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Volume 4, Issue 1, Pages 41-46 (January 2010)


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Relationship of aortic valve calcification with coronary artery calcium severity: The Multi-Ethnic Study of Atherosclerosis (MESA)

Khurram Nasir, MD MPHaCorresponding Author Informationemail address, Ronit Katz, DPhilb, Mouaz Al-Mallah, MDc, Junichiro Takasu, MDd, David M. Shavelle, MDd, Jeffery J. Carr, MDe, Richard Kronmal, PhDb, Roger S. Blumenthal, MDa, Kevin O'Brien, MDb, Matthew J. Budoff, MDd

Received 26 June 2009; received in revised form 10 November 2009; accepted 4 December 2009. published online 14 December 2009.

Background

Aortic valve calcification (AVC) and atherosclerosis share causative and pathologic features.

Objective

We evaluated the relationship between AVC and coronary artery calcium (CAC) severity in the Multi-Ethnic Study of Atherosclerosis (MESA).

Methods

Men and women aged 45–84 years (n=6809; mean age, 62 years) were studied. The presence and burden of AVC and CAC were determined by noncontrast cardiac computed tomography. Relative risk regression was used to model the probability of AVC as a function of CAC>0 as well as CAC categories (0, 1–99, 100–399, and ≥400) with the reference group being CAC=0.

Results

The prevalence of AVC and CAC was 13% and 50%, respectively. Among those without CAC, the prevalence of AVC was 5% and increased across levels of CAC severity such that 14%, 25%, and 38% had AVC with increasing CAC scores of 1–99, 100–399, and ≥400, respectively (P for trend<0.0001). After controlling for patient demographic factors and cardiovascular risk factors, the prevalence ratio of AVC among those with mild CAC (1–99) was 1.83 (95% CI, 1.45–2.31) and increased to 3.36 (95% CI, 2.56–4.42) for CAC400. Similar statistically significant increased risk of AVC was found when CAC was assessed as a continuous variable.

Conclusion

Our study shows that AVC is independently associated with increasing severity of CAC.

a Division of Cardiology, Blalock 524 C, Johns Hopkins University, 600N Wolfe Street, Baltimore, MD 21287, USA

b University of Washington, Seattle, WA, USA

c Division of Cardiology, Henry Ford Hospital, Detroit, MI, USA

d Division of Cardiology, Harbor-UCLA Medical Center Research and Education Institute, Torrance, CA, USA

e Department of Radiology, Wake Forest University, Winston Salem, NC, USA

Corresponding Author InformationCorresponding author.

 Conflict of interest: The authors report no conflicts of interest.

 This research was supported by R01 HL071739 and contracts N01-HC-95159 through N01-HC-95165 and N01 HC 95169 from the National Heart, Lung, and Blood Institute.

PII: S1934-5925(09)00637-6

doi:10.1016/j.jcct.2009.12.002


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