Geriatric Aspects of Aortic Stenosis

Abstract

Currently, AS is the most frequent heart valve disease in industrialized countries and its prevalence sharply increases with age (Iung et al., 2003; Nkomo et al., 2006). Thus with the prolongation of life expectancy, the population of old patients with AS is expected to grow in the future. In elderly patients AS is most frequently caused by progressive calcification and degeneration of the tricuspid aortic cusps (Otto et al., 1997; Lindroos et al., 1994). The comissures are not fused as in rheumatic AS. Traditionally, AS has been thought of as a passive degenerative ”wear and tear” disease associated with aging. Certain clinical factors like coronary artery disease (CAD), hypertension, obesity, diabetes mellitus, smoking, hyperlipidemia and chronic kidney disease (CKD) are associated with AS. However, the studies of Otto CM et al. support that the histopathological property of calcific aortic valve disease represents an active process with some similarities to atherosclerosis, including lipid deposition, macrophage and T cell infiltration, basement membrane disruption and microscopic calcification (Otto et al., 1994). Both AS and atherosclerosis have many clinical risk factors in common such as diabetes mellitus, hypertension, dyslipidemia, CKD, and tobacco use. (Peltier et al., 2003). Ortlepp JR et al observed that genetic factors may be important in the development of valve calcification (Ortlepp et al., 2001). They showed that patients with AS had significant difference in vitamin D receptor genotypes compared to individuals without AS. The research of Stewart Bf et al. revealed that in 5201 men and women older than 65 years, 26% of study participants had frank aortic sclerosis (thickening of or calcific deposits on the aortic valve cusps with a peak velocity across the aortic valve of <1.5 msn) (Stewart et al., 1997). In the initial stages, aortic sclerosis is present without stenosis, but as the disease advances the valve leaflets which become less mobile eventually fuse together and cause left ventricular outflow tract (LVOT) obstruction. The study by Cosmi JE et al., in which more than 2000 patients with aortic sclerosis were examined, %16 developed AS (Cosmi et al., 2002). Of these patients mild, moderate and severe AS developed in 10.5, 3, and 2.5%