Aortic sclerosis pathophysiology
Aortic sclerosisMicrochapters |
Diagnosis |
---|
Treatment |
Case Studies |
Aortic sclerosis pathophysiology On the Web |
American Roentgen Ray Society Images of Aortic sclerosis pathophysiology |
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,[1] macrophage and T-cellular infiltration,[2] basement membrane disruption and extracellular matrix formation that cause progressive thickening of the aortic valve.[3][4]
Pathophysiology
- Otto et al,[4] 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.[5]
References
- ↑ O'Brien KD, Reichenbach DD, Marcovina SM, Kuusisto J, Alpers CE, Otto CM (1996). "Apolipoproteins B, (a), and E accumulate in the morphologically early lesion of 'degenerative' valvular aortic stenosis". Arteriosclerosis, Thrombosis, and Vascular Biology. 16 (4): 523–32. PMID 8624774. Retrieved 2012-04-11. Unknown parameter
|month=
ignored (help) - ↑ Olsson M, Dalsgaard CJ, Haegerstrand A, Rosenqvist M, Rydén L, Nilsson J (1994). "Accumulation of T lymphocytes and expression of interleukin-2 receptors in nonrheumatic stenotic aortic valves". Journal of the American College of Cardiology. 23 (5): 1162–70. PMID 8144784. Retrieved 2012-04-11. Unknown parameter
|month=
ignored (help) - ↑ 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) - ↑ 4.0 4.1 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)