**Part 4**

**Aortic Sclerosis/Aortic Stenosis** 

118 Aortic Valve

Watkin RW, Lang S, Lambert PA, Littler WA & Elliott TS (2006). The serological diagnosis of

Wilson W, Taubert KA, Gewitz M, Lockhart PB, Baddour LM, Levison M, et al. (2007).

Research Interdisciplinary Working Group. *Circulation*; 116(15):1736-54.

Prevention of infective endocarditis: guidelines from the American Heart Association: a guideline from the American Heart Association Rheumatic Fever, Endocarditis, and Kawasaki Disease Committee, Council on Cardiovascular Disease in the Young, and the Council on Clinical Cardiology, Council on Cardiovascular Surgery and Anesthesia, and the Quality of Care and Outcomes

staphylococcal infective endocarditis. *J Infect*; 53:301–307.

**6** 

*USA* 

**The Progression of** 

**Aortic Sclerosis to Aortic Stenosis** 

Uzma Jalal Serageldin Raslan and Farouk Mookadam *Department of Cardiovascular Diseases, Mayo Clinic, Scottsdale, AZ,* 

Aortic stenosis is the most frequent valvular heart disease in the western world and its incidence continues to rise. Until recently, aortic valve sclerosis (AVS) was considered to be a normal degenerative process associated with aging. For this reason, the common and well recognized soft, basal ejection murmur of aortic sclerosis was generally regarded by physicians to be of little or no clinical significance. In the last decade, AVS has been the focus of both clinical and animal research. AVS has emerged as a biomarker for cardiovascular risk, and ultimately leads to aortic stenosis in 16% of adults (Stewart et al., 1997; Cosmi et al., 2002). Calcific aortic valve disease ranges from aortic sclerosis, defined as focal, irregular thickening of aortic valve leaflets with no hemodynamically significant derangement (i.e., peak velocity of ≤ 2 m/s and no significant aortic regurgitation), to severe calcification (with impaired leaflet motion and an aortic jet velocity of ≥ 2.5 m/s) referred to as aortic stenosis. The paradigm of aortic stenosis has shifted from being considered a degenerative aging process; it is now recognized as a dynamic inflammatory process with features similar to atherosclerotic plaque. These features include endothelial disruption, focal deposition of low density lipoprotein (LDL) cholesterol and lipoprotein A, accumulation of macrophages and

Aortic valve sclerosis is present in approximately 25% of people 65 to 74 years old and in 50 % of people over 84 years (Lindroos et al., 1993; Stewart et al., 1997; Otto et al., 1999), while aortic stenosis affects 2% of the population over 65 years old, 3 % over 75 years old, and 4% over 85 years old (Stewart, 1997). The severity of aortic sclerosis on a scale of 0-3 has been quantified by echocardiography for echogenicity, thickening, or calcification of the

• 2- Moderate (Minor involvement of two leaflets or extensive involvement of one leaflet) • 3- Severe (Extensive involvement of two leaflets or involvement of all three leaflets) In adults, valvular aortic stenosis is due to degenerative calcific changes of a trileaflet valve, rheumatic disease, or secondary calcification of a congenitally bicuspid valve (Roberts, 1970; Selzer, 1987). In developed countries, the most common cause of adult acquired aortic

T lymphocytes, and calcification (Freeman et al., 2004).

**2. Epidemiology and etiology** 

• 0- Normal (No involvement)

valve leaflet as follows (Chandra et al., 2004):

• 1- Mild (Minor involvement of one leaflet)

**1. Introduction** 
