Academic literature on the topic 'Established aneurysm'
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Journal articles on the topic "Established aneurysm"
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Lyu, Yanxia, Jie Luo, Yonghong Zhang, et al. "An Effective and Simple Way to Establish Elastase-Induced Middle Carotid Artery Fusiform Aneurysms in Rabbits." BioMed Research International 2020 (August 26, 2020): 1–12. http://dx.doi.org/10.1155/2020/6707012.
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Objective. Elastase-induced aneurysms in rabbits have been proposed as a preclinical tool for device development, but there is still much deficiency in those aneurismal models. So we need to explore the efficient and convenient animal models for the investigation of intracranial aneurysms. Then, we compared and analyzed three methods of elastase-induced carotid artery aneurysms in rabbits and aimed to find a simple, effective, and reproducible method for creating elastase-induced aneurysms. Methods. 42 standard feeding male adult Japanese white rabbits (3.05±0.65 kg) were randomly divided into 3 groups and treated with elastase ablation to create common carotid artery (RCCA) aneurysm models: Group A (root-RCCA medication group, n=12), Group B (mid-RCCA medication group, n=18), and Group C (ligated RCCA+medication group, n=12). For Group A, the origin of the RCCA was blocked by two temporary aneurysm clips, and the resulting 2 cm cavity was infused with elastase for 20 min, then the clip was removed and the RCCA was not ligated. For Group B, the middle part of RCCA was treated the same way as Group A and the RCCA was not ligated. For Group C, the middle part of RCCA was treated as Group B, but the distal RCCA was ligated. After the aneurysm models were created for 3 weeks, prior to sacrificing the animals, color Doppler ultrasound and angiography were performed for blood flow measurements inside the aneurysms. Histological analysis (such as SMA-α, CD31, CD34, CD68, collagen IV, and Ki67) and the other relevant indexes were compared between the ideal model’s aneurysmal tissues and the human intracranial aneurysm’s tissues to confirm whether we have successfully established elastase-induced aneurysm models. Results. Compared with human intracranial aneurysm specimens by the color Doppler ultrasound, angiography, and changes in the inner diameter of arteries, all three methods have successfully established the elastase-induced aneurysm models. Histology showed that biological responses were similar to both human cerebral aneurysms and previously published elastase-induced rabbit aneurysm models. Group A and Group B had the same morphology, but Group A had a higher mortality rate than Group B. Group B and Group C had different morphology. The aneurysm of Group C was more similar to human cerebral aneurysms but had a higher mortality rate than Group B. Group B was confirmed not only as an alternative method but also as a more safe and effective method for creating elastase-induced aneurysm models. Conclusion. Through analysis and comparison, the Group B is proven to be the simplest, reproducible, and most effective modeling method. The aneurysm model established by Group B can be used for basic research related to aneurysm mechanism. We have provided a new and effective method for basic research on aneurysm.
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Swiatek, Vanessa M., Belal Neyazi, Jorge A. Roa, et al. "Aneurysm Wall Enhancement Is Associated With Decreased Intrasaccular IL-10 and Morphological Features of Instability." Neurosurgery 89, no. 4 (2021): 664–71. http://dx.doi.org/10.1093/neuros/nyab249.
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Abstract BACKGROUND High-resolution vessel wall imaging plays an increasingly important role in assessing the risk of aneurysm rupture. OBJECTIVE To introduce an approach toward the validation of the wall enhancement as a direct surrogate parameter for aneurysm stability. METHODS A total of 19 patients harboring 22 incidental intracranial aneurysms were enrolled in this study. The aneurysms were dichotomized according to their aneurysm-to-pituitary stalk contrast ratio using a cutoff value of 0.5 (nonenhancing < 0.5; enhancing ≥ 0.5). We evaluated the association of aneurysm wall enhancement with morphological characteristics, hemodynamic features, and inflammatory chemokines directly measured inside the aneurysm. RESULTS Differences in plasma concentration of chemokines and inflammatory molecules, morphological, and hemodynamic parameters were analyzed using the Welch test or Mann-Whitney U test. The concentration ΔIL-10 in the lumen of intracranial aneurysms with low wall enhancement was significantly increased compared to aneurysms with strong aneurysm wall enhancement (P = .014). The analysis of morphological and hemodynamic parameters showed significantly increased values for aneurysm volume (P = .03), aneurysm area (P = .044), maximal diameter (P = .049), and nonsphericity index (P = .021) for intracranial aneurysms with strong aneurysm wall enhancement. None of the hemodynamic parameters reached statistical significance; however, the total viscous shear force computed over the region of low wall shear stress showed a strong tendency toward significance (P = .053). CONCLUSION Aneurysmal wall enhancement shows strong associations with decreased intrasaccular IL-10 and established morphological indicators of aneurysm instability.
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Brinjikji, Waleed, Bong Jae Chung, Carlos Jimenez, Christopher Putman, David F. Kallmes, and Juan R. Cebral. "Hemodynamic differences between unstable and stable unruptured aneurysms independent of size and location: a pilot study." Journal of NeuroInterventional Surgery 9, no. 4 (2016): 376–80. http://dx.doi.org/10.1136/neurintsurg-2016-012327.
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BackgroundWhile clinical and angiographic risk factors for intracranial aneurysm instability are well established, it is reasonable to postulate that intra-aneurysmal hemodynamics also have a role in aneurysm instability.ObjectiveTo identify hemodynamic characteristics that differ between radiologically unstable and stable unruptured intracranial aneurysms.Materials and methods12 pairs of unruptured intracranial aneurysms with a 3D rotational angiographic set of images and followed up longitudinally without treatment were studied. Each pair consisted of one stable aneurysm (no change on serial imaging) and one unstable aneurysm (demonstrated growth of at least 1 mm diameter or ruptured during follow-up) of matching size (within 10%) and locations. Patient-specific computational fluid dynamics models were created and run under pulsatile flow conditions. Relevant hemodynamic and geometric variables were calculated and compared between groups using the paired Wilcoxon test.ResultsThe area of the aneurysm under low wall shear stress (low shear stress area (LSA)) was 2.26 times larger in unstable aneurysms than in stable aneurysms (p=0.0499). The mean aneurysm vorticity was smaller by a factor of 0.57 in unstable aneurysms compared with stable aneurysms (p=0.0499). No statistically significant differences in geometric variables or shape indices were found.ConclusionsThis pilot study suggests there may be hemodynamic differences between unstable and stable unruptured cerebral aneurysms. In particular, the area under low wall shear stress was larger in unstable aneurysms. These findings should be considered tentative until confirmed by future larger studies.
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Colovic, R., L. Davidovic, D. Bilanovic, et al. "Splenic artery aneurysms." Acta chirurgica Iugoslavica 53, no. 1 (2006): 41–44. http://dx.doi.org/10.2298/aci0601041c.
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Although the third most frequent aneurysm in the abdomen, after aneurysms of the aorta and iliac arteries, and most frequent aneurisms of visceral arteries, splenic artery aneurysms are rare, but not very rare. Thanks to the new imaging techniques, first of all ultrasonography, they have been discovered with increasing frequency. We present a series of 9 splenic artery aneurysms. Seven patients were female and two male of average age 49 years (ranging from 28 to 75 years). The majority of affected women were multiparae, with average 3 children (ranging from 1 to 6). One patient had a subacute rupture, and 2 had ruptures into the splenic vein causing portal hypertension. The spleen was enlarged in 7 out of 9 patients. The average size of aneurysms was 3,2 cm (ranging from 2 to 8 cm). The preoperative diagnosis of splenic artery aneurysm was established in 6 patients while in 3 patients aneurism was accidentally found during other operations, during splenectomy in 2, and during the excision of a retroperitoneal tumor in 1 patient. Aneurysmectomy was carried out in 7 patients, while a ligation of the incoming and out coming wessels was performed in 2 patients with arteriovenous fistula. Splenectomy was performed in 6 patients, while pancreatic tail resection, cholecystectomy and excision of the retroperitoneal tumor were performed in 3 patients. Additional resection of the abdominal aortic aneurysm with reconstruction of aortoiliac segment was performed in 2 patients. There were no mortality and the postoperative recovery was uneventful in all patients.
