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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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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:
  1. Subendothelial thickening on the aortic side of the leaflet, between the basement membrane and elastic lamina,
  2. Presence of large amounts of intracellular and extracellular neutral lipids and fine, stippled mineralization, and
  3. Disruption of the basement membrane overlying the lesion.
  4. 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

  1. 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. 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)
  3. 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)

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