Background: Calcific aortic valve disease is common in an aging population. It is an active
atheroinflammatory process that has an initial pathophysiology and similar risk factors as atherosclerosis.
However, the ultimate disease phenotypes are markedly different. While coronary heart
disease results in rupture-prone plaques, calcific aortic valve disease leads to heavily calcified and
ossified valves. Both are initiated by the retention of low-density lipoprotein particles in the subendothelial
matrix leading to sterile inflammation. In calcific aortic valve disease, the process towards
calcification and ossification is preceded by valvular thickening, which can cause the first clinical
symptoms. This is attributable to the accumulation of lipids, inflammatory cells and subsequently
disturbances in the valvular extracellular matrix. Fibrosis is also increased but the innermost extracellular
matrix layer is simultaneously loosened. Ultimately, the pathological changes in the
valve cause massive calcification and bone formation - the main reasons for the loss of valvular
function and the subsequent myocardial pathology.
Conclusion: Calcification may be irreversible, and no drug treatments have been found to be effective,
thus it is imperative to emphasize lifestyle prevention of the disease. Here we review the
mechanisms underpinning the early stages of the disease.