Aortic sclerosis pathophysiology
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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:
- 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
- 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)