Are aortic aneurysms caused by atherosclerosis?

Reed, Daniel M.; Reed, C. I.; Stemmermann, Grant N.; Hayashi, T.

doi:10.1161/01.cir.85.1.205

Cited by 283 publications

(186 citation statements)

References 25 publications

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“…The process of development from atherosclerosis to rupture of aortic aneurysms may be longer and more complicated than that from atherosclerosis to infarction of coronary arteries. Epidemiologic studies have also demonstrated a 2 to 8-fold increased risk of aortic aneurysms in heavy smokers compared to nonsmokers (Hirayama 1992;Reed et al 1992). However, in Japan the sharply increasing mortality rates of aortic aneurysms were inconsistent with a declining trend for the proportion of smokers during the same period (Ministry of Health and Welfare 1993).…”

Section: Discussionmentioning

confidence: 99%

Increasing Trends in Mortality Rate of Aortic Aneurysms in Japan, 1955-90.

Hu¹,

Shimizu²,

Kawakami³

et al. 1993

Tohoku J. Exp. Med.

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To know the characteristics of mortality from aortic aneurysms in Japan, the age-adjusted and age-specific mortality rates of the diseases were calculated based on the Vital Statistics of Japan published from the Statistics and Information Department, Minister's Secretariat, Ministry of Health and Welfare. The overall age-adjusted mortality rate increased 24.8-fold from 0.43 to 10.98 per 100,000 for males, and 18.6-fold from 0.23 to 4.54 per 100,000 for females from 1955-90. The most common type was abdominal aortic aneurysms followed by dissecting and thoracic aortic aneurysms. The mortality rates of dissecting and thoracic aortic aneurysms increased greater than that of abdominal aortic aneurysms. The mortality rate of dissecting aneurysms was higher than that of abdominal and thoracic aortic aneurysms in age groups of 64 years or under. The mortality rate of abdominal aortic aneurysms was the most common in age groups of 65 years or over, mortality; aortic aneurysms It is reported that mortality rate of abdominal aortic aneurysms has increased, whereas the rates of dissecting and thoracic aortic aneurysms have decreased in recent decades in England and Wales, the USA and Western Australia (Castleden et al. 1985;Lilienfeld et al. 1987;Fowkes et al. 1989). Hirayama reported that the number of deaths due to aortic aneurysms has sharply increased in Japan from 1955 -90 (Hirayama 1992. He also reported that the increasing trends in deaths from dissecting and thoracic aortic aneurysms were greater than that from abdominal aortic aneurysms, although he did not show the mortality rates. We calculated the age-adjusted mortality rates of the disease according to type of aneurysms in Japan comparing those in England and Wales, and the USA. MATERIALS AND METHODSWe obtained number of deaths from aortic aneurysms and population, 1955-90 , by sex and age from the Vital Statistics in Japan.We defined the following diseases as aortic aneurysms based on the International Classification of Diseases (ICD) diagnostic codes: ICD

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Section: Discussionmentioning

confidence: 99%

Increasing Trends in Mortality Rate of Aortic Aneurysms in Japan, 1955-90.

Hu¹,

Shimizu²,

Kawakami³

et al. 1993

Tohoku J. Exp. Med.

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“…30 -32 Leukocyte recruitment and expression of pro-inflammatory cytokines characterize early atherogenesis. 1 AAA typically arise in the setting of severe atherosclerosis, 33 and several studies suggest that the aneurysmal disease may progress from occlusive disease. 34 Because AAA frequently coexist with generalized atherosclerosis, they are frequently termed "atherosclerotic aneurysms."…”

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confidence: 99%

Inflammation and Cellular Immune Responses in Abdominal Aortic Aneurysms

Shimizu

Mitchell

Libby

2006

ATVB

562

478

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Abstract-Expansion and rupture of abdominal aortic aneurysms (AAA) result in high morbidity and mortality rates. Like stenotic atherosclerotic lesions, AAA accumulate inflammatory cells, but usually exhibit much more extensive medial damage. Leukocyte recruitment and expression of pro-inflammatory Th1 cytokines typically characterize early atherogenesis of any kind, and modulation of inflammatory mediators mutes atheroma formation in mice. 1 However, the mechanistic differences between stenotic and aneurysmal manifestations of atherosclerosis remain unexplained. We recently showed that aortic allografts deficient in interferon-␥ (IFN-␥) signaling developed AAA correlating with skewed Th2 cytokine environments, suggesting important regulatory roles for Th1/Th2 cytokine balance in modulating matrix remodeling and important implications for the pathophysiology of aortic aneurysm and atherosclerosis. Key Words: aortic aneurysm Ⅲ atherosclerosis Ⅲ cytokine Ⅲ pathogenesis Ⅲ T-lymphocytes Ⅲ transplantation A ortic aneurysms are permanent and localized aortic dilations defined as having diameters 1.5-times greater than normal (ie, Ͼ3 cm diameter for abdominal aortic aneurysms [AAA]). In comparison, the term aortic ectasia describes localized aortic enlargement Ͻ1.5-times normal diameter. 2 Although most aneurysms remain asymptomatic and undiagnosed, risk of rupture increases dramatically when diameters exceed 5.5 cm. Despite surgical advances, the prognosis of ruptured AAA remains poor, and the overall mortality remains high (80% to 90%). 3 Although surgical or endovascular repair constitutes the major therapeutic options for AAA Ͼ5.5 cm, such invasive procedures provide no therapeutic advantage for AAA Ͻ5.5 cm diameter.Most AAA develop below the renal arteries and end above the bifurcation of the iliac arteries; they typically exhibit a fusiform morphology, with symmetrical circumferential enlargement involving all layers of the aortic wall. Less frequently, aneurysms have a saccular form, with aneurysmal degeneration affecting only part of the aortic circumference. The AAA wall usually becomes laminated with thrombus and its intraluminal diameter often appears relatively normal by angiography. Important histological features of aneurysms include chronic adventitial and medial inflammatory cell infiltration, elastin fragmentation and degeneration, and medial attenuation. Collagen (especially types I and III) in the media and adventitia provides tensile strength to the aortic wall. Collagen synthesis increases during the early stages of aneurysm formation, suggesting a repair process. 4 However, in later stages, collagen degradation exceeds its synthesis (accompanied by excessive degradation of other extracellular matrix macromolecules, notably elastin), ultimately favoring AAA rupture. Indeed, AAA exhibit increased local production of enzymes capable of degrading collagen and elastin extracellular matrix proteins. [5][6][7] In AAA, inflammatory cells (polymorphonuclear neutrophils, T cells, B cells, macrophages, mast c...

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“…In these disorders, a chronic inflammatory infiltrate of the aortic medial and adventitial vasa vasorum is present, with many lymphocytes, macrophages and multinucleated giant cells (6,(8)(9)(10). Giant cell arteritis patients have 2.4 times the risk of developing aortic aneurysms compared with the general population (3,11,12).…”

Section: Discussionmentioning

confidence: 99%