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(Circulation. 2008;117:2938-2948.)
© 2008 American Heart Association, Inc.

Basic Science for Clinicians

Vascular Calcification

Pathobiology of a Multifaceted Disease

Linda L. Demer, MD, PhD; Yin Tintut, PhD

From the Departments of Medicine (L.L.D., Y.T.) and Physiology (L.L.D.), University of California at Los Angeles.

Correspondence to Linda Demer, MD, PhD, Division of Cardiology, University of California at Los Angeles, School of Medicine, 10833 Le Conte Ave, Mail Box 951679, Los Angeles, CA 90095-1679. E-mail ldemer@mednet.ucla.edu

Key Words: atherosclerosis • calcium • genetics • lipids • inflammation • phosphates • vasculature

An extract of the first 250 words of the full text is provided, because this article has no abstract.

	Introduction

 
Most individuals aged >60 years have progressively enlarging deposits of calcium mineral in their major arteries.¹ This vascular calcification reduces aortic and arterial elastance, which impairs cardiovascular hemodynamics, resulting in substantial morbidity and mortality^2–4 in the form of hypertension, aortic stenosis, cardiac hypertrophy, myocardial and lower-limb ischemia, congestive heart failure, and compromised structural integrity.^5–7 The severity and extent of mineralization reflect atherosclerotic plaque burden⁸ and strongly and independently predict cardiovascular morbidity and mortality.⁹

Previously considered passive and degenerative, vascular calcification is now recognized as a pathobiological process sharing many features with embryonic bone formation. As evidence of this change in paradigm, research on vascular calcification has accelerated dramatically in the past decade. A search of PubMed (www.ncbi.nlm.nih.gov; US National Library of Medicine) under the key words vascular calcification returned 16 articles in 1982, 100 in 1994, and 250 in 2004. This year, 400 new publications are expected, for a total >3500.

A breakthrough in this field was the recognition of its similarity to bone development and metabolism, in which endothelial, mesenchymal, and hematopoietic cells interact and respond to mechanical, inflammatory, metabolic, and morphogenetic signals governing skeletal mineralization; their counterparts in the artery wall govern arterial mineralization. With increasing age and dysmetabolic conditions in our population, the clinical burden of vascular calcification will continue to increase.

	Clinical Impact of Arterial Calcification

 
Aortic calcification promotes congestive heart failure by eroding compliance and elastance. The hemodynamic demands of the cardiovascular system require that the aorta store energy in its elastance during systole and release it during diastole, which . . . [Full Text of this Article]

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