IB
formulation of such problems, derived here from the principle of least action,
involves both Eulerian and Lagrangian variables, linked by the Dirac
delta function. Spatial discretization of the IB equations is based on a fixed
Cartesian mesh for the Eulerian variables, and a moving curvilinear mesh for
the Lagrangian variables. The two types of variables are linked by interaction
equations that involve a smoothed approximation to the Dirac delta function.
Eulerian/Lagrangian identities govern the transfer of data from one mesh to
the other. Temporal discretization is by a second-order Runge–Kutta method.
Current and future research directions are pointed out, and applications of
the IB method are briefly discussed.
Thoracic endovascular aortic repair is a promising means of treating patients with complicated type B aortic dissection by excluding the intimomedial tears. This study aims to characterize the location of tears and to propose a classification of type B aortic dissections based on these findings.
Advanced protocols in computed tomography scans of patients with type B aortic dissection were used to identify the size and location of intimomedial tears in relation to the origin of the left subclavian artery. Aortic imaging details in 72 un-operated patients were used as a reference standard. From 1999 to 2005, 44 patients underwent primary endovascular treatment for complications of type B aortic dissection.
Each patient had an average of 2.8 +/- 2.11 intimomedial tears. The median intimomedial tear surface area was 0.63 cm(2). The presence of >or=3 or >or=5 intimomedial tears in the descending thoracic aorta did not correlate with aortic branch malperfusion (P > .05). Thirteen of 26 (50%) patients with a tear >1.9 cm(2) had aortic branch malperfusion (P = .032). Ten of 14 (71%) patients with a tear >4.86 cm(2) (mean plus one standard deviation) had aortic branch malperfusion (P = .002). The location of tears ranged from -6 mm to +459.2 mm from the left subclavian artery orifice: 80.5% (n = 99) of these tears were above the reference origin of the celiac artery. Eight of 13 patients (62%) with a tear distal to 282 mm (the orifice of the celiac artery) had aortic branch malperfusion in (P = .04). A classification for the location of intimomedial tears is proposed with potential clinical relevance to endovascular repair: type 1 has no identifiable tears; type 2 has one or more tears with no tears distal to the orifice of the celiac artery; type 3 has tears involving the branch vessels of the abdominal aorta; and type 4 has intimomedial tears distal to the aortic bifurcation.
Characterization and location of intimomedial tears using computed tomography (CT) imaging is feasible and represents an important step in the management of type B aortic dissection. The location and surface area of tears is associated with malperfusion. Based on the proposed classification and anatomic reference data, three out of every four patients may have a favorable constellation of intimomedial tears (type 1 or 2) that would be amenable to endovascular repair and reverse aortic remodeling. The clinical correlation will be established in upcoming studies.
Impact on survival of different treatment strategies was analyzed in 571 patients with acute type B aortic dissection enrolled from 1996 to 2005 in the International Registry of Acute Aortic Dissection.
The optimal treatment for acute type B dissection is still a matter of debate.
Information on 290 clinical variables were compared, including demographics; medical history; clinical presentation; physical findings; imaging studies; details of medical, surgical, and endovascular management; in-hospital clinical events; and in-hospital mortality.
Of the 571 patients with acute type B aortic dissection, 390 (68.3%) were treated medically, 59 (10.3%) with standard open surgery and 66 (11.6%) with an endovascular approach. Patients who underwent emergency endovascular or open surgery were younger (mean age 58.8 years, p < 0.001) than their counterparts treated conservatively, and had male preponderance and hypertension in 76.9%. Patients submitted to surgery presented with a wider aortic diameter than patients treated by interventional techniques or by medical therapy (5.36 +/- 1.7 cm vs. 4.62 +/- 1.4 cm vs. 4.47 +/- 1.4 cm, p = 0.003). In-hospital complications occurred in 20% of patients subjected to endovascular technique and in 40% of patients after open surgical repair. In-hospital mortality was significantly higher after open surgery (33.9%) than after endovascular treatment (10.6%, p = 0.002). After propensity and multivariable adjustment, open surgical repair was associated with an independent increased risk of in-hospital mortality (odds ratio: 3.41, 95% confidence interval: 1.00 to 11.67, p = 0.05).
