Adiponectin, leptin, and resistin in patients with aortic stenosis without concomitant atherosclerotic vascular disease

Abstract

IntroductIon Aortic stenosis (AS) is the most common valvular heart disease in adults, with the highest prevalence among elderly patients. Aortic valvular lesions have some similarities to atherosclerosis including chronic inflammation, the presence of lipoproteins, cholesterol, macrophages, T cells, 1 and calcification. 2 Growing evidence indicates that AS is an active, potentially modifiable inflammatory process.In contrast to multiple cytokines involved in the development of AS, adipocytokines in AS have attracted less inter est despite their role in atherosclerosis. Adiponectin, leptin, and resistin play a major role in glucose meta bolism, insulin

Severe degenerative aortic stenosis with preserved ejection fraction does not change adipokines serum levels

“…Recently, Gucuk Ipek et al [27] showed, similar to the present findings, that there is no relationship between the adiponectin levels and calcific AVD. In contrast, Kolasa-Trela et al [28] published an article suggesting that adipokines may be involved in the progression of AS. In 2010, Mohty et al [29] observed that older patients with AS had a higher plasma level of resistin, which was associated with the degree of valvular calcification and inflammation.…”

Degenerative Aortic Stenosis, Dyslipidemia and Possibilities of Medical Treatment

“…Scientific research has proven that development of DAS is similar to the development process of atherosclerosis [ 2 , 7 , 11 , 18 ]. It has been determined that both AV calcinosis and atherosclerosis cover endothelial dysfunction, lipid infiltration, inflammation, neoangiogenesis and calcinosis.…”

“…In case of MS, flow velocity through AV increases by 0.25 ± 0.21 m/s per year on average, while for those without MS–0.19 ± 0.19 m/s per year ( p = 0.03) [ 27 ]. Even in cases when intensive lipid-reducing therapy is applicated and recommended LDL levels are achieved, DAS progresses twice as fast as for patients without MS [ 11 ].…”

“…Penetration and oxidation are significant pathogenic mechanisms which stimulate inflammatory reaction in aortic valve endotelium. Close relationship between lipids, inflammation and DAS was determined [ 7 , 11 , 12 ]. LDL and Lp(a) infiltrate the location of injury and oxidize.…”

“…Calcinosis of aortic valve was the disease of the elderly; however, it has been proven that DAS is not a consequence of aging only [ 7 ]. Histopathological tests have shown that calcinosis of aortic valve is an active process which resembles development of atherosclerosis [ 10 , 11 ]. Endothelial dysfunction, lipid infiltration, calcification and ossification are evidenced in both diseases [ 10 , 12 ].…”