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      Optimization of the Model of Abdominal Aortic Aneurysm – Experiment in an Animal Model

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          Background: Many studies have been performed in order to model abdominal aortic aneurysm (AAA) in an experimental animal, most commonly in small laboratory animals. In our study, we tried to find the best AAA model in a pig by using various mechanical and enzymatic mechanisms. Methods: Twenty-two pigs were operated on. We combined 3 mechanisms of creating an AAA, using an intraluminal infusion of porcine pancreatic elastase into the abdominal aortic segment, application of plastic cuff below the renal arteries causing turbulent blood flow, and inserting a patch into the longitudinal aortotomy. Results: We found different results in different groups according to the mechanisms used. In group A, with a combination of the intraluminal elastase infusion and application of a stenosing cuff, AAA developed in all 7 animals (100%). In this group, we also found the largest histological changes in the abdominal aorta samples. Conclusion: The use of intraluminal pancreatic elastase infusion, together with increased turbulent flow caused by the stenosing cuff, seems to be the best model of AAA in pigs. This model is suitable for further research in the etiopathology of AAA. In fact, it is the first successful approach to a large-caliber native aneurysm model.

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          Most cited references 9

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          Multicenter prospective study of nonruptured abdominal aortic aneurysm. Part II. Variables predicting morbidity and mortality.

          A previous article (Part I) described the patient population and operative management of 666 patients who had surgery for nonruptured abdominal aortic aneurysms. This article details the perioperative complications and, by chi-square and logistic regression analysis, identifies the variables that are associated with each complication. In summarizing the results (below) the incidence of each complication is listed, along with the predictive risk factors in parentheses that have significance levels less than 0.05. Vascular morbidity data are as follows: intraoperative bleeding, 4.8%; postoperative bleeding requiring transfusion, 2.3% or repeat operation, 1.4% (large volume of blood transfusion and/or use of an autotransfusion device); intraoperative limb ischemia, 3.5%; graft thrombosis, 0.9% (femoropopliteal disease and/or distal anastomosis at the femoral level); distal thromboembolism, 3.3% (male sex, femoral popliteal disease, and/or intraoperative graft thrombosis); amputation, 1.2%; graft infection, 1 case. General morbidity data are as follows: cerebrovascular event, 0.6%; paraplegia, 1 case; cardiac event, 15.1% (age, previous episode of congestive heart failure, and/or electrocardiogram [ECG] evidence of a previous myocardial infarction); myocardial infarction, 5.2% (advancing age, angina, and/or prolonged aortic cross-clamp time); congestive heart failure, 8.9% (previous history of congestive heart failure, ECG evidence of ischemia, and/or chronic obstructive lung disease); arrhythmia requiring treatment, 10.5% (preoperative ventricular premature beats and/or respiratory failure requiring ventilation for more than 48 hours); new arrhythmia, 8.4% (angina and/or chronic obstructive lung disease); respiratory failure, 8.4% (chronic obstructive lung disease, large volume of blood transfused, and/or occurrence of postoperative bleeding, cerebrovascular accident, congestive heart failure, or myocardial infarction); renal damage with rise in creatinine or blood urea nitrogen, 5.4% and/or renal failure requiring dialysis, 0.6% (elevated preoperative creatinine, suprarenal aortic cross-clamping, and/or renal vein ligation); diarrhea without evidence of ischemia colitis, 7.1% and ischemic colitis, 0.6% (pelvic flow interrupted); prolonged ileus, 11.0% (aortoiliac occlusive disease, deterioration of renal function, prolonged ventilation, and/or preoperative history of angina); superficial wound infection, 1.5% and deep infection, 0.5% (femoral anastomosis and/or female sex); coagulopathy, 1.1% (large volume of blood transfused).(ABSTRACT TRUNCATED AT 400 WORDS)
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            Pathogenesis of abdominal aortic aneurysm.

            The pathogenesis of abdominal aortic aneurysm involves many factors acting over time. However, destruction of elastin in the aortic wall is a key event that shifts the load produced by blood pressure on to collagen. This is exacerbated in the presence of hypertension. Smoking and age are further important factors, as is the site; elastic lamellae are relatively less common in the abdominal aorta. Once the shielding effect of elastin is lost, further dilatation and rupture of the aorta depend on the physical properties of the collagen present.
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              Two decades of abdominal aortic aneurysm repair: have we made any progress?

              Over the past 20 years, there have been numerous advances in our ability to detect and to treat abdominal aortic aneurysms (AAAs). We hypothesized that these advances would lead to (1) an increase in the rate of elective repair and a decrease in the incidence of ruptured AAA (rAAA) and (2) a decrease in operative deaths for both elective AAA (eAAA) and rAAA. To test these hypotheses, we investigated the incidence and outcomes of eAAA and rAAA surgery between 1979 and 1997, using the National Hospital Discharge Survey. This data set is a randomized, stratified sample representing discharges from the nation's acute care, nonfederally funded hospitals. Codes from the International Classification of Diseases, Ninth Revision were used to identify our study population. Over the past 19 years, there has been no change in the incidence rate of eAAA repair (range, 44.1-77.9 per 100,000). Moreover, the incidence of rAAAs presenting to the nation's hospitals has not changed (range, 6.6-16.3 per 100,000). There has been no consistent improvement over time in operative deaths associated with either eAAA or rAAA repair (average rates over the study period: eAAA, 5.6%; rAAA, 45.7%). Significant predictors of death from eAAA in patients included an age older than 80 years, African American race, congestive heart failure (CHF), and diabetes (P<.0001 for all). Significant predictors of death from rAAA in patients included age older than 70 years, African American race, female sex, renal failure, and a hospital bed size more than 500 (P<.05 for all). On a national level, over the past 19 years, our ability to identify and to treat patients with AAA has not improved. Advances in technology and critical care have not affected outcome. Regionalization of care, screening of high-risk populations, and endovascular repair are strategies that might allow further improvement in the outcome of patients with aneurysmal disease.

                Author and article information

                J Vasc Res
                Journal of Vascular Research
                S. Karger AG
                December 2008
                31 May 2008
                : 46
                : 1
                : 1-5
                Departments of aVascular Surgery and bPediatry, University Hospital, and cInstitute of Histology and Embryology, Medical Faculty, Charles University, Pilsen, Czech Republic
                135659 J Vasc Res 2009;46:1–5
                © 2008 S. Karger AG, Basel

                Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                Page count
                Figures: 6, Tables: 1, References: 14, Pages: 5
                Methods in Vascular Biology


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