In the International Registry of Acute Aortic Dissection, the less invasive nature of endovascular treatment seems to provide better in-hospital survival in patients with acute type B dissection; larger randomized trials or comprehensive registries are needed to access impact on outcomes.
The incidence of peripheral vascular complications in 272 patients with aortic dissection during a 25-year span was determined, as was outcome after a uniform, aggressive surgical approach directed at repair of the thoracic aorta. One hundred twenty-eight patients (47%) presented with acute type A dissection, 70 (26%) with chronic type A, 40 (15%) with acute type B, and 34 (12%) with chronic type B dissections. Eighty-five patients (31%) sustained one or more peripheral vascular complications: Seven (3%) had a stroke, nine (3%) had paraplegia, 66 (24%) sustained loss of a peripheral pulse, 22 (8%) had impaired renal perfusion, and 14 patients (5%) had compromised visceral perfusion. Following repair of the thoracic aorta, local peripheral vascular procedures were unnecessary in 92% of patients who presented with absence of a peripheral pulse. The operative mortality rate for all patients was 25% +/- 3% (68 of 272 patients). For the subsets of individuals with paraplegia, loss of renal perfusion, and compromised visceral perfusion, the operative mortality rates (+/- 70% confidence limits) were high: 44% +/- 17% (4 of 9 patients), 50% +/- 11% (11 of 22 patients), and 43% +/- 14% (6 of 14 patients), respectively. The mortality rates were lower for patients presenting with stroke (14% +/- 14% [1 of 7 patients]) or loss of peripheral pulse (27% +/- 6% [18 of 66 patients]). Multivariate analysis revealed that impaired renal perfusion was the only peripheral vascular complication that was a significant independent predictor of increased operative mortality risk (p = 0.024); earlier surgical referral (replacement of the appropriate section of the thoracic aorta) or more expeditious diagnosis followed by surgical renal artery revascularization after a thoracic procedure may represent the only way to improve outcome in this high-risk patient subset. Early, aggressive thoracic aortic repair (followed by aortic fenestration and/or abdominal exploration with or without direct visceral or renal vascular reconstruction when necessary) can save some patients with compromised visceral perfusion; however, once visceral infarction develops the prognosis is also poor. Increased awareness of these devastating complications of aortic dissection and the availability of better diagnostic tools today may improve the survival rate for these patients in the future. The initial surgical procedure should include repair of the thoracic aorta in most patients.
Blood velocity waveforms from the fetal thoracic aorta, obtained by a combination of real-time and Doppler ultrasound and a spectral analyser, detected a total end-diastolic block in the curve in nine pregnancies with chronic fetal hypoxia. Simultaneous cardiotocographic recordings were normal except in one patient. These findings suggest that hypoxia causes an increase of peripheral vascular resistance in the tissues distal to the thoracic aorta and that this change appears earlier than pathological changes in the cardiotocogram. The potential clinical value of this technique justifies further research.
Densitometry by video dilution permits regional blood estimation by a modification of the indicator dilution technique originally described by Stewart and Hamilton. Contrast mass is measured from the video fluoroscopic image rather than from dye concentration in blood withdrawn through a sampling catheter. From more than 400 studies, 70 patients who presumably had normal regional flows were selected. Flows in the cerebral, splanchnic, renal, and extremity circulations were determined as a percentage of ascending aortic flow (cardiac output). The regional flow determined by video dilution technique compare well with results of other techniques described in the literature. It is now possible to measure distribution of cardiac output to any major artery during routine angiography, thus providing another determinant of arterial adequacy. These normal values are currently used by the investigators as standards for the evaluation of patients with a variety of vascular diseases.
To determine the anatomic, hemodynamic, and radiologic characteristics of branch-vessel compromise in patients with aortic dissection.
