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. 2012 Aug;5(8):781-8.
doi: 10.1016/j.jcmg.2011.12.025.

Associations of LV hypertrophy with prevalent and incident valve calcification: Multi-Ethnic Study of Atherosclerosis

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Associations of LV hypertrophy with prevalent and incident valve calcification: Multi-Ethnic Study of Atherosclerosis

Sammy Elmariah et al. JACC Cardiovasc Imaging. 2012 Aug.

Abstract

Objectives: The aim of this study was to evaluate the relationship between percentage of predicted left ventricular mass (%PredLVM) and valve calcification in the MESA (Multi-Ethnic Study of Atherosclerosis) study.

Background: Cardiac valve calcification has been associated with left ventricular hypertrophy (LVH), which portends cardiovascular events. However, this relationship and its mediators are poorly understood.

Methods: The MESA study is a longitudinal cohort study of men and women 45 to 84 years of age without clinical cardiovascular disease in whom serial cardiac magnetic resonance and computed tomography imaging were performed. The relationships between baseline %PredLVM and the prevalence, severity, and incidence of aortic valve (AVC) and mitral annulus calcification (MAC) were determined by regression modeling.

Results: Prevalent AVC was observed in 630, and MAC was observed in 442 of 5,042 subjects (median 55.9 and 71.1 Agatston units, respectively). After adjustment for age, sex, body mass index (BMI), ethnicity, socioeconomic status, physical activity, diabetes, cholesterol levels, blood pressure, smoking, kidney function, serum lipids, and antihypertensive and statin medications, %PredLVM was associated with prevalent AVC (odds ratio [OR]: 1.18/SD increase in %PredLVM [95% confidence interval (CI): 1.08 to 1.30]; p = 0.0004) and MAC (OR: 1.18 [95% CI: 1.06 to 1.32]; p = 0.002). Similarly, %PredLVM was associated with increased severity of prevalent AVC (risk difference = 0.26 [95% CI: 0.15 to 0.38]; p < 0.0001) and MAC (risk difference = 0.20 [95% CI: 0.03 to 0.37]; p = 0.02). During follow-up (mean 2.4 ± 0.9 years), 153 subjects (4%) developed AVC, and 198 (5%) developed MAC. The %PredLVM was associated with incident AVC (OR: 1.24 [95% CI: 1.04 to 1.47]; p = 0.02) and MAC (OR: 1.18 [95% CI: 1.01 to 1.40]; p = 0.04). Further adjustment for inflammatory markers and coronary artery calcification did not attenuate these associations. Specifically, concentric LVH most strongly predicted incident valve calcification.

Conclusions: Within the MESA cohort, LVH was associated with prevalence, severity, and incidence of valve calcification independent of hypertension and other identified confounders.

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Figures

Figure 1
Figure 1. Relationship of LV mass to prevalent valve calcification
Unadjusted prevalence of aortic valve and mitral annulus calcification increases across quartiles of percent of predicted left ventricular mass. %PredLVM = percent of predicted left ventricular mass; LV = left ventricular.
Figure 2
Figure 2. Relationship of LV mass to incident valve calcification
Unadjusted incidence of aortic valve and mitral annulus calcification stratified by quartile of percent of predicted left ventricular mass demonstrates that increased %PredLVM at baseline evaluation is associated with the development of incident valve calcification at both anatomic sites. %PredLVM = percent of predicted left ventricular mass; LV = left ventricular.

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