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Suzuki, Tomoaki, Christopher J. Stapleton, Matthew J. Koch, et al. "Decreased wall shear stress at high-pressure areas predicts the rupture point in ruptured intracranial aneurysms." Journal of Neurosurgery 132, no. 4 (2020): 1116–22. http://dx.doi.org/10.3171/2018.12.jns182897.
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OBJECTIVEDegenerative cerebral aneurysm walls are associated with aneurysm rupture and subarachnoid hemorrhage. Thin-walled regions (TWRs) represent fragile areas that may eventually lead to aneurysm rupture. Previous computational fluid dynamics (CFD) studies reported the correlation of maximum pressure (Pmax) areas and TWRs; however, the correlation with aneurysm rupture has not been established. This study aims to investigate this hemodynamic correlation.METHODSThe aneurysmal wall surface at the Pmax areas was intraoperatively evaluated using a fluid flow formula under pulsatile blood flow conditions in 23 patients with 23 saccular middle cerebral artery (MCA) bifurcation aneurysms (16 unruptured and 7 ruptured). The pressure difference (Pd) at the Pmax areas was calculated by subtracting the average pressure (Pave) from the Pmax and normalized by dividing this by the dynamic pressure at the aneurysm inlet side. The wall shear stress (WSS) was also calculated at the Pmax areas, aneurysm dome, and parent artery. These hemodynamic parameters were used to validate the correlation with TWRs in unruptured MCA aneurysms. The characteristic hemodynamic parameters at the rupture points in ruptured MCA aneurysms were then determined.RESULTSIn 13 of 16 unruptured aneurysms (81.2%), Pmax areas were identified that corresponded to TWRs. In 5 of the 7 ruptured cerebral aneurysms, the Pmax areas coincided with the rupture point. At these areas, the Pd values were not higher than those of the TWRs in unruptured cerebral aneurysms; however, minimum WSS, time-averaged WSS, and normalized WSS at the rupture point were significantly lower than those of the TWRs in unruptured aneurysms (p < 0.01).CONCLUSIONSAt the Pmax area of TWRs, decreased WSS appears to be the crucial hemodynamic parameter that indicates the risk of aneurysm rupture.
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Chen, Chunguang, Fei Liang, Yupeng Zhang, and Chuhan Jiang. "Modified Intravascular Interventional Operation of Balloon-Bound Elastase Induction Method to Establish Rabbit Aneurysm Model Using Cardiovascular Angiography." Journal of Medical Imaging and Health Informatics 10, no. 6 (2020): 1389–94. http://dx.doi.org/10.1166/jmihi.2020.3023.
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Objective: In this paper, we establish a simple, efficient and stable rabbit aneurysm model using modified intravascular interventional operation of balloon-bound elastase induction method. Methods: We selected 20 healthy adult New Zealand white rabbits. An aortic aneurysm model of rabbit right common carotid artery was established by modified intravascular interventional balloon-binding elastase induction method using cardiovascular angiography. The cerebral angiography confirmed the model successfully after 4 weeks. Some animals were given paraffin-embedded H-E staining and elastic fiber staining after sacrifice. Angiography was performed for all experiments to build our models and to confirm our findings. Results: Two rabbits died during postoperative feeding, and the remaining 18 rabbits were cultured for 4 weeks and confirmed by angiography to make an aneurysm model. The success rate of aneurysm was 90%, the diameter of the tumor-bearing artery was 3.12±0.20, the short diameter of the tumor was 3.41±0.88, the long diameter of the tumor was 6.30±1.65, and the width of the neck was 3.49±0.80. HE pathology showed that the destruction of the elastic layer of the aneurysm disappeared, similar to the pathological changes of human aneurysms. Conclusions: The rabbit model of aneurysm was established by modified intravascular intervention combined with elastase induction based on angiography. It is similar to human aneurysm in morphology, histology and hemodynamics. The method is simple, the damage is small, the aneurysmal formation rate is high, and the performance is high. Stable and reliable, low production cost, it is an ideal animal model for the development of preclinical neurological interventional devices.
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Verikokos, Christos, Georgios Karaolanis, Mikes Doulaptsis, et al. "Giant Popliteal Artery Aneurysm: Case Report and Review of the Literature." Case Reports in Vascular Medicine 2014 (2014): 1–4. http://dx.doi.org/10.1155/2014/780561.
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Popliteal artery aneurysms (PAAs) are rare in general population but represent the second most common peripheral arterial aneurysms following those located in the aortoiliac segment. They usually affect men over 60 years old with established cardiovascular disease caused by atherosclerosis. Other more unusual conditions such as trauma, congenital popliteal aneurysm, mycotic aneurysm, inflammatory arteritis, or popliteal entrapment are responsible. The authors report the first ever case of a male diagnosed with chronic renal failure with giant popliteal artery aneurysm. We have successfully resected the aneurysm and revascularized with synthetic graft.
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Yokoi, Toshihiro, Takahiro Isono, Makoto Saitoh, Yayoi Yoshimura та Kazuhiko Nozaki. "Suppression of cerebral aneurysm formation in rats by a tumor necrosis factor–α inhibitor". Journal of Neurosurgery 120, № 5 (2014): 1193–200. http://dx.doi.org/10.3171/2014.1.jns13818.
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Object Although cerebral aneurysmal subarachnoid hemorrhage is a devastating disease for humans, effective medical treatments have not yet been established. Recent reports have shown that regression of some inflammatory-related mediators has protective effects in experimental cerebral aneurysm models. This study corroborated the effectiveness of tumor necrosis factor–α (TNF-α) inhibitor for experimentally induced cerebral aneurysms in rats. Methods Five-week-old male rats were prepared for induction of cerebral aneurysms and divided into 3 groups, 2 groups administered different concentrations of a TNF-α inhibitor (etanercept), and 1 control group. One month after aneurysm induction, 7-T MRI was performed. The TNF-α inhibitor groups received subcutaneous injection of 25 μg or 2.5 μg of etanercept, and the control group received subcutaneous injection of normal saline every week. The TNF-α inhibitor administrations were started at 1 month after aneurysm induction to evaluate its suppressive effects on preexisting cerebral aneurysms. Arterial circles of Willis were obtained and evaluated 3 months after aneurysm induction. Results Rats administered a TNF-α inhibitor experienced significant increases in media thickness and reductions in aneurysmal size compared with the control group. Immunohistochemical staining showed that treatment with a TNF-α inhibitor suppressed matrix metalloproteinase (MMP)–9 and inducible nitric oxide synthase (iNOS) expression through the luminal surface of the endothelial cell layer, the media and the adventitia at the site of aneurysmal formation, and the anterior cerebral artery–olfactory artery bifurcation. Quantitative polymerase chain reaction also showed suppression of MMP-9 and iNOS by TNF-α inhibitor administration. Conclusions Therapeutic administration of a TNF-α inhibitor significantly reduced the formation of aneurysms in rats. These data also suggest that TNF-α suppression reduced some inflammatory-related mediators that are in the downstream pathway of nuclear factor-κB.
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Ishida, Wataru, Masayuki Sato, Tatsuo Amano, and Yuji Matsumaru. "The significant impact of framing coils on long-term outcomes in endovascular coiling for intracranial aneurysms: how to select an appropriate framing coil." Journal of Neurosurgery 125, no. 3 (2016): 705–12. http://dx.doi.org/10.3171/2015.7.jns15238.
