Abstract
Arterial calcification is an active process resulting from the interaction of factors that both promote and inhibit the process. Interaction of these factors results in phenotype transdifferentiation of vacular smooth muscle cells and pericytes into osteoblast-like cells. In addition to this active process, oversaturation of extracellular fluid with high serum calcium and phosphate contributes to calcium apatite precipitation. Arterial calcifications exist in two frequently interrelated types: intimal and medial. Intimal calcification is a part of advanced atherosclerosis and results in plaque development, arterial lumen decrease or occlusion, and ischemic lesions downstream. Medial calcifications result in the stiffening of arterial walls, with increased systolic and decreased diastolic pressures, resulting in cardiac pressure overload, left-ventricular hypertrophy, and decreased myocardial perfusion. Both types are associated with increased cardiovascular morbidity and mortality.
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London, G.M., Pannier, B., Marchais, S.J. (2010). Disturbed Calcium-Phosphorus Metabolism/Arterial Calcifications: Consequences on Cardiovascular Function and Clinical Outcome. In: Berbari, A.E., Mancia, G. (eds) Cardiorenal Syndrome. Springer, Milano. https://doi.org/10.1007/978-88-470-1463-3_20
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DOI: https://doi.org/10.1007/978-88-470-1463-3_20
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