(NVKP-16-1-2016-0017 National Heart Program) Támogató: NKFIH
(2020-4.1.1.-TKP2020)
(Therapeutic Development and Bioimaging thematic programmes of the Semmelweis University)
Aortic valve stenosis (AS) is the most common valvular heart disease. The incidence
of AS increases with age, however, a significant proportion of elderly people have
no significant AS, indicating that both aging and nonaging pathways are involved in
the pathomechanism of AS. Age-related and stress-induced cellular senescence accompanied
by further active processes represent the key elements of AS pathomechanism. The early
stage of aortic valve degeneration involves dysfunction and disruption of the valvular
endothelium due to cellular senescence and mechanical stress on blood flow. These
cells are replaced by circulating progenitor cells, but in an age-dependent decelerating
manner. When endothelial denudation is no longer replaced by progenitor cells, the
path opens for focal lipid deposition, initiating subsequent oxidation, inflammation
and micromineralisation. Later stages of AS feature a complex active process with
extracellular matrix remodeling, fibrosis and calcification. Echocardiography is the
gold standard method for diagnosing aortic valve disease, although computed tomography
and cardiac magnetic resonance are useful additional imaging methods. To date, no
medical treatment has been proven to halt the progression of AS. Elucidation of differences
and similarities between vascular and valvular calcification pathomechanisms may help
to find effective medical therapy and reduce the increasing health burden of the disease.
