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]


Calcific aortic valve disease includes both aortic sclerosis and aortic stenosis.[1]

In patients with calcific aortic valve disease, microscopic examination reveals lipoprotein accumulation,[2] macrophage and T-cellular infiltration,[3] basement membrane disruption and extracellular matrix formation that lead to progressive thickening of the aortic valve.[4][5][1]


  • Otto et al,[5] 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
  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.[6]
  • Disturbances in mineral metabolism such as higher serum phosphate concentration has shown to contribute to the development of aortic sclerosis.[7][8]


  1. 1.0 1.1 O'Brien KD (2006). "Pathogenesis of calcific aortic valve disease: a disease process comes of age (and a good deal more)". Arteriosclerosis, Thrombosis, and Vascular Biology. 26 (8): 1721–8. doi:10.1161/ PMID 16709942. Retrieved 2012-04-11. Unknown parameter |month= ignored (help)
  2. 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)
  3. 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)
  4. 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)
  5. 5.0 5.1 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)
  6. 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)
  7. Linefsky JP, O'Brien KD, Katz R, de Boer IH, Barasch E, Jenny NS, Siscovick DS, Kestenbaum B (2011). "Association of serum phosphate levels with aortic valve sclerosis and annular calcification: the cardiovascular health study". Journal of the American College of Cardiology. 58 (3): 291–7. doi:10.1016/j.jacc.2010.11.073. PMID 21737022. Retrieved 2012-04-11. Unknown parameter |month= ignored (help)
  8. Adeney KL, Siscovick DS, Ix JH, Seliger SL, Shlipak MG, Jenny NS, Kestenbaum BR (2009). "Association of serum phosphate with vascular and valvular calcification in moderate CKD". Journal of the American Society of Nephrology : JASN. 20 (2): 381–7. doi:10.1681/ASN.2008040349. PMC 2637048. PMID 19073826. Retrieved 2012-04-11. Unknown parameter |month= ignored (help)

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