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Arteriosclerosis, Thrombosis, and Vascular Biology. 2007;27:642-648
Published online before print December 21, 2006, doi: 10.1161/01.ATV.0000255952.47980.c2
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*Heart Valve Diseases
(Arteriosclerosis, Thrombosis, and Vascular Biology. 2007;27:642.)
© 2007 American Heart Association, Inc.


Atherosclerosis and Lipoproteins

Aortic Valve Calcification

Determinants and Progression in the Population

David Messika-Zeitoun; Lawrence F. Bielak; Patricia A. Peyser; Patrick F. Sheedy; Stephen T. Turner; Vuyisile T. Nkomo; Jerome F. Breen; Joseph Maalouf; Christopher Scott; A. Jamil Tajik; Maurice Enriquez-Sarano

From the Divisions of Cardiovascular Diseases and Internal Medicine (D.M.-Z., V.T.N., J.M., A.J.T., M.E.-S.), Radiology (P.F.S., J.F.B.), Hypertension (S.T.T.), and Biostatistics (C.S.), Mayo Clinic, Rochester, Minn; and Epidemiology (L.F.B., P.A.P.), University of Michigan, Ann Arbor.

Correspondence to Dr Maurice Enriquez-Sarano, MD, Division of Cardiovascular Diseases and Internal Medicine, Mayo Clinic, 200 First Street SW, Rochester, MN 55905. E-mail sarano.maurice{at}mayo.edu

Background— Aortic valve calcification (AVC) is considered degenerative. Recent data suggested links to atherosclerosis or coronary disease (CAD).

Methods and Results— AVC and coronary artery calcifications (CAC) were prospectively assessed by Electron-Beam-Computed-Tomography in 262 population-based research participants ≥60 years. AVC was frequent (27%) with aging (P<0.01) and in men (P<0.05). AVC was associated with diabetes, hypertension, higher body-mass-index, and serum glucose (all P<0.05). AVC was a marker of higher prevalence (P<0.01) and severity of CAD (CAC score: 441±802 versus 265±566, P<0.05) independently of age. After follow-up of 3.8±0.9 years, AVC score increased (94±271 versus 54±173, P<0.01, +11±32 U/year), faster with higher baseline AVC score (P<0.01). Compared with participants remaining free of AVC, de novo acquisition of AVC was associated with higher LDL-cholesterol (141±31 versus 121±27 mg/dL, P<0.05) and faster CAC progression (+78±87 versus +28±47 U/year, P<0.05). In multivariate analysis, LDL-cholesterol independently determined AVC acquisition while higher baseline AVC scores determined faster progression of existing AVC.

Conclusion— In the population, AVC is frequent with aging and atherosclerotic risk factors. AVC is a marker of subclinical CAD. AVC is progressive, appearing de novo with progressive atherosclerosis whereas established AVC progresses independently of atherosclerotic risk factors and faster with increasing initial AVC loads.

Aortic valve calcification (AVC) in 262 population-based participants ≥60 years was frequent (27%) with aging, with diabetes, and with coronary calcification. After 3.8±0.9 years, AVC score and prevalence increased. New AVC acquisition occurs with high LDL-cholesterol and progressive atherosclerosis. Larger established AVC determines faster AVC progression independently of atherosclerotic risk factors.


Key Words: aortic valve • computed tomography • calcification • atherosclerosis • epidemiology




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