Abstract

Calcific aortic stenosis (CAS) more frequently was found in aged patients with elevated homocysteine (Hcy) levels. Endothelial dysfunction, oxidative stress, sub-endothelial accumulation of lipids and inflammatory cells, reactive oxygen species (ROS) production, extracellular matrix (ECM) remodeling and others are the leading causes inducing aortic stenosis (AS). Subsequently, these valvular aortic areas can converge in large calcified masses, causing CAS. On the other hand, risk factors acting on aortic valvular leaflets can also cause atherosclerotic coronary artery disease (CAD). The coexistence of CAS and CAD rather occurs in aged patients, but more frequently is present in those with HHcy. Traditional therapeutic interventions, such as surgical aortic valve replacement (SAVR) + coronary artery by-pass grafting (CABG), must be performed in patients contemporarily suffering of severe CAS and symptomatic CAD. But, a mini-invasive treatment, such as percutaneous coronary intervention (PCI), can be coupled to SAVR (“hybrid” treatment), or with transcatheter aortic valve implantation (TAVI) when the aged patients have a high-risk or are inoperable. Folic acid or vitamins B6-12 supplementation, even if decreases HHcy don’t reduce the incidence of AS. On the contrary, Angiotensin converting enzyme inhibitors and/or angiotensin receptor blockers can be used to delay AS when systemic hypertension coesists. Likely, some anti-lipemic drugs, as Niacin, can be employed in the presence of contemporary hyperlipemia. Finally, specific compounds, such as Biphosphonates, Denosumab or vitamin K must be given for reduce or delay the aortic valve calcification.

Keywords

calcific aortic stenosis, CAS, homocysteine, coronary artery disease, CAD, ROS, reactive oxygen species, ECM, extracellular matrix, Hcy, homocysteine, AS, aortic stenosis, CABG, coronary artery by-pass grafting, SAVR, surgical aortic valve replacement, TAVI, transcatheter aortic valve implantation, LDL, low-density lipoproteins