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Calcific aortic valve stenosis (CAVS) in the elderly, is a condition becoming progressively more widespread during the last decades, representing, today, the most common heart valve pathology in the Western Countries, following the almost complete disappearance of rheumatic valve disease and the progressive aging of the population. A Swedish population study estimated CAVS prevalence between 2% and 4% in the age group 65–79 years, reaching almost 10% over the age of 80years. A recent population study, OxVALVE, in which 2500 patients with an age >65years underwent echocardiography, revealed that 34% of the subjects had sclerosis of the aortic valve and 1.3% had aortic valve stenosis. Valvular aortic stenosis is a slowly progressive condition, well tolerated for several years, and, often, the diagnosis is only made when symptoms occur, in older, and frailer patients. Severe symptomatic CAVS has a high mortality rate, up to 50% per year, worse than most malignant tumours. In an effort to improve the classical surgical aortic valve replacement procedure, minimally invasive surgical approaches were developed, and during the last decade, percutaneous transcatheter aortic valve implantation procedures. Along these technical innovations, there has been a renewed interest in the pathophysiology of CAVS, with the goal of devising therapeutic strategies to prevent or at least delay the progression of the disease. The pathogenic process leading to CAVS is not fully understood, but it starts with an initial thickening of the cusps, then calcification and rigidity, at the beginning with a transvalvular gradient within normal limits (valvular sclerosis), and eventually developing in a true valvular stenosis, characterized by extensive thickening and calcifications determining a left ventricular outflow obstruction. Histology shows the characteristics lesions, initially on the aortic side of the cusps, with endothelial damage and buildup of extracellular lipids and lipoproteins, with inflammatory cells infiltration and calcification. Similar to atherosclerosis, CAVS for years has been considered an inevitable consequence of the aging process. This assumption has been challenged by the 1993 publication identifying a morphogenic protein typical of bone tissue in calcific tissue from human carotids. Further experimental studies confirmed that CAVS, as well as atherosclerosis, is a consequence of an active process involving lipid deposition, inflammation, and production of bone tissue. The link between CAVS and coronary artery disease has been pointed out by a large meta-analysis of observational studies, in which the presence of the valve disorder was associated with significantly increased risk of coronary events [hazard ratio (HR) 1.68], stroke (HR 1.27), cardiovascular mortality (HR 1.69), and overall mortality (HR 1.27). Albeit CAVS and atherosclerosis share many similarities, they diverge in some details, first among which is a prominent early mineralization of the aortic valve with relative paucity of smooth muscle cells and the absence of significant coronary artery disease in over half of the patients, such that, although a similar pathogenesis appears to be likely, this is not totally coincident. The search for factors facilitating this condition has drawn attention to the impact of the basic processes of calcium homoeostasis in tissues calcification. There are two variants of vitamin K, K1 (phylloquinone), with liver uptake for the synthesis of vitamin K-dependent coagulation factors, and K2 (menaquinone), also used in the synthesis of coagulation factors, but predominantly recirculated to reach peripheral tissues, mainly the bone where it regulates cell activities, and vascular walls and valve cusps where it controls carboxylation of a matrix protein, glutamic acid, in gamma-carboxyglutamic acid. Gammacarboxyglutamic acid is a powerful inhibitor of vascular

Aortic stenosis in the elderly can be prevented: old risk factors and a new pathological condition