Sixty-two patients with aortic dissection were evaluated with aortography (n = 62), intravascular ultrasound (US) (n = 35), and manometry (n = 56). Branch-vessel compromise with ischemia was suspected in 40 of these patients. Radiologic and manometric findings were correlated with clinical findings of ischemia. Femoral artery pulse strength was correlated with access from the respective femoral artery to the true and false lumina of the dissected aorta.
Twenty-six of 40 patients suspected of having ischemia had angiographic evidence of branch-vessel compromise, and intravascular US helped identify two types of branch-vessel compromise in them: static (dissection intersected and narrowed the vessel origin) and dynamic (dissection spared the vessel origin, but the dissection flap appeared to compress the true lumen at or above the origin and covered the origin). False-lumen pressure in classic dissections exceeded (n = 16) or equaled (n = 30) true-lumen pressure. Branch vessels that arose exclusively from the false lumen were well perfused. Findings of a dissection flap oriented concave toward the false lumen were 91% sensitive and 72% specific for a true-lumen pressure deficit.
Intravascular US and manometric findings clarify the mechanisms of branch-vessel compromise after aortic dissection and provide a rational guide for percutaneous treatment.
Thrombosis occurs in a dynamic rheological field that constantly changes as the thrombus grows to occlusive dimensions. In the initiation of thrombosis, flow conditions near the vessel wall regulate how quickly reactive components are delivered to the injured site and how rapidly the reaction products are disseminated. Whereas the delivery and removal of soluble coagulation factors to the vessel is thought to occur via classic convection-diffusion phenomena, the movement of cells and platelets to the injured wall is strongly augmented by flow-dependent cell-cell collisions that enhance their ability to interact with the wall. In addition, increased shear conditions have been shown to activate platelets, alter the cellular localization of proteins such as tissue factor (TF) and TF pathway inhibitor, and regulate gene production. In the absence of high shearing forces, red cells, leukocytes, and platelets can form stable aggregates with each other or cells lining the vessel wall, which, in addition to altering the biochemical makeup of the aggregate or vessel wall, effectively increases the local blood viscosity. Thus, hemodynamic forces not only regulate the predilection of specific anatomic sites to thrombosis, but they strongly influence the biochemical makeup of thrombi and the reaction pathways involved in thrombus formation.
Despite its comparatively small size, the brain receives a disproportionate amount of blood flow compared with most other organ systems. Cerebral blood flow is closely coupled to brain metabolism and can be affected by respiratory-induced CO2 changes and arterial blood pressure. Autoregulation is the intrinsic capacity of resistance vessels in end organs, such as heart, kidney, and brain, to dilate and constrict in response to dynamic perfusion pressure changes, maintaining blood flow relatively constant (Figure). This rapid vascular response occurs within seconds of arterial pressure fluctuations. The exact mediators of cerebral autoregulation are not completely understood. However, neurogenic stimuli; metabolic factors, such as adenosine accumulation during low perfusion; and direct intravascular pressure effects on smooth muscle or mediated via endothelial-derived relaxation factor (ie, NO) and constriction factor (ie, endothelin-1) have been implicated.1
Autoregulation maintains cerebral blood flow relatively constant between 50 and 150 mm Hg mean arterial pressure. The range is right shifted in chronically hypertensive patients.
The cerebral resistance vessels in normotensive individuals are known to autoregulate across a broad range of mean arterial pressures. Perfusion pressures below the lower limit result in initially increased oxygen extraction …
The aim of this study was to assess the significance of malperfusion syndromes in patients with acute type A aortic dissection following a contemporary surgical management algorithm and the effects on morbidity, hospital mortality, and long-term survival. We believe that obliteration of the primary tear site with restoration of flow in the true aortic lumen results in decreased need for revascularization of malperfused organ systems.
