Takanen Niklasson, C. Självrapporterad hälsa hos män som genomgått screening av bukaorta. Examensarbete i omvårdnad 15 högskolepoäng. Malmö Högskola: Hälsa och Samhälle. Utbildningsområde omvårdnad 2012.Abdominellt aortaaneurysm (AAA) är den 13:e vanligaste orsaken till dödsfall i västvärlden på män över 65 år och är fyra gånger vanligare hos män än hos kvinnor. Sedan 2010 erbjuder Region Skåne ultraljuds screening av bukaorta till alla män är 65 år för att upptäcka ev. AAA. AAA uppkommer genom förhöjt kolesterol, rökning kombinerat med högt blodtryck. Även en genetisk faktor spelar roll. Syfte: Studiens syfte var att kartlägga självrapporterat hälsotillstånd och rökvanor hos patienter som via screening diagnostiserats med aortaaneurysm i jämförelse med män med normal aorta. Metod: Studien är en deskriptiv tvärsnittsstudie som bygger på självskattade hälsoformulär som har tagits fram för screeningverksamheten. Dessa fylldes i av männen i hemmet som de sedan lämnade på screeningmottagningen. Data analyserades manuellt i antal och procent i jämförelse mellan män med AAA och de med normal aorta. Resultat: Studiens resultat visade att män med AAA hade högt BMI (Body Mass Index) och led av andra sjukdomar. Vidare hade männen med AAA låg utbildning. Nästan hälften av männen med AAA rökte. Däremot beskrev männen oavsett grupp sin hälsa på liknande sätt i den öppna frågan rörande deras nuvarande hälsotillstånd. Slutsats: Resultatet kan indikera tidigare forskning som visat alla riskfaktorer som leder till ateroskleros även kan leda till utveckling av AAA. Men eftersom ingen statistik har använts i resultatet för att belägga skillnader kan datan endast ses som en trend. Denna kunskap kan utgöra en bas för sjuksköterskans preventiva arbete i mötet med patienter som diagnostiserats med AAA. / Takanen Niklasson, C. Self-reported health of men who underwent abdominal aortascreening. Degree Project, 15 Credit Points. Malmö University: Health and Society, Department of Nursing, 2012.Abdominal aortic aneurysm (AAA) is the 13:th most common cause of death in the western world in men over 65 years old and is four times more common in men than in women. The County Council of Skåne started in 2010 a screening program in men 65 years of age to possibly discover AAA. AAA generates through elevated cholesterol and smoking combined with high blood pressure. There is also a genetic factor involved. Aim: The aim of this study was to chart self-reported state of health and smoking habits of men diagnosed with AAA through screening compared with men with normal aorta. Method: the study is a descriptive cross-sectional survey built on self-rated health questionnaires which was developed for use in the screening program. These were filled out by the men at home and gathered at the screening examination. The data was analyzed manually in numbers and percent and compared between men with AAA and those with normal aorta. Results: The results showed that men with AAA had high BMI (Body Mass Index) and suffered from other diseases. Further had men with AAA a low educational level. Almost 50% of the men with AAA were also smoking. However, all men, irrespective of having AAA or not, described their health in a similar way in the open question regarding their current health status. Conclusion: The result can indicate previous research showing that all risk factors associated with development of atherosclerosis also is associated with the development of AAA. However, no statistics were being used in the result to claim differences so the data can only be a trend. This knowledge can constitute a base for nursing prevention measures in the care of men diagnosed with AAA.

Aortic aneurysms are the 14th leading cause of death in the United States. Annually, abdominal aortic aneurysm (AAA) ruptures are responsible for 4500 deaths. There are another 45,000 repair procedures performed to prevent rupture, and of these approximately 1400 lead to deaths. With proper detection, the aneurysm may be treated using endovascular aneurysm repair (EVAR). Understanding how the flow of the blood within the artery is affected by the aneurysm is important in determining the growth of the aneurysm, as well as how to properly treat the aneurysm. The goal of this project was to develop a physical construct of the AAA, and use this construct to validate a computational model of the same aneurysm through flow visualization. The hypothesis was that the fluid velocities within the physical construct would accurately mimic the fluid velocities used in the computational model. The physical model was created from a CT scan of an AAA using 3D printing and polymer casting. The result was a translucent box containing a region in the shape of the aneurysm. Fluid was pumped through the construct to visualize and quantify the velocity of the fluid within the aneurysm. COMSOL Multiphysics® was used to create a computational model of the same aneurysm, as well as obtain velocity measurements to statistically compare to those from the physical construct. There was no significant difference between the velocity values for the physical construct and the COMSOL Multiphysics® model, confirming the hypothesis. This study used a CT scan to create an anatomically accurate model of an AAA that was used to validate a computational model using a novel technique of flow visualization. As EVAR technologies continue to progress, it will become increasingly important to understand how the blood flow within the aneurysm affects the growth and treatment of AAAs.

