Anatomic and clinical significance of calcification of the aortic knob visualized radiographically∗

Chapman, Irving

doi:10.1016/0002-9149(60)90315-5

Cited by 16 publications

(6 citation statements)

References 2 publications

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“…For more than half a century, it has been associated with a poor prognosis attributable to vascular disease. 1 Its presence is a strong indicator of chronic inflammatory disease, usually atherosclerosis, and its extent directly relates to the overall burden of atherosclerotic disease. 2 Despite its clinical relevance, research on the mechanism of mineral deposition in arteries has been limited and remains at an early scientific stage relative to research on other aspects of atherosclerosis, such as lipoprotein biochemistry and inflammation.…”

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confidence: 99%

Vascular Calcification

Abedin

Tintut

Demer

2004

ATVB

783

220

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Abstract-Vascular calcification, long thought to result from passive degeneration, involves a complex, regulated process of biomineralization resembling osteogenesis. Evidence indicates that proteins controlling bone mineralization are also involved in the regulation of vascular calcification. Artery wall cells grown in culture are induced to become osteogenic by inflammatory and atherogenic stimuli. Furthermore, osteoclast-like cells are found in calcified atherosclerotic plaques, and active resorption of ectopic vascular calcification has been demonstrated. In general, soft tissue calcification arises in areas of chronic inflammation, possibly functioning as a barrier limiting the spread of the inflammatory stimulus. Atherosclerotic calcification may be one example of this process, in which oxidized lipids are the inflammatory stimulus. Calcification is widely used as a clinical indicator of atherosclerosis. It progresses nonlinearly with time, following a sigmoid-shaped curve. The relationship between calcification and clinical events likely relates to mechanical instability introduced by calcified plaque at its interface with softer, noncalcified plaque. In general, as calcification proceeds, interface surface area increases initially, but eventually decreases as plaques coalesce. Key Words: calcification Ⅲ atherosclerosis Ⅲ inflammation Ⅲ bone Ⅲ vascular V ascular calcification is an important manifestation of atherosclerosis. For more than half a century, it has been associated with a poor prognosis attributable to vascular disease. 1 Its presence is a strong indicator of chronic inflammatory disease, usually atherosclerosis, and its extent directly relates to the overall burden of atherosclerotic disease. 2 Despite its clinical relevance, research on the mechanism of mineral deposition in arteries has been limited and remains at an early scientific stage relative to research on other aspects of atherosclerosis, such as lipoprotein biochemistry and inflammation. Mechanisms of Vascular CalcificationVascular calcification recapitulates embryonic osteogenesis. Pathologists in the 19th century recognized the presence of bone-like tissue within atherosclerotic arteries, with lamellar structure, osteoblast-like cells, and hematopoietic elements. 3 Yet, for most of the 20th century, vascular calcification has been regarded as a passive, unregulated, degenerative process occurring within advanced atherosclerotic plaques. The concept of regulated ossification as the mechanism behind vascular calcification has re-emerged only in the past decade. 4,5 Ossification has been identified histologically in 60% of restenotic aortic valves after balloon valvuloplasty. 6 Approximately 15% of carotid atherosclerotic plaque specimens 7 and calcified cardiac valve tissue 8 have ossification. Vascular calcification may include both osteogenic and chondrogenic differentiation. In humans, it is primarily osteogenic with bone tissue formation, whereas in mice, it is primarily chondrogenic with cartilage formation. Although osteoblas...

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confidence: 99%

Vascular Calcification

Abedin

Tintut

Demer

2004

ATVB

783

220

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“…For more than half a century, it has been associated with a poor prognosis attributable to vascular disease. 10 However, the process reduces the vascular resilience required for hemodynamic function and introduces high mechanical failure stress in the artery wall & hence the importance of calcium score in CAD. Diffuse calcification of the length of dorsal aorta continuously upto a significant part of the abdominal aorta is rare.…”

Section: Resultsmentioning

confidence: 99%

Upper Body Hypertension with Gross Atherosclerotic Narrowing and Diffuse Calcification of the Descending and Abdominal Aorta

1970

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Of the hypertensive patients presenting to the primary care providers, 95-99% have essential hypertension. Remaining 1-5% have an underlying diagnosis.1 Narrowing of the aorta distal to the origin of the arteries to the head, neck & upper limbs causes upper body hypertension. Coarctation of the aorta, a congenital narrowing of the aorta just distal to the insertion of ductus arteriosus, is the major cause of upper body hypertension. Gross atherosclerotic narrowing & diffuse calcification of the descending & abdominal aorta rarely emulates the features of coarctation of the aorta. We report a case of upper body hypertension due to gross atherosclerotic narrowing & diffuse calcification of the descending & abdominal aorta after extensive medline search we have not come across of such reports yet. Â doi:10.3329/jom.v10i3.2014 Â J Medicine 2009; 10 (Supplement 1): 32-35

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“…Vascular calcification is an important manifestation of atherosclerosis. For more than half a century, it has been associated with a poor prognosis attributable to vascular disease [8]. Its presence is a strong indicator of chronic inflammatory Fig.…”

Section: Discussionmentioning

confidence: 99%

Effects of emotional and physiological stress on plaque instability in apolipoprotein E knockout mice

et al. 2011

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In the present study, we sought to investigate the effects of emotional and physiological stress on plaque instability in atherosclerosis. We used different stress-treated apolipoprotein E (ApoE)-deficient mice, which have been shown to spontaneously develop atherosclerosis with features similar to those seen in humans, as an animal model. Morphology study showed that emotional stress (ES) obviously promoted the development of atherosclerotic plaques and plaque instability evidenced by significantly increasing plaque size, plaque-to-surface ratio and plaque calcification, and enhancing the frequency of large necrotic core and medial erosion compared with control ApoE(-/-) mice (P<0.01). Physiological stress (PS) treatment alone did not affect the plaque stability compared with control ApoE(-/-) mice (P>0.05). However, the combination of ES and PS treatment (CS) initiated much stronger plaque instability compared with ES treatment alone (P<0.01), increased the frequency of thin fibrous caps, and even triggered plaque rupture and buried fibrous cap. Immunohistochemical analysis indicated that both ES and CS treatment led to an increase in the accumulation of macrophages and T cells and a decrease of smooth muscle cells, reflecting an unstable atherosclerotic plaque phenotype, in the atherosclerotic lesions in ApoE(-/-) mice. PS alone did not affect plaque cellular components. Similarly, CS-mediated changes in atherosclerotic plaque composition were stronger than that caused by ES alone (P<0.01). Taken together, ES treatment alone is sufficient to promote plaque instability. PS alone does not affect atherosclerotic plaque development, but can potentiate ES-mediated plaque destabilization.

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Anatomic and clinical significance of calcification of the aortic knob visualized radiographically∗

Cited by 16 publications

References 2 publications

Vascular Calcification

Vascular Calcification

Upper Body Hypertension with Gross Atherosclerotic Narrowing and Diffuse Calcification of the Descending and Abdominal Aorta

Effects of emotional and physiological stress on plaque instability in apolipoprotein E knockout mice

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