(Circulation. 2007;115:297-299.)
© 2007 American Heart Association, Inc.
Editorial |
From the Center for Cardiovascular Research, Washington University School of Medicine, Department of Internal Medicine, Bone and Mineral Diseases, St Louis, Mo.
Correspondence to Dwight A. Towler, MD, PhD, Internal MedicineBMD, Washington University School of Medicine, Barnes-Jewish Hospital North Campus Box 8301, 660 South Euclid Ave, St Louis, MO 63110. E-mail dtowler@im.wustl.edu
Key Words: Editorials aorta atherosclerosis calcium imaging inflammation muscle, smooth
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
Aortic calcification increasingly afflicts our aging and dysmetabolic population.1 In the past decade, multiple studies from preclinical and clinical investigators have identified that active osteogenic/chondrogenic mechanisms contribute to aortic calcium load.2 Cellular and matricrine signals control vascular calcium phosphate mineral deposition via processes resembling membranous and endochondral bone formation.24 Clinical consequences also have begun to emerge.2,4 Atherosclerotic calcification of the aortic arch portends ischemic cerebrovascular events in women, although mitral annulus calcification may be a better predictor.5 Medial artery calcification, a nonobstructive form of aortofemoral calcium accumulation, is a characteristic vascular pathology seen in patients with type II diabetes or chronic renal failure.3 Medial artery calcification not only is a predictor of cardiovascular mortality but also increases the risk for lower extremity amputation6; vascular stiffening perturbs normal aortofemoral Windkessel physiology, thus compromising distal tissue perfusion while increasing afterload, pulse pressure, and myocardial workload.3,4 Aortic valve calcium accumulation assessed by echocardiography is a strong predictor of disease progression in patients with initially asymptomatic aortic stenosis.7 In end-stage renal disease patients on dialysis, the presence of aortic valve calcification is a particularly ominous risk factor for cardiovascular mortality.8 All forms of aortic and aortic valve calcification are increased along the metabolic syndrome to type II diabetes continuum.1 The detailed analysis by Katz et al1 of the Multiethnic Study of Atherosclerosis cohort revealed stepwise increases in aortic valve calcification risk with accrual of metabolic syndrome risk factors.1 As highlighted by Bostrom,9 vascular mineralization not only promotes further epitaxial mineral deposition but also
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