Yes / Abdominal aortic aneurysm (AAA) is a silent, progressive disease with high mortality and increasing prevalence with aging. Smooth muscle cell (SMC) dysfunction contributes to gradual dilatation and eventual rupture of the aorta. Here we studied phenotypic characteristics in SMC cultured from end-stage human AAA (5cm) and cells cultured from a porcine carotid artery (PCA) model of early and end-stage aneurysm. Human AAA-SMC presented a secretory phenotype and expressed elevated levels of differentiation marker miR-145 (2.2-fold, P<.001) and senescence marker SIRT-1 (1.3-fold, P<.05), features not recapitulated in aneurysmal PCA-SMC. Human and end-stage porcine aneurysmal cells were frequently multi-nucleated (3.9-fold, P<.001 and 1.8-fold, P<.01 respectively, versus control cells) and displayed aberrant nuclear morphology. Human AAA-SMC exhibited higher levels of the DNA damage marker H2AX (3.9-fold, P<.01 vs. control SMC). These features did not correlate with patients’ chronological age; and are therefore potential markers for pathological premature vascular aging. Early-stage PCA-SMC (control and aneurysmal) were indistinguishable from one another across all parameters. The principal limitation of human studies is tissue availability only at end-stage disease. Refinement of a porcine bioreactor model would facilitate study of temporal modulation of SMC behaviour during aneurysm development and potentially identify therapeutic targets to limit AAA progression. / Supported in part by a grant from the Leeds Teaching Hospitals Charitable Foundation (9R11/8002)

Yes / (1) Abdominal aortic aneurysm (AAA) is a silent, progressive disease with significant mortality from rupture. Whilst screening programmes are now able to detect this pathology early in its development, no therapeutic intervention has yet been identified to halt or retard aortic expansion. The inability to obtain aortic tissue from humans at early stages has created a necessity for laboratory models, yet it is essential to create a timeline of events from EARLY to END stage AAA progression. (2) We used a previously validated ex vivo porcine bioreactor model pre-treated with protease enzyme to create "aneurysm" tissue. Mechanical properties, histological changes in the intact vessel wall, and phenotype/function of vascular smooth muscle cells (SMC) cultured from the same vessels were investigated. (3) The principal finding was significant hyperproliferation of SMC from EARLY stage vessels, but without obvious histological or SMC aberrancies. END stage tissue exhibited histological loss of α-smooth muscle actin and elastin; mechanical impairment; and, in SMC, multiple indications of senescence. (4) Aortic SMC may offer a therapeutic target for intervention, although detailed studies incorporating intervening time points between EARLY and END stage are required. Such investigations may reveal mechanisms of SMC dysfunction in AAA development and hence a therapeutic window during which SMC differentiation could be preserved or reinstated. / This research was funded in part by The Leeds Teaching Hospitals Charitable Foundation (R11/8002). E.R.C. was supported by a PhD studentship from the Engineering and Physical Sciences Research Council (EPSRC; EP/F500513/1). R.J.H. was the recipient of an Intercalated Batchelor of Science Degree in Science award from the Royal College of Surgeons of England. M.A.B.(FS/18/12/33270 and FS/12/54/29671), K.I.B. (FS/12/26/29395), and K.J.G. (FS/11/91/29090) were supported by BHF Clinical Research Training Fellowships.

Yes / Early vascular ageing (EVA) is a pathological phenomenon whereby the vascular system ages more quickly than chronological age. This underpins many cardiovascular diseases including the complications of type 2 diabetes, aneurysm formation and hypertension. Smooth muscle cells (SMC) are the principal cell type in the vascular wall and maintain vascular tone. EVA-related phenotypic switching of these cells contributes towards disease progression. EVA is distinct from chronological ageing, and research is ongoing to identify a definitive molecular signature of EVA. This will facilitate the discovery of new clinical tests for early detection of EVA and identify therapeutic targets to halt (or prevent) EVA in SMC, thus reducing macrovascular morbidity and mortality.

No description available.

Abdominal aortic aneurysm (AAA) is a major cardiovascular disease and involves enhancement of renin-angiotensin system and recruitment/activation of inflammatory factors such as matrix metalloproteases (MMP's). Caveolae has been shown to play a role in a number of different cardiovascular diseases through different mechanisms including regulation of oxidative stress, inflammation and degradation of extracellular matrix components through MMP's. In addition, endothelial cell caveolae are known to localize the Ang-II (AT1) receptor and regulate renin-angiotensin signaling. Based on these findings, we evaluated the role of caveolae in AAA formation in the murine model. Here, eight week old mice were co-infused with Ang-II and BAPN, a lysyl oxidase inhibitor, to induce AAA. We found that mice lacking the main structural protein of caveolae, caveolin-1, did not develop AAA compared to WT animals in spite of hypertensive blood pressures measured by telemetry in both groups. This finding suggests that intact Ang-II signaling remains in place in caveolin-1 knockout mice. To begin to address the underlying mechanism by which caveolae contributes to AAA, we measured the level of oxidative stress and MMP's in aneurysms. We found an increased expression of MMP-2 and MMP-9 in vessels of WT mice displaying aneurysms. This increase in expression was not observed in Cav-1 knockout mice. Furthermore, KO mice showed less oxidative stress then their WT counterparts as assessed by anti-nitrotyrosine staining. Next we examined the characteristics of early AAA formation in wild-type mice. We found caveolae associated proteins, endothelial nitric oxide synthase (eNOS) and NADPH oxidase 2 (Nox2), were upregulated in early AAA formation, particularly in the endothelium. Also, Vascular Cell Adhesion Molecule (VCAM) was upregulated in the endothelium. However, macrophage infiltration and MMP-2 activation was not observed in early AAA development. In order to elucidate the role of endothelial caveolae in the formation of AAA, we induced AAA, as previously described, in endothelial specific cav-1 knockout mice. Preliminarily findings show endothelial specific knockout mice do not form AAA as compared to their WT littermates. In conclusion, caveolae appears to play a critical role in the formation of AAA in mice via oxidative stress, and recruitment and/or activation of MMPs, specifically MMP-2 and MMP-9. Early markers of AAA formation include VCAM, NOX2, eNOS, and protein nitration. Also, preliminary results indicate that endothelial specific knockout mice do not develop AAA. / Cell Biology

