The prevalence of moderate to severe calcific aortic valve stenosis in patients ≥75 years old is 2.8% and only 40% of patients with surgical indication undergo aortic valve replacement because of high perioperative risk, older age, lack of symptoms, and patient/family refusal . In the absence of hemodynamically significant left ventricular (LV) outflow obstruction, calcific aortic valve disease (CAVD) prevalence raises up to 25% in patients aged from 65 to 74 years old [2,3] and independently predicts cardiovascular (CV) event, overall and CV mortality. As the population ages and CAVD incidence and prevalence increase, it is crucial a deeper understanding of the patho-physiology of heart valve calcification that could provide novel insight into medical therapeutic approaches to delay or modify the disease course. In the human body, several physiological processes of calcification take places and mineralized deposits are present, as bones, enamel and dentin. More than that, pathological mineralization can lead to ectopic calcification and pathologies as urinary stones, vascular calcification and calcific heart valve stenosis. Macroscopically, in aortic valve sclerosis there is an initial thickening of the valve leaflets and formation of calcium nodules, usually corresponding to the nodules of Arantio near the aortic surface, in association to angiogenesis, while end-stage calcific aortic stenosis is characterized by large, heavily calcific, nodular masses within the aortic cusps that protrude into the sinuses of Valsalva, thus interfering with valve opening along the aortic surface. While in the past heart valve calcification was seen as a passive, degenerative course of aging, evidences have shown that is an active, cell-mediated process with similarities to bone development (osseus metaplasia) .
Published on: Oct 22, 2016 Pages: 45-46