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Aneurysm: Epidemiology Aetiology and Pathophysiology

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Biomechanics and Mechanobiology of Aneurysms

Part of the book series: Studies in Mechanobiology, Tissue Engineering and Biomaterials ((SMTEB,volume 7))

Abstract

Abdominal aortic aneurysm (AAA) disease is a chronic degenerative disorder and is an important cause of preventable deaths in older patients. Prevalence rates are estimated between 1.3 and 8.9% in men and between 1.0 and 2.2% in women. However, with the aging of the population and the increasing number of smokers, the incidence of the AAA is rising. The prevalence and incidence of thoracic aortic aneurysms (TAA) is more difficult to assess than for the abdominal portion of the aorta due to poorer access to screening. The overall incidence rate of TAAs is estimated at 10.4 per 100,000 person-years. The classical risk factors for atherosclerosis, such as tobacco smoking, male sex, age, hypertension, and hyperlipidemia have all been found to be also risk factors for AAA. The pathophysiology of the aorta above and below the diaphragm has shown significant differences in biomechanical properties, atherosclerotic distribution, proteolytic pattern, and cell signaling pathways that have implications in the development of an aortic aneurysm. During the last decades an overwhelming amount of evidence has been accumulated in support of genetic risk factors contributing to the development, growth and rupture of aneurysms in different segments of the arterial tree. Inflammation and matrix metalloproteinases (MMPs) also play a key role in the pathogenesis of AAA by causing proteolytic degradation of structural proteins. The size of an aneurysm is a universally recognized factor in predicting the probability of rupture; the risk of rupture increases as the diameter of the aneurysm increases. Rupture occasionally occurs in small aneurysms. The risk of rupture and dissection of TAAs also increase with increasing diameter. In addition, not only the size but also the growth rate of the aneurysm has been consistently shown to be critical in predicting rupture.

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Acknowledgments

The original work (Genetics) carried out in the Kuivaniemi laboratory was funded in part by the National Heart, Lung, and Blood Institute of the NIH (grants HL045996 and HL064310 to H.K.).

The Department of Cardiovascular surgery University hospital of Liège is supported by the European Union integrated project ‘‘Fighting Aneurysmal Disease’’ (FAD, http://www.fighting-aneurysm.org/).

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Authors and Affiliations

  1. Department of Cardiovascular Surgery, University Hospital of Liège, Liège, Belgium

    Natzi Sakalihasan, Rodolphe Durieux & Jean-Olivier Defraigne

  2. Sigfried and Janet Weis Center for Research, Geisinger Clinic, Danville, PA, USA

    Helena Kuivaniemi

  3. Laboratory of Connective Tissues Biology, University of Liège, Liège, Belgium

    Betty Nusgens

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Correspondence to Natzi Sakalihasan .

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Sakalihasan, N., Kuivaniemi, H., Nusgens, B., Durieux, R., Defraigne, JO. (2010). Aneurysm: Epidemiology Aetiology and Pathophysiology. In: McGloughlin, T. (eds) Biomechanics and Mechanobiology of Aneurysms. Studies in Mechanobiology, Tissue Engineering and Biomaterials, vol 7. Springer, Berlin, Heidelberg. https://doi.org/10.1007/8415_2010_47

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