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OBJECTIVE The importance of a framing coil (FC)—the first coil inserted into an aneurysm during endovascular coiling, also called a lead coil or a first coil—is recognized, but its impact on long-term outcomes, including recanalization and retreatment, is not well established. The purposes of this study were to test the hypothesis that the FC is a significant factor for aneurysmal recurrence and to provide some insights on appropriate FC selection. METHODS The authors retrospectively reviewed endovascular coiling for 280 unruptured intracranial aneurysms and gathered data on age, sex, aneurysm location, aneurysm morphology, maximal size, neck width, adjunctive techniques, recanalization, retreatment, follow-up periods, total volume packing density (VPD), volume packing density of the FC, and framing coil percentage (FCP; the percentage of FC volume in total coil volume) to clarify the associated factors for aneurysmal recurrence. RESULTS Of 236 aneurysms included in this study, 33 (14.0%) had recanalization, and 18 (7.6%) needed retreatment during a mean follow-up period of 37.7 ± 16.1 months. In multivariate analysis, aneurysm size (odds ratio [OR] = 1.29, p < 0.001), FCP < 32% (OR 3.54, p = 0.009), and VPD < 25% (OR 2.96, p = 0.015) were significantly associated with recanalization, while aneurysm size (OR 1.25, p < 0.001) and FCP < 32% (OR 6.91, p = 0.017) were significant predictors of retreatment. VPD as a continuous value or VPD with any cutoff value could not predict retreatment with statistical significance in multivariate analysis. CONCLUSIONS FCP, which is equal to the FC volume as a percentage of the total coil volume and is unaffected by the morphology of the aneurysm or the measurement error in aneurysm length, width, or height, is a novel predictor of recanalization and retreatment and is more significantly predictive of retreatment than VPD. To select FCs large enough to meet the condition of FCP ≥ 32% is a potential relevant factor for better long-term outcomes. These findings support our hypothesis that the FC is a significant factor for aneurysmal recurrence.
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Reynolds, Matthew R., Robert T. Buckley, Santoshi S. Indrakanti, et al. "The safety of vasopressor-induced hypertension in subarachnoid hemorrhage patients with coexisting unruptured, unprotected intracranial aneurysms." Journal of Neurosurgery 123, no. 4 (2015): 862–71. http://dx.doi.org/10.3171/2014.12.jns141201.
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OBJECT Vasopressor-induced hypertension (VIH) is an established treatment for patients with aneurysmal subarachnoid hemorrhage (SAH) who develop vasospasm and delayed cerebral ischemia (DCI). However, the safety of VIH in patients with coincident, unruptured, unprotected intracranial aneurysms is uncertain. METHODS This retrospective multiinstitutional study identified 1) patients with aneurysmal SAH and 1 or more unruptured, unprotected aneurysms who required VIH therapy (VIH group), and 2) patients with aneurysmal SAH and 1 or more unruptured, unprotected aneurysms who did not require VIH therapy (non-VIH group). All patients had previously undergone surgical or endovascular treatment for the presumed ruptured aneurysm. Comparisons between the VIH and non-VIH patients were made in terms of the patient characteristics, clinical and radiographic severity of SAH, total number of aneurysms, number of ruptured/unruptured aneurysms, aneurysm location/size, number of unruptured and unprotected aneurysms during VIH, severity of vasospasm, degree of hypervolemia, and degree and duration of VIH therapy. RESULTS For the VIH group (n = 176), 484 aneurysms were diagnosed, 231 aneurysms were treated, and 253 unruptured aneurysms were left unprotected during 1293 total days of VIH therapy (5.12 total years of VIH therapy for unruptured, unprotected aneurysms). For the non-VIH group (n = 73), 207 aneurysms were diagnosed, 93 aneurysms were treated, and 114 unruptured aneurysms were left unprotected. For the VIH and non-VIH groups, the mean sizes of the ruptured (7.2 ± 0.3 vs 7.8 ± 0.6 mm, respectively; p = 0.27) and unruptured (3.4 ± 0.2 vs 3.2 ± 0.2 mm, respectively; p = 0.40) aneurysms did not differ. The authors observed 1 new SAH from a previously unruptured, unprotected aneurysm in each group (1 of 176 vs 1 of 73 patients; p = 0.50). Baseline patient characteristics and comorbidities were similar between groups. While the degree of hypervolemia was similar between the VIH and non-VIH patients (fluid balance over the first 10 days of therapy: 3146.2 ± 296.4 vs 2910.5 ± 450.7 ml, respectively; p = 0.67), VIH resulted in a significant increase in mean arterial pressure (mean increase over the first 10 days of therapy relative to baseline: 125.1% ± 1.0% vs 98.2% ± 1.2%, respectively; p < 0.01) and systolic blood pressure (125.6% ± 1.1% vs. 104.1% ± 5.2%, respectively; p < 0.01). CONCLUSIONS For small, unruptured, unprotected intracranial aneurysms in SAH patients, the frequency of aneurysm rupture during VIH therapy is rare. The authors do not recommend withholding VIH therapy from these patients.
Dissertations / Theses on the topic "Established aneurysm"
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Liu, Jing. "THE ROLE OF APOB-CONTAINING LIPOPROTEINS IN ABDOMINAL AORTIC ANEURYSM." UKnowledge, 2015. http://uknowledge.uky.edu/pharmacol_etds/12.
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Abdominal aortic aneurysm (AAA) is a devastating disease that exhibits permanent lumen expansion typically in the infrarenal aorta. AAA is prevalent among aged population, especially in males. Despite the incidence in women is lower, studies indicate the tortuosity is more severe and aortic rupture risk is higher in women. In most patients, AAA remains asymptomatic until it ruptures leading to sudden and fatal hemorrhage.
To date, there is no proven medical therapy that can prevent the expansion or rupture. Human observational studies implicate the presence of AAA is associated with both high plasma low-density lipoprotein-cholesterol (HDL-C) and low plasma high-density lipoprotein-cholesterol (HDL-C) concentrations. To examine the role of specific lipoproteins in development of AAA, angiotensin (Ang) II-induced AAA was firstly determined in apolipoprotein AI deficient (apoAI -/-) mice in both C57BL/6 and LDL receptor deficient (LDL receptor -/-) backgrounds. The deletion of apoAI led to a significant decrease of HDL-C concentrations. However, we were unable to define any exacerbation of AngII-induced AAA in either normo- or hyperlipidemic mice with apoAI deficiency. Next we compared AngII-induced AAA formation using multiple mouse strains with dietary manipulation to generate different severities of hypercholesterolemia. We demonstrated the apolipoprotein B (apoB)-containing lipoproteins promoted the development of AngII-induced AAA. Moreover, ezetimibe administration significantly reduced both apoB-containing lipoproteins and AAA formation. Together, our studies demonstrate that elevated apoB-containing lipoproteins, contribute to the development of AngII-induced AAA.
To investigate the role of apoB-containing lipoproteins on established AAA, male LDL receptors -/- mice fed a Western diet were infused with AngII for 4 weeks to induced AAA. Then mice with AAA were stratified into either a group maintained on western diet or switched to a normal diet. AngII infusion was continued for an additional 8 weeks. The diet switch resulted in significantly reduced plasma cholesterol concentrations, which was attributable to the decrease of apoB-containing lipoproteins. We found a profound inhibition of aneurysm progression in diet switched mice associated with attenuated macrophage accumulation and medial thickening. Collectively, our data demonstrate that apoB-containing lipoproteins promote the progression of established AAA.
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Chiang, Yu-Lin Fan, and 范姜郁琳. "Application of Next Generation Sequencing to Establish the Genetic Testing Platform for Thoracic Aortic Aneurysm and Dissection Syndrome." Thesis, 2017. http://ndltd.ncl.edu.tw/handle/92030430283610040366.
