Aortic sclerosis pathophysiology: Difference between revisions
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:#Disruption of the basement membrane overlying the lesion. | :#Disruption of the basement membrane overlying the lesion. | ||
:#Regions of the fibrosa adjacent to these lesions were characterized by thickening and by protein, lipid, and calcium accumulation. | :#Regions of the fibrosa adjacent to these lesions were characterized by thickening and by protein, lipid, and calcium accumulation. | ||
*Aortic sclerosis is '''''non-obstructive degeneration''''' of the aortic valve developed consequently to calcification of the aortic valve and macrophage accumulation which is dependent on the synthesis of osteopontin protein.<ref name="pmid7554197">{{cite journal |author=O'Brien KD, Kuusisto J, Reichenbach DD, Ferguson M, Giachelli C, Alpers CE, Otto CM |title=Osteopontin is expressed in human aortic valvular lesions |journal=[[Circulation]] |volume=92 |issue=8 |pages=2163–8 |year=1995 |month=October |pmid=7554197 |doi= |url=http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=7554197 |accessdate=2012-04-11}}</ref> | |||
==References== | ==References== | ||
Revision as of 16:33, 11 April 2012
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Aortic sclerosisMicrochapters |
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Diagnosis |
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Treatment |
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Case Studies |
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Aortic sclerosis pathophysiology On the Web |
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American Roentgen Ray Society Images of Aortic sclerosis pathophysiology |
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Risk calculators and risk factors for Aortic sclerosis pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Lakshmi Gopalakrishnan, M.B.B.S. [2]
Overview
Microscopic changes reveal lipoprotein accumulation, macrophage and T-cellular infiltration, basement membrane disruption and extracellular matrix formation that cause progressive thickening of the aortic valve.[1][2]
Pathophysiology
- Otto et al,[2] demonstrated the following histological characteristics observed in patients with aortic sclerosis:
- Subendothelial thickening on the aortic side of the leaflet, between the basement membrane and elastic lamina,
- Presence of large amounts of intracellular and extracellular neutral lipids and fine, stippled mineralization, and
- Disruption of the basement membrane overlying the lesion.
- Regions of the fibrosa adjacent to these lesions were characterized by thickening and by protein, lipid, and calcium accumulation.
- Aortic sclerosis is non-obstructive degeneration of the aortic valve developed consequently to calcification of the aortic valve and macrophage accumulation which is dependent on the synthesis of osteopontin protein.[3]
References
- ↑ Freeman RV, Otto CM (2005). "Spectrum of calcific aortic valve disease: pathogenesis, disease progression, and treatment strategies". Circulation. 111 (24): 3316–26. doi:10.1161/CIRCULATIONAHA.104.486738. PMID 15967862. Retrieved 2012-04-10. Unknown parameter
|month=ignored (help) - ↑ 2.0 2.1 Otto CM, Kuusisto J, Reichenbach DD, Gown AM, O'Brien KD (1994). "Characterization of the early lesion of 'degenerative' valvular aortic stenosis. Histological and immunohistochemical studies". Circulation. 90 (2): 844–53. PMID 7519131. Retrieved 2012-04-11. Unknown parameter
|month=ignored (help) - ↑ O'Brien KD, Kuusisto J, Reichenbach DD, Ferguson M, Giachelli C, Alpers CE, Otto CM (1995). "Osteopontin is expressed in human aortic valvular lesions". Circulation. 92 (8): 2163–8. PMID 7554197. Retrieved 2012-04-11. Unknown parameter
|month=ignored (help)