Our operative approach aims at replacing the entire ascending aorta, resuspension of the aortic valve with repair or replacement of the sinus segment, and routine open replacement of the arch under hypothermic circulatory arrest with retrograde cerebral perfusion with obliteration of false lumen at the distal arch/proximal descending thoracic aorta, thus reestablishing normal flow in the descending thoracic true lumen. From January 1993 to December 2004, 221 consecutive patients underwent repair of acute type A aortic dissection at our institution. Data were collected retrospectively and prospectively. Various types of malperfusion syndromes were present in 26.7% of patients. The organ systems with malperfusion were as follows: cardiac, 7.2%; cerebral, 7.2%; ileofemoral, 12.7%; renal, 4.1%; mesenteric, 1.4%; innominate, 5.4%; and spine, 2.2%.
Coronary malperfusion required coronary revascularization in 62.5% of cases. Distal revascularization was needed in 42.9% of patients with ileofemoral malperfusion. Patients with malperfusion were more likely to suffer perioperative myocardial infarction (p<0.001), postoperative coma (p=0.012), delirium (p=0.011), sepsis (p=0.006), acute renal failure (p=0.017), dialysis (p=0.018), and acute limb ischemia (p<0.001). The in-hospital mortality was 30.5% in patients presenting with any malperfusion syndrome while only 6.2% in patients without malperfusion syndrome (p<0.001). Both cardiac (p=0.020) and cerebral malperfusions (p<0.001) were risk factors for in-hospital mortality. The actuarial long-term survival in patients with malperfusion syndrome was estimated by Kaplan-Meier methods to be 67.8%+/-6.1% at 1 year, 54.0%+/-7.0% at 5 years, and 43.1%+/-8.0% at 10 years and for patient without malperfusion 82.7%+/-3.0% at 1 year, 66.3%+/-3.9% at 5 years, and 46.1%+/-6.7% at 10 years (log rank 2.55, p=0.110). Cerebral malperfusion was a significant risk factor for decreased long-term survival (p=0.0002).
The occurrence of malperfusion in patients with acute type A dissection is associated with significant increased risk of in-hospital mortality and complications. Additional revascularization is generally needed in patients with coronary malperfusion and ileofemoral malperfusion. Patients presenting with cardiac and cerebral malperfusions have a high hospital mortality and preoperative cerebral malperfusion is associated with dismal long-term survival.
Clinical profiles and outcomes of patients with acute type B aortic dissection have not been evaluated in the current era.
Accordingly, we analyzed 384 patients (65+/-13 years, males 71%) with acute type B aortic dissection enrolled in the International Registry of Acute Aortic Dissection (IRAD). A majority of patients had hypertension and presented with acute chest/back pain. Only one-half showed abnormal findings on chest radiograph, and almost all patients had computerized tomography (CT), transesophageal echocardiography, magnetic resonance imaging (MRI), and/or aortogram to confirm the diagnosis. In-hospital mortality was 13% with most deaths occurring within the first week. Factors associated with increased in-hospital mortality on univariate analysis were hypotension/shock, widened mediastinum, periaortic hematoma, excessively dilated aorta (>or=6 cm), in-hospital complications of coma/altered consciousness, mesenteric/limb ischemia, acute renal failure, and surgical management (all P<0.05). A risk prediction model with control for age and gender showed hypotension/shock (odds ratio [OR] 23.8, P<0.0001), absence of chest/back pain on presentation (OR 3.5, P=0.01), and branch vessel involvement (OR 2.9, P=0.02), collectively named 'the deadly triad' to be independent predictors of in-hospital death.
Our study provides insight into current-day profiles and outcomes of acute type B aortic dissection. Factors associated with increased in-hospital mortality ("the deadly triad") should be identified and taken into consideration for risk stratification and decision-making.
Epidemiology and Clinicopathology of Aortic Dissection
Changing Pathology of the Thoracic Aorta From Acute to Chronic Dissection: Literature Review and Insights
The Immersed Boundary Method
Aortic Intimal Tears: Detection With Spiral Computed Tomography
- L E Quint
- J F Platt
- S S Sonnad
- G M Deeb
- D M Williams
Quint, L. E., Platt, J. F., Sonnad, S. S., Deeb, G. M., and Williams, D. M., 2003,
"Aortic Intimal Tears: Detection With Spiral Computed Tomography," J. Endovascular Ther., 10(3), pp. 505-510.