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碩士<br>國立臺灣大學<br>分子醫學研究所<br>105<br>Thoracic Aortic Aneurysm and Dissection syndrome (TAAD) can be divided into two main categories according to clinical features: (1) Syndromic, often accompanied by multiple groups of organ damage, including Marfan syndrome (MFS), Loeys-Dietz syndrome (LDS), Ehlers-Danlos syndrome (EDS), Aneurysms-Osteoarthritis syndrome (AOS), and transforming growth factor-β signaling related diseases; (2) Non-syndromic, only in the aortic disease, generally divided into familial TAAD and sporadic TAAD. However, the diversity of clinical features or symptoms are not clear, and it not only resulting in the difficulties of clinical diagnosis, but also suffering greater pain to patients and their families.
In this study, we enrolled patients from National Taiwan University Hospital "Cardiology Outpatient", "Pediatric Cardiology Outpatient" and "Department of Medical Genetics";30 patients with clinically diagnosed TAAD- Aneurysm/Dissection, and 19 patients with TAAD-non Aneurysm/Dissection but the clinical manifestations of suspected Marian syndrome (MFS) were included. We extracted gDNA from peripheral blood of these 49 patients, and detected 27 genes related to Syndromic TAAD and Non-syndromic TAAD by next-generation sequencing (NGS). Total detection rate was 49.0% (24/49), with 63.3% (19/30) for 30 TAAD- Aneurysm/Dissection diagnosed patients, and 26.3% (5/19) for 19 TAAD-non Aneurysm/Dissection cases. The accuracy rate was 100% (20/20) for the doubling check with Sanger sequencing. According to the ACMG (American College of Medical Genetics and Genomics) guidelines, we found 8 variants on FBN1 and 1 variant on FBN2 to be pathogenic or likely pathogenic, and they were genetic variants which not yet been reported so far.
Comparing with traditional sequencing methods, NGS is a combination of micro-technologies to do millions of DNA sequencing simultaneously; it generates high throughputs with high resolution within several days, which help us to save time and money. With this method, we can help patients to find out their causes of thoracic aorta. Furthermore, the understanding of genetic composition of Taiwan patients expands our understanding of this disease.
Books on the topic "Established aneurysm"
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Pirson, Yves, and Dominique Chauveau. Management of intracranial aneurysms. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0310.
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An asymptomatic intracranial aneurysm (ICA) is found by screening in about 8% of patients with autosomal dominant polycystic kidney disease (ADPKD), with a trend to cluster in some families. Though most ICAs will remain asymptomatic, a minority of them may rupture, causing subarachnoid haemorrhage (SAH). Given the grave prognosis of ICA rupture, screening and prophylactic repair of unruptured ICAs have to be considered, with the aim to identify patients with a risk of ICA rupture that exceeds the risk of a prophylactic procedure, surgical or endovascular. Relying on a decision analysis model established in the general population, widespread screening in ADPKD patients is today not recommended. However, the chapter authors advise screening in ADPKD patients with a familial history of ICA or SAH. Additional acceptable indications are high-risk occupations and patient anxiety despite adequate information. Screening is preferably performed by high-resolution, three-dimensional, time-of-flight magnetic resonance imaging. When an asymptomatic ICA is found, a recommendation for whether to intervene depends on its size, site, morphology, patient life expectancy, and general health as well as the experience of the neuroradiologist–neurosurgeon team. Since the risk of new ICAs or enlargement of an existing one is very low in those with small (< 6 mm) ICAs, conservative management is usually recommended. Elimination of tobacco use and aggressive treatment of hypertension are strongly recommended.
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Lancellotti, Patrizio, and Bernard Cosyns. Ischaemic Cardiac Disease (ICD). Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198713623.003.0006.
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Echocardiography has established appropriate areas in the evaluation of patients with known or suspected ischaemic heart disease. This chapter highlights the main risk stratifications for assessment of acute myocardial infarction. It illustrates the main complications of acute myocardial infarction (e.g. wall rupture, ventricular aneurysm, ventricular pseudoaneurysm, thrombus, pericardial effusion, mitral regurgitation) with details of incidence, timing, echocardiographic findings and implications. This chapter also details poor prognosis risk factors found in echocardiographic examination of patients with chronic ischaemic heart disease.
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Banerjee, Amitava, and Kaleab Asrress. Screening for cardiovascular disease. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0351.
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Screening involves testing asymptomatic individuals who have risk factors, or individuals who are in the early stages of a disease, in order to decide whether further investigation, clinical intervention, or treatment is warranted. Therefore, screening is classically a primary prevention strategy which aims to capture disease early in its course, but it can also involve secondary prevention in individuals with established disease. In the words of Geoffrey Rose, screening is a ‘population’ strategy. Examples of screening programmes are blood pressure monitoring in primary care to screen for hypertension, and ultrasound examination to screen for abdominal aortic aneurysm. The effectiveness and feasibility of screening are influenced by several factors. First, the diagnostic accuracy of the screening test in question is crucial. For example, exercise ECG testing, although widely used, is not recommended in investigation of chest pain in current National Institute for Health and Care Excellence guidelines, due to its low sensitivity and specificity in the detection of coronary artery disease. Moreover, exercise ECG testing has even lower diagnostic accuracy in asymptomatic patients with coronary artery disease. Second, physical and financial resources influence the decision to screen. For example, the cost and the effectiveness of CT coronary angiography and other new imaging modalities to assess coronary vasculature must be weighed against the cost of existing investigations (e.g. coronary angiography) and the need for new equipment and staff training and recruitment. Finally, the safety of the investigation is an important factor, and patient preferences and physician preferences should be taken into consideration. However, while non-invasive screening examinations are preferable from the point of view of patients and clinicians, sometimes invasive screening tests may be required at a later stage in order to give a definitive diagnosis (e.g. pressure wire studies to measure fractional flow reserve in a coronary artery). The WHO’s principles of screening, first formulated in 1968, are still very relevant today. Decision analysis has led to ‘pathways’ which guide investigation and treatment within screening programmes. There is increasing recognition that there are shared risk factors and shared preventive and treatment strategies for vascular disease, regardless of arterial territory. The concept of ‘vascular medicine’ has gained credence, leading to opportunistic screening in other vascular territories if an individual presents with disease in one territory. For example, post-myocardial infarction patients have higher incidence of cerebrovascular and peripheral arterial disease, so carotid duplex scanning and measurement of the ankle–brachial pressure index may be valid screening approaches for arterial disease in other territories.
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López-Sendón, José, and Esteban López de Sá. Mechanical complications of myocardial infarction. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0045.
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Mechanical complications after an acute infarction include different forms of heart rupture, including free wall rupture, interventricular septal rupture, and papillary muscle rupture. Its incidence decreased dramatically with the widespread use of reperfusion therapies but may occur in 2–3% of ST-elevation myocardial infarction patients, and mortality is very high if not properly diagnosed, as surgery is the only effective treatment. Echocardiography is the most important tool for diagnosis that should be suspected in patients with hypotension, heart failure, or recurrent chest pain. Awareness and well-established protocols are crucial for an early diagnosis. Modern imaging techniques permit a more reliable and direct identification of left ventricular free wall rupture, which is almost impossible to identify with conventional echocardiography. Mitral regurgitation, secondary to papillary muscle ischaemia or necrosis or left ventricular dilatation and remodelling, without papillary muscle rupture, is frequent after myocardial infarction and is considered as an independent risk factor for outcomes. Revascularization to control ischaemia and surgical repair should be considered in all patients with severe or symptomatic mitral regurgitation in the absence of severe left ventricular dysfunction. Other mechanical complications include true aneurysms and thrombus formation in the left ventricle. Again, these complications have decreased with the use of early reperfusion therapies and, for thrombus formation, with aggressive antithrombotic treatment. In a single large randomized trial (STICH), surgical remodelling of the left ventricle failed to demonstrate a significant improvement in outcomes, although it still may be an option in selected patients.
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López-Sendón, José, and Esteban López de Sá. Mechanical complications of myocardial infarction. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199687039.003.0045_update_001.