Obstructive sleep apnea (OSA) is common in older U.S. adults and the prevalence is anticipated to rise in this age group along with obesity, a prominent risk factor for OSA. Recently, OSA was determined to be highly prevalent among patients with abdominal aortic aneurysm (AAA) disease. Objectives: Examine associations between OSA risk and physical activity (PA), metabolic syndrome (MetSyn), and exercise responses to cardiopulmonary exercise testing (CPET) in elderly patients with AAA disease. Methods: Elderly patients (n=326 for Studies 1 and 2; n=114 for Study 3) newly diagnosed with small AAAs (aortic diameter "2.5 and < 5.5 cm) were recruited. Data collection for all participants included: extraction of medical history and drug information from medical records; completion of a physical examination to assess resting vital signs and anthropometrics; fasting blood draw for several biochemical analyses; completion of a cardiopulmonary exercise test (CPET); and completion of interviews and questionnaires for health history, PA, and OSA risk. Results: 57% of subjects were High-risk for OSA and 17% were classified in the highest-risk Berlin Risk Score (BRS) 3 group; these subjects reported fewer blocks walked/day, flights of stairs climbed/day, and expended fewer Calories when engaged in these activities compared to Low-risk counterparts, independent of obesity. Among those at High-risk for OSA, 45% had MetSyn. Subjects with the highest BRS also had the highest prevalence of MetSyn and values for the MetSyn component biomarkers. Exercise capacity and physiological responses at rest, during exercise, and recovery were similar between groups at High- and Low-risk for OSA. Conclusions: Reduced levels of PA among elderly AAA patients at High-risk for OSA could have unfavorable implications for cardiovascular disease (CVD) risk and all-cause and CVD mortality.  Subjects demonstrating the most clinical symptoms of OSA showed a significantly higher prevalence for MetSyn and several of the biomarkers that determine MetSyn. In clinical practice, the BRS may be useful for identifying those AAA patients at increased risk for both OSA and MetSyn. / Ph. D.

Diss. Linköping : Linköpings universitet, 2005.

Abdominal Aortic Aneurysm (AAA) is a disease that mainly affects elderly men, and ruptured AAA (rAAA) is associated with a mortality of &gt; 80%. AAA seldom gives any symptoms prior to rupture. The aims of this thesis were to investigate different aspects of how to affect mortality from rAAA. In Study I, we identified 849 patients treated for rAAA during 1987-2004, and studied the 30-day survival after surgery, depending on whether they came directly to the treating hospital (one-stop) or were transferred via another hospital (two-stop). A two-stop referral pattern resulted in a 27% lower population-based survival rate for patients 65-74 years of age. However, the consequences would be small even if a one-stop referral pattern could be generally accomplished, due to the huge over-all mortality related to rAAA, hence an argument to find and treat AAA before rupture, e.g. by screening. In Study II, we examined the AAA-prevalence and the risk factors for AAA among 70-year-old men. The screening-detected AAA-prevalence was 2.3%, thus less than half the predicted. The most important risk factor was smoking. In Study III, we compared the screening-detected AAA-prevalence, the attendance rate, and the rate of opportunistic detection of AAA, between almost 8000 65- and 6000 70-year-old men. There was no difference in the screening-detected prevalence; probably due to the fact that almost 40% of the AAAs among the 70-year-old were already known prior to screening, compared to roughly 25% in the 65-year-old. The attendance rate was higher among the 65-year-old men, 85.7% compared 84.0% in the 70-year-old. Thus, there is no benefit of screening for AAA among 70- instead of 65-year-old men. In Study IV, a cost-effectiveness analysis, we found that screening for AAA still appears to be cost-effective, despite profound changes in disease pattern and AAA-management. In conclusion, we found that mortality from rAAA is not affected in any substantial way by different referral patterns and hence centralisation of services for AAA/rAAA is not a solution. A better alternative is to prevent rupture through early detection by screening. Screening 65-year-old men for AAA still appears to be cost-effective, despite profound changes in disease pattern and AAA-management during the last decade. Screening 70- instead of 65-year-old men will not increase the efficacy of screening.