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María Manuela Izquierdo-Gómez [1] and Iván Hernández-Betancor [1] and Javier García-Niebla [2] and Belén Marí-López [1] and Ignacio Laynez-Cerdeña [1] and Juan Lacalzada-Almeida [1]

Academic Editor: Giacomina Brunetti

1, Department of Cardiology, Hospital Universitario de Canarias, Tenerife, Spain, huc.es

2, Servicios Sanitarios del Área de Salud de El Hierro, Valle del Golfo Health Center, El Hierro, Spain

Received Apr 5, 2017; Accepted Jun 20, 2017

This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

1. Introduction

Although aortic valvular sclerosis and aortic stenosis (AS) have long been thought of as two independent entities, they are now considered to be different stages of the same process. This disease manifests initially as valve thickening caused by lipocalcified deposits, leading to progressive reduction of the valve orifice which, over time, causes hemodynamically significant stenosis.

Aortic valve sclerosis is present in approximately 20–30% of individuals aged over 65 years and in 48% of patients over 85 years, while significant stenosis affects 2-3% of those over 65 years of age and up to 8% of those over 85 years [1, 2]. Thus its incidence increases exponentially with age and hence was long considered a simple passive age-related degenerative process with calcium buildup. However, several studies have shown that, in addition to age, calcific aortic valve disease (CAVD) is related to the presence of cardiovascular risk factors such as male sex, arterial hypertension, diabetes mellitus, dyslipidemia, and smoking, sharing many similarities with the process that regulates atherosclerosis [1–8]. There is therefore a direct relationship between the presence of valvular calcium deposits and the development of coronary disease and cardiovascular events [8–11], to the point that some authors even consider aortic calcification a possible marker of atherosclerosis and subclinical coronary artery disease [10, 12]. In 1986, Roberts [3] suggested that the presence of aortic mitral and valvular annular calcification was a form of atherosclerosis and numerous authors have since demonstrated this fact [6, 13–16]. In the Cardiovascular Health Study, the presence of aortic sclerosis in patients without previous coronary disease increased the risk of myocardial infarction and cardiovascular mortality 1.4 and 1.5 times, respectively [10]. In another prospective study involving 1,980...

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