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Mechanical complications after an acute infarction include different forms of heart rupture, including free wall rupture, interventricular septal rupture, and papillary muscle rupture. Its incidence decreased dramatically with the widespread use of reperfusion therapies but may occur in 2–3% of ST-elevation myocardial infarction patients, and mortality is very high if not properly diagnosed, as surgery is the only effective treatment. Echocardiography is the most important tool for diagnosis that should be suspected in patients with hypotension, heart failure, or recurrent chest pain. Awareness and well-established protocols are crucial for an early diagnosis. Modern imaging techniques permit a more reliable and direct identification of left ventricular free wall rupture, which is almost impossible to identify with conventional echocardiography. Mitral regurgitation, secondary to papillary muscle ischaemia or necrosis or left ventricular dilatation and remodelling, without papillary muscle rupture, is frequent after myocardial infarction and is considered as an independent risk factor for outcomes. Revascularization to control ischaemia and surgical repair should be considered in all patients with severe or symptomatic mitral regurgitation in the absence of severe left ventricular dysfunction. Other mechanical complications include true aneurysms and thrombus formation in the left ventricle. Again, these complications have decreased with the use of early reperfusion therapies and, for thrombus formation, with aggressive antithrombotic treatment. In a single large randomized trial (STICH), surgical remodelling of the left ventricle failed to demonstrate a significant improvement in outcomes, although it still may be an option in selected patients.
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López-Sendón, José, and Esteban López de Sá. Mechanical complications of myocardial infarction. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199687039.003.0045_update_002.
Full textAbstract:
Mechanical complications after an acute infarction include different forms of heart rupture, including free wall rupture, interventricular septal rupture, and papillary muscle rupture. Its incidence decreased dramatically with the widespread use of reperfusion therapies but may occur in 2–3% of ST-elevation myocardial infarction patients, and mortality is very high if not properly diagnosed, as surgery is the only effective treatment. Echocardiography is the most important tool for diagnosis that should be suspected in patients with hypotension, heart failure, or recurrent chest pain. Awareness and well-established protocols are crucial for an early diagnosis. Modern imaging techniques permit a more reliable and direct identification of left ventricular free wall rupture, which is almost impossible to identify with conventional echocardiography. Mitral regurgitation, secondary to papillary muscle ischaemia or necrosis or left ventricular dilatation and remodelling, without papillary muscle rupture, is frequent after myocardial infarction and is considered as an independent risk factor for outcomes. Revascularization to control ischaemia and surgical repair should be considered in all patients with severe or symptomatic mitral regurgitation in the absence of severe left ventricular dysfunction. Other mechanical complications include true aneurysms and thrombus formation in the left ventricle. Again, these complications have decreased with the use of early reperfusion therapies and, for thrombus formation, with aggressive antithrombotic treatment. In a single large randomized trial (STICH), surgical remodelling of the left ventricle failed to demonstrate a significant improvement in outcomes, although it still may be an option in selected patients.
7
López-Sendón, José, and Esteban López de Sá. Mechanical complications of myocardial infarction. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199687039.003.0045_update_003.
Full textAbstract:
Mechanical complications after an acute infarction involve different forms of heart rupture, including free wall rupture, interventricular septal rupture, and papillary muscle rupture. Its incidence decreased dramatically with the widespread use of reperfusion therapies occurring in <1% of ST-elevation myocardial infarction patients, and mortality is very high if not properly diagnosed, as surgery is the only effective treatment (Ibanez et al, 2017). Echocardiography is the most important tool for diagnosis that should be suspected in patients with hypotension, heart failure, or recurrent chest pain. Awareness and well-established protocols are crucial for an early diagnosis. Modern imaging techniques permit a more reliable and direct identification of left ventricular free wall rupture, which is almost impossible to identify with conventional echocardiography. Mitral regurgitation, secondary to papillary muscle ischaemia or necrosis or left ventricular dilatation and remodelling, without papillary muscle rupture, is frequent after myocardial infarction and is considered as an independent risk factor for outcomes. Revascularization to control ischaemia and surgical repair should be considered in all patients with severe or symptomatic mitral regurgitation in the absence of severe left ventricular dysfunction. Other mechanical complications include true aneurysms and thrombus formation in the left ventricle. Again, these complications have decreased with the use of early reperfusion therapies and, for thrombus formation, with aggressive antithrombotic treatment. In a single large randomized trial (STICH), surgical remodelling of the left ventricle failed to demonstrate a significant improvement in outcomes, although it still may be an option in selected patients.
8
Dewhurst, Alexander Timothy, and Brigitta Brandner. Intensive care management after vascular surgery. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0370.
Full textAbstract:
Vascular patients require admission to an intensive care unit at a number of stages during their hospital stay. They often have multiple co-morbidities and are at risk of major complications. Their management strategy requires a multidisciplinary approach with locally agreed pathways taking national frameworks into account. Vascular emergencies require immediate resuscitation and transfer to a tertiary cardiovascular centre. Vascular disease occurs throughout the arterial vascular tree, affecting both large and small vessels. The major cause is atherosclerosis. The management of vascular conditions is complex, and includes both medical and surgical interventions. Disease can be classified as non-occlusive where there is restricted blood flow or occlusive where the vessels are completely obstructed. Aneurysmal disease occurs when vessels walls weaken. The surgical treatment of these lesions is to either replace the diseased segment of artery with a vascular graft or to exclude it with an endovascular stent. Occlusive vascular disease can occur because of atherosclerotic emboli or thrombosis, and can be treated by embolectomy, bypass, or endovascular procedures. Medical therapy with β-blockade, lipid-lowering agents, anti-hypertensives agents, and control of diabetes reduces cardiovascular risk. Recent advances in medical technology have shifted treatment options from open surgical to endovascular procedures. The long-term outcome and cost benefit of endovascular procedures is yet to be established.
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Pipitone, Nicolò, Annibale Versari, and Carlo Salvarani. Large-vessel vasculitis. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0133.
Full textAbstract:
Large-vessel vasculitis includes giant cell arteritis (GCA) and Takayasu's arteritis (TAK). GCA affects patients aged over 50, mainly of white European ethnicity. GCA occurs together with polymyalgia rheumatica (PMR) more frequently than expected by chance. In both conditions, females are affected two to three times more often than males. GCA mainly involves large- and medium-sized arteries, particularly the branches of the proximal aorta including the temporal arteries. Vasculitic involvement results in the typical manifestations of GCA including temporal headache, jaw claudication, and visual loss. A systemic inflammatory response and a marked response to glucocorticoids is characteristic of GCA. GCA usually remits within 6 months to 2 years from disease onset. However, some patients have a chronic-relapsing course and may require long-standing treatment. Mortality is not increased, but there is significant morbidity mainly related to chronic glucocorticoid use and cranial ischaemic events, especially visual loss. The diagnosis of GCA rests on the characteristic clinical features and raised inflammatory markers, but temporal artery biopsy remains the gold standard to support the clinical suspicion. Imaging techniques are also used to demonstrate large-vessel involvement in GCA. Glucocorticoids are the mainstay of treatment for GCA, but other therapeutic approaches have been proposed and novel ones are being developed. TAK mainly involves the aorta and its main branches. Women are particularly affected with a female:male ratio of 9:1. In most patients, age of onset is between 20 and 30 years. Early manifestations of TAK are non-specific and include constitutional and musculoskeletal symptoms. Later on, vascular complications become manifest. Most patients develop vessel stenoses, particularly in the branches of the aortic artery, leading to manifestations of vascular hypoperfusion. Aneurysms occur in a minority of cases. There are no specific laboratory tests to diagnose TAK, although most patients have raised inflammatory markers, therefore, imaging techniques are required to secure the diagnosis. Glucocorticoids are the mainstay of treatment of TAK. However, many patients have an insufficient response to glucocorticoids alone, or relapse when they are tapered or discontinued. Immunosuppressive agents and, in refractory cases, biological drugs can often attain disease control and prevent vascular complications. Revascularization procedures are required in patients with severe established stenoses or occlusions.
10
Pipitone, Nicolò, Annibale Versari, and Carlo Salvarani. Large-vessel vasculitis. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199642489.003.0133_update_003.
Full textAbstract:
Large-vessel vasculitis includes giant cell arteritis (GCA) and Takayasu’s arteritis (TAK). GCA affects patients aged over 50, mainly of white European ethnicity. GCA occurs together with polymyalgia rheumatica (PMR) more frequently than expected by chance. In both conditions, females are affected two to three times more often than males. GCA mainly involves large- and medium-sized arteries, particularly the branches of the proximal aorta including the temporal arteries. Vasculitic involvement results in the typical manifestations of GCA including temporal headache, jaw claudication, and visual loss. A systemic inflammatory response and a marked response to glucocorticoids is characteristic of GCA. GCA usually remits within 6 months to 2 years from disease onset. However, some patients have a chronic-relapsing course and may require longstanding treatment. Mortality is not increased, but there is significant morbidity mainly related to chronic glucocorticoid use and cranial ischaemic events, especially visual loss. The diagnosis of GCA rests on the characteristic clinical features and raised inflammatory markers, but temporal artery biopsy remains the gold standard to support the clinical suspicion. Imaging techniques are also used to demonstrate large-vessel involvement in GCA. Glucocorticoids are the mainstay of treatment for GCA, but other therapeutic approaches have been proposed and novel ones are being developed. TAK mainly involves the aorta and its main branches. Women are particularly affected with a female:male ratio of 9:1. In most patients, age of onset is between 20 and 30 years. Early manifestations of TAK are non-specific and include constitutional and musculoskeletal symptoms. Later on, vascular complications become manifest. Most patients develop vessel stenoses, particularly in the branches of the aortic artery, leading to manifestations of vascular hypoperfusion. Aneurysms occur in a minority of cases. There are no specific laboratory tests to diagnose TAK, although most patients have raised inflammatory markers, therefore, imaging techniques are required to secure the diagnosis. Glucocorticoids are the mainstay of treatment of TAK. However, many patients have an insufficient response to glucocorticoids alone, or relapse when they are tapered or discontinued. Immunosuppressive agents and, in refractory cases, biological drugs can often attain disease control and prevent vascular complications. Revascularization procedures are required in patients with severe established stenoses or occlusions.
Book chapters on the topic "Established aneurysm"
1
Miller, Craig A. "Houston: 1956–1960." In A Time for All Things. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780190073947.003.0007.
Full textAbstract:
DeBakey and his team conquer aortic aneurysms in the chest, as well as occluded arteries throughout the body. The Baylor team invents and perfects new instruments and prosthetic arterial substitutes, transforming the practice of vascular surgery. With the new heart-lung machine the Houston group enthusiastically embraces open-heart surgery. The demanding Baylor surgery residency develops. DeBakey becomes a key member of the Second Hoover Commission, which helps establish the National Library of Medicine. DeBakey begins to spread the word of the new surgery by visiting centers worldwide, including in the Soviet Union at the height of the Cold War.
2
Ameddah, Hacene, and Hammoudi Mazouz. "3D Printing Analysis by Powder Bed Printer (PBP) of a Thoracic Aorta Under Simufact Additive." In Additive Manufacturing Technologies From an Optimization Perspective. IGI Global, 2019. http://dx.doi.org/10.4018/978-1-5225-9167-2.ch005.
Full textAbstract:
In recent decades, vascular surgery has seen the arrival of endovascular techniques for the treatment of vascular diseases such as aortic diseases (aneurysms, dissections, and atherosclerosis). The 3D printing process by addition of material gives an effector of choice to the digital chain, opening the way to the manufacture of shapes and complex geometries, impossible to achieve before with conventional methods. This chapter focuses on the bio-design study of the thoracic aorta in adults. A bio-design protocol was established based on medical imaging, extraction of the shape, and finally, the 3D modeling of the aorta; secondly, a bio-printing method based on 3D printing that could serve as regenerative medicine has been proposed. A simulation of the bio-printing process was carried out under the software Simufact Additive whose purpose is to predict the distortion and residual stress of the printed model. The binder injection printing technique in a Powder Bed Printer (PBP) bed is used. The results obtained are very acceptable compared with the results of the error elements found.
3
Ameddah, Hacene, and Hammoudi Mazouz. "3D Printing Analysis by Powder Bed Printer (PBP) of a Thoracic Aorta Under Simufact Additive." In Research Anthology on Emerging Technologies and Ethical Implications in Human Enhancement. IGI Global, 2021. http://dx.doi.org/10.4018/978-1-7998-8050-9.ch039.
Full textAbstract:
In recent decades, vascular surgery has seen the arrival of endovascular techniques for the treatment of vascular diseases such as aortic diseases (aneurysms, dissections, and atherosclerosis). The 3D printing process by addition of material gives an effector of choice to the digital chain, opening the way to the manufacture of shapes and complex geometries, impossible to achieve before with conventional methods. This chapter focuses on the bio-design study of the thoracic aorta in adults. A bio-design protocol was established based on medical imaging, extraction of the shape, and finally, the 3D modeling of the aorta; secondly, a bio-printing method based on 3D printing that could serve as regenerative medicine has been proposed. A simulation of the bio-printing process was carried out under the software Simufact Additive whose purpose is to predict the distortion and residual stress of the printed model. The binder injection printing technique in a Powder Bed Printer (PBP) bed is used. The results obtained are very acceptable compared with the results of the error elements found.
4
Farne, Hugo, Edward Norris-Cervetto, and James Warbrick-Smith. "Groin lump." In Oxford Cases in Medicine and Surgery. Oxford University Press, 2015. http://dx.doi.org/10.1093/oso/9780198716228.003.0030.
Full textAbstract:
Considering the anatomy and associated pathology in a systematic fashion, the lump may represent: • Psoas sheath → psoas abscess or psoas bursa • Femoral nerve → neuroma • Femoral artery → femoral aneurysm or pseudoaneurysm • Femoral vein/long saphenous vein → saphena varix (dilated great saphenous vein due to incompetence at the saphenofemoral junction) • Lymph nodes → lymphadenopathy (infectious or malignant) • Hernial orifices → inguinal hernia, femoral hernia • Testicular apparatus → ectopic testis, undescended testis, hydrocele of cord • Skin/subcutis → lipoma, infected abscess (e.g. from intravenous (IV) drug use), sebaceous cyst. In common with lumps anywhere on the body, you will need to establish: • How long has the lump been there? Many of the diagnoses listed in Figure 24.1 will develop rather insidiously, but there are some that may have a rather shorter history. For example, a patient may develop a femoral artery pseudoaneurysm (a collection of blood outside the vessel lumen) following angiography, a direct inguinal hernia may be precipitated by a period of heavy lifting, or inguinal lymphadenopathy may follow a lower limb infection. Ectopic or undescended testes would be present from birth, but it is extremely unlikely that a man would reach adulthood in the Western world without having had this defect corrected by orchidopexy (orchid = testis, -pexy = fixation in correct position) or orchidectomy (orchid = testis, -ectomy = removal). • Is the lump always there? Does it reduce when the patient lies down? This question relates to hernias and saphena varix. Increases in intra-abdominal pressure, for example during coughing or straining at stool, may cause hernias to increase in size. A saphena varix may increase in size if the patient stands for long periods of time as retrograde flow through incompetent venous valves will allow blood to pool. A saphena varix will disappear completely when the patient lies down. • Has the lump got bigger, smaller, or stayed the same size? Almost all of the pathologies on our differential (with the possible exception of ectopic/undescended testes) may change in size over time.
5
Pipitone, Nicolò, Annibale Versari, and Carlo Salvarani. "Large-vessel vasculitis." In Oxford Textbook of Rheumatology. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0133_update_004.
Full textAbstract:
Large-vessel vasculitis includes giant cell arteritis (GCA) and Takayasu’s arteritis (TAK). GCA affects patients aged over 50, mainly of white European ethnicity. GCA occurs together with polymyalgia rheumatica (PMR) more frequently than expected by chance. In both conditions, females are affected two to three times more often than males. GCA mainly involves large- and medium-sized arteries, particularly the branches of the proximal aorta including the temporal arteries. Vasculitic involvement results in the typical manifestations of GCA including temporal headache, jaw claudication, and visual loss. A systemic inflammatory response and a marked response to glucocorticoids is characteristic of GCA. GCA usually remits within 6 months to 2 years from disease onset. However, some patients have a chronic-relapsing course and may require longstanding treatment. Mortality is not increased, but there is significant morbidity mainly related to chronic glucocorticoid use and cranial ischaemic events, especially visual loss. The diagnosis of GCA rests on the characteristic clinical features and raised inflammatory markers, but temporal artery biopsy remains the gold standard to support the clinical suspicion. Imaging techniques are also used to demonstrate large-vessel involvement in GCA. Glucocorticoids are the mainstay of treatment for GCA, but other therapeutic approaches have been proposed and novel ones are being developed. TAK mainly involves the aorta and its main branches. Women are particularly affected with a female:male ratio of 9:1. In most patients, age of onset is between 20 and 30 years. Early manifestations of TAK are non-specific and include constitutional and musculoskeletal symptoms. Later on, vascular complications become manifest. Most patients develop vessel stenoses, particularly in the branches of the aortic artery, leading to manifestations of vascular hypoperfusion. Aneurysms occur in a minority of cases. There are no specific laboratory tests to diagnose TAK, although most patients have raised inflammatory markers, therefore, imaging techniques are required to secure the diagnosis. Glucocorticoids are the mainstay of treatment of TAK. However, many patients have an insufficient response to glucocorticoids alone, or relapse when they are tapered or discontinued. Immunosuppressive agents and, in refractory cases, biological drugs can often attain disease control and prevent vascular complications. Revascularization procedures are required in patients with severe established stenoses or occlusions.
6
Pipitone, Nicolò, Annibale Versari, and Carlo Salvarani. "Large-vessel vasculitis." In Oxford Textbook of Rheumatology. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0133_update_005.
Full textAbstract:
Large-vessel vasculitis includes giant cell arteritis (GCA) and Takayasu’s arteritis (TAK). GCA affects patients aged over 50, mainly of white European ethnicity. GCA occurs together with polymyalgia rheumatica (PMR) more frequently than expected by chance. In both conditions, females are affected two to three times more often than males. GCA mainly involves large- and medium-sized arteries, particularly the branches of the proximal aorta including the temporal arteries. Vasculitic involvement results in the typical manifestations of GCA including temporal headache, jaw claudication, and visual loss. A systemic inflammatory response and a marked response to glucocorticoids is characteristic of GCA. GCA usually remits within 6 months to 2 years from disease onset. However, some patients have a chronic-relapsing course and may require longstanding treatment. Mortality is not increased, but there is significant morbidity mainly related to chronic glucocorticoid use and cranial ischaemic events, especially visual loss. The diagnosis of GCA rests on the characteristic clinical features and raised inflammatory markers, but temporal artery biopsy remains the gold standard to support the clinical suspicion. Imaging techniques are also used to demonstrate large-vessel involvement in GCA. Glucocorticoids are the mainstay of treatment for GCA, but other therapeutic approaches have been proposed and novel ones are being developed. TAK mainly involves the aorta and its main branches. Women are particularly affected with a female:male ratio of 9:1. In most patients, age of onset is between 20 and 30 years. Early manifestations of TAK are non-specific and include constitutional and musculoskeletal symptoms. Later on, vascular complications become manifest. Most patients develop vessel stenoses, particularly in the branches of the aortic artery, leading to manifestations of vascular hypoperfusion. Aneurysms occur in a minority of cases. There are no specific laboratory tests to diagnose TAK, although most patients have raised inflammatory markers, therefore, imaging techniques are required to secure the diagnosis. Glucocorticoids are the mainstay of treatment of TAK. However, many patients have an insufficient response to glucocorticoids alone, or relapse when they are tapered or discontinued. Immunosuppressive agents and, in refractory cases, biological drugs can often attain disease control and prevent vascular complications. Revascularization procedures are required in patients with severe established stenoses or occlusions.
Conference papers on the topic "Established aneurysm"
1
Lieber, B. B., C. Sadasivan, D. J. Fiorella, et al. "Preliminary In Vitro Estimates of Intra-Aneurysmal Void Sizes After Endovascular Coiling." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53349.
Full textAbstract:
Endovascular coiling has become a well-established treatment method for cerebral aneurysms. The primary drawback of the technique is aneurysm recanalization requiring periodic angiographic follow-ups and possible aneurysm re-treatment. A recent review [1] estimates that 20% of treated aneurysms re-canalize and that half of those aneurysms (10%) are re-treated. Aneurysm recanalization is, in turn, largely caused by compaction of the coil mass due to hemodynamic impingement forces every cardiac cycle. Currently, the only quantitative measure used to characterize effectiveness of the treatment is the aneurysm packing density (ratio of total volume of coils inserted into the aneurysm and the volume of the aneurysm). Lower packing densities have been correlated with higher coil compaction rates [2], so aneurysms are generally coiled to maximal packing. A wider aneurysm neck is also correlated with higher coil-compaction rates. Coiling in such wide-neck aneurysms is performed either with the support of a balloon that is removed post-coiling or with the support of an intracranial stent that is implanted. Such assist devices also improve aneurysm packing densities [3].
2
Lieber, Baruch B., Mohammad Ali-Aziz Sultan, Chander Sadasivan, et al. "A Novel Method for Excluding Aneurysms From the Cerebral Circulation: Preliminary Results in Rabbits." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206795.
Full textAbstract:
Despite many advances in the treatment of cerebral aneurysms in the last few decades, none of the available methods provide an unequivocal solution for all aneurysm sizes and morphologies. The feasibility of successfully treating aneurysms solely by the placement of an intravascular flow-diverting mesh across the aneurysm neck was established more than a decade ago [1]. Flow diverters disrupt the momentum exchange between the parent artery and aneurysm and significantly reduce intraaneurysmal hydrodynamic vorticity and kinetic energy. The resultant flow stasis promotes thrombus formation within the aneurysm sac, which eventually matures into fibrotic tissue, leading to exclusion of the aneurysm from the circulation. With the increased use of stents in the intracranial circulation, cases where coiling is not feasible, or is staged as a secondary procedure, are providing clinical evidence of the successful treatment of aneurysms with stents alone [2,3]. Methodological evidence of the performance of appropriately designed flow diverters in treating cerebral aneurysms has recently become available in the literature [4,5].
3
Gee, Michael W., and Wolfgang A. Wall. "Model Complexity and Prestressing in Abdominal Aortic Aneurysm Simulation." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-204593.
Full textAbstract:
Rupture of abdominal aortic aneurysm (AAA) is the 13th leading cause of death in western society and is fatal in 70–90%. In consequence, precise prediction of AAA rupture risk is essential. With the current, well established CT-morphological parameters such as maximum aortic diameter, aneurysm shape and AAA expansion, only at best the relative, but not the individual rupture risk can be determined. Hence, AAA rupture may occur unexpectedly in small aneurysms below the critical diameter limits whereas many large aneurysms may remain stable throughout patient’s lifetime, without prophylactic surgery.
4
Embong, A. H., A. M. Al-Jumaily, G. Mahadevan, A. Lowe, and S. Sugita. "Development of an Abdominal Aortic Aneurysm Ruptures Mechanism Using a Geometric Analytical Technique." In ASME 2014 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2014. http://dx.doi.org/10.1115/imece2014-39823.
Full textAbstract:
Current ultrasound approaches practice probe for diagnosing instantaneous abdominal aortic aneurysms (AAA) based on arterial tissue deformation. However, tracking the progression of potential aneurysms, and predicting the risk of rupture is based on the diameter of the aneurysm and is still an insufficient method: Larger diameter aneurysms do not always lead to ruptures, and smaller diameter aneurysms unexpectedly rupture. In order to improve diagnostic accuracy of ultrasound imaging techniques, this paper presents geometric analyses of patient-specific instant deformations as a means to develop an aneurysm rupture mechanism. Segmented AAA images were used to analyze dependent elements that contribute to a three-dimensional (3-D) aneurysm reconstructive model using proposed Patient-Specific Aneurysm Rupture Predictor (P-SARP) method. The outcomes indicate that the proposed technique has the ability to associate the distortion of wall deformation with geometric analyses. This method can positively be integrated with established ultrasound techniques for improvements in the accuracy of future diagnoses of potential AAA ruptures.
5
Sadasivan, Chander, Baruch B. Lieber, Liliana Cesar, Jaehoon Seong, and Ajay K. Wakhloo. "Treatment of Cerebral Aneurysms With Flow Divertors: Long Term Results in an In Vivo Model." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176277.
Full textAbstract:
Subarachnoid hemorrhagic stroke is a devastating illness with a 30-day mortality rate of 45% and is mostly caused due to the rupture of an intracranial aneurysm. Although these aneurysms are currently treated surgically by clipping, or, endovascularly by coiling and stent-assisted coiling, the feasibility of successfully treating aneurysms solely by the placement of an intravascular flow-diverting mesh across the aneurysm neck was established more than a decade ago [1]. Flow divertors disrupt the momentum exchange between the parent artery and aneurysm and significantly reduce intraaneurysmal hydrodynamic vorticity. The resultant flow stasis promotes thrombus formation within the aneurysm sac, which eventually matures into fibrotic tissue, leading to the exclusion of the aneurysm from the circulation. With the increased use of stents in the intracranial circulation, cases where coiling is not feasible, or is staged as a secondary procedure, are providing clinical evidence of the successful treatment of aneurysms with stents alone [2,3]. Such reports are sporadic and, moreover, the devices used are not designed to be flow divertors. Methodological evidence of the performance of appropriately designed flow divertors in treating cerebral aneurysms is currently unavailable.
6
Lieber, Baruch B., Chander Sadasivan, David J. Fiorella, and Henry H. Woo. "Phototherapy Enhanced Exclusion of Aneurysms From the Cerebral Circulation." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14135.
Full textAbstract:
Accumulated experience using flow diverters in humans suggests that complete cure of the aneurysm is usually a protracted process that can last up to twelve months [1]. While it is well established that a properly designed flow diverter serves as a scaffold for neointimal proliferation, the process of its formation over the aneurysm neck is delayed until the aneurysm cavity itself is occluded by a thrombus, negating flow of fresh blood through the neck, and thus allowing the neointimal formation to bridge the aneurysm neck. The notion that induction of some injury to the luminal surface of the aneurysmal tissue, particularly to the endothelium, may result in a healing response that is faster than just placing a flow diverter and waiting for thrombus formation within the aneurysm has been tried in the past using various experimental models. Some of the injuries to the aneurysm tissue that have been tried in the past include mechanical scraping, thermal heating and UV irradiation. All these attempts, while showing that hastening the thrombus formation is feasible, have not resulted in any success due to the fact that the processes that were tried suffered from lack of proper control to be implemented in actual aneurysmal tissue that is weakened and diseased a priori.
7
Le, Trung Bao, and Lahcen Akerkouch. "On the Modal Analysis of Blood Flow Dynamics in Brain Aneurysms." In 2020 Design of Medical Devices Conference. American Society of Mechanical Engineers, 2020. http://dx.doi.org/10.1115/dmd2020-9100.
Full textAbstract:
Abstract Complex, unstable inflow jet has been linked to aneurysm growth and rupture. However, methodologies to characterize this inflow jet have not been well established. Our previous works (Le et al., J. Biomech. Engr., 2010 and Le et al., Annals Biomedical Eng., 2013) have shown a possible transition from the stable mode (cavity) to the unstable mode (vortex ring) of this jet. We have proposed the use of a non-dimensional index called Aneurysm Number to characterize this transition (Le et al., 2013). However, the quantification of such a transition is lacking. Currently, there have no efforts in quantifying unstable flows in intracranial aneurysms, which is essential in stratifying rupture risks. In this work, the aneurysmal geometries from three patients at Sanford Health, North Dakota are reconstructed from Magnetic Resonance Angiogram and Digital Subtraction Angiogram data. Using our in-house CFD code (Virtual Flow Simulator), high-resolution flow data is obtained via numerical simulation. We perform modal analysis of blood flow dynamics for these cases using Proper Orthogonal Decomposition. Our results show that there are up to five dominant modes in the flow arising from the interaction of the incoming jet and the aneurysm dome. The spatial distribution of these modes reflect the characteristics of the inflow jet and can be used to quantify flow unsteadiness. Future works will be needed to apply the same procedure for a larger population of patients to examine its relevance in clinical practice.
8
Haskett, Darren, Urs Utzinger, Mohamad Azhar, and Jonathan Vande Geest. "Progressive Alterations in Biomechanical Response of a Mouse Model of Aneurysm." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80321.
Full textAbstract:
Abdominal aortic aneurysm (AAA) is a complex disease that leads to a localized dilation of the infrarenal aorta, the rupture of which is associated with significant morbidity and mortality, however the underlying mechanisms by which such changes remains an important unanswered question in the literature. Animal models of AAA can be used to study how changes in the microstructural and biomechanical behavior of aortic tissues develop as disease progresses in these animals. We chose here to investigate changes in mechanical characteristics with time in the established Apolipoprotein E deficient (ApoE−/−) angiotensin II (AngII) infused mouse model of AAA.
9
Trachet, Bram, Marjolijn Renard, Gianluca De Santis, et al. "A Quantitative Comparison Between Baseline Hemodynamics and End-Stage Aneurysm Formation in ApoE −/− Mice." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53452.
Full textAbstract:
The pathogenesis of abdominal aortic aneurysm (AAA) formation still remains debated. Hemodynamics have been suggested to play a (modulating) role, but no follow-up studies have been performed due to (a.o.) a lack of human data before disease initiation. We therefore used an established mouse model of AAA [1] to study whether AAA develops at locations experiencing disturbed flow. We set up a framework to obtain mouse-specific Computational Fluid Dynamics (CFD) simulations of the mouse abdominal aorta, combining: (i) an in vivo assessed geometric model [2] and (ii) in vivo measured boundary conditions. A distance map was generated to link baseline and end-stage aortic morphologies after AAA development, and the relationship between baseline hemodynamics and end-stage dilatation was quantified.
10
Di Martino, Elena S., Ajay Bohra, Christine Scotti, Ender Finol, and David A. Vorp. "Wall Stresses Before and After Endovascular Repair of Abdominal Aortic Aneurysms." In ASME 2004 International Mechanical Engineering Congress and Exposition. ASMEDC, 2004. http://dx.doi.org/10.1115/imece2004-61556.
Full textAbstract:
Endovascular aneurysm repair (EVAR) technique is a minimally invasive procedure approach to abdominal aortic aneurysm (AAA) repair. Following EVAR, isolated aortic tissue starts remodeling after the new blood path is established. The commercially available endovascular grafts (EVG) have been found to be prone to Type I endoleak, which is re-pressurization of the degenerated AAA sac following a breach in the seal mechanism of the EVG or migration due to failure of the mechanism holding the graft in place (Chuter, 2002) These inadequacies of EVGs might be attributed to the effect of non-optimal design of graft anchoring system. In the present study, we utilized pre-operative and post-operative computer tomography (CT) data with previously derived material properties to construct three-dimensional finite element (FE) models for AAA before and after the EVAR procedure. We studied the nature of stresses acting on the aorta before and after EVAR. In particular we investigated the physical forces acting on the EVG and how they are transferred to the aortic wall at graft anchoring sites.