Daniele Massera1, Petra Buzkova2, Anna E Bortnick3, David S Owens4, SongShou Mao5, Dong Li6, Ian H De Boer7, Bryan R Kestenbaum8, Matthew J Budoff9, Jorge R Kizer10. 1. Leon H. Charney Division of Cardiology, NYU Grossman School of Medicine, New York, NY, USA. Electronic address: Daniele.Massera@nyulangone.org. 2. Department of Biostatistics, University of Washington, Seattle, WA, USA. Electronic address: buzkova@uw.edu. 3. Divisions of Cardiology and Geriatrics, Montefiore Medical Center, Bronx, NY, USA. Electronic address: abortnic@montefiore.org. 4. Division of Cardiology, University of Washington, Seattle, WA, USA. Electronic address: dsowens@u.washington.edu. 5. Los Angeles Biomedical Research Institute at Harbor-UCLA, Torrance, CA, USA. Electronic address: smao@lundquist.org. 6. Division of Hospital Medicine, Emory University, Atlanta, GA, USA. Electronic address: dong.li2@emory.edu. 7. Division of Nephrology and Kidney Research Institute, Department of Medicine, University of Washington, Seattle, WA, USA. Electronic address: deboer@uw.edu. 8. Division of Nephrology and Kidney Research Institute, Department of Medicine, University of Washington, Seattle, WA, USA. Electronic address: brk@u.washington.edu. 9. Los Angeles Biomedical Research Institute at Harbor-UCLA, Torrance, CA, USA. Electronic address: mbudoff@labiomed.org. 10. Cardiology Section, San Francisco Veterans Affairs Health Care System, and Department of Medicine, University of California San Francisco, San Francisco, CA, USA; Department of Epidemiology and Biostatistics, University of California San Francisco, San Francisco, CA, USA. Electronic address: jorge.kizer@ucsf.edu.
Abstract
BACKGROUND AND AIMS: Bone and mineral metabolism has been implicated in the pathophysiology of cardiac valve calcification. Whether bone demineralization, a common aging-related disorder, promotes calcific valve disease remains uncertain. We tested the hypothesis that low bone mineral density (BMD) is associated with greater incidence/progression of cardiac valve calcification in the Multi-Ethnic Study of Atherosclerosis. METHODS: Using linear mixed-effects models, we related baseline measurement of BMD of the thoracic vertebrae by computed tomography (CT) in 6768 participants to serial CT assessments of aortic valve calcification (AVC) and mitral annular calcification (MAC) obtained over a >10-year period. RESULTS: After multivariable adjustment, lower BMD (per SD decrement) was associated with accelerated increase in AVC over time in women (0.76 [95% CI 0.42,1.09] Agatston -units [AU]/year) and men (1.41 [95% CI 0.48,2.33] AU/year), as well as for MAC in women (3.22 [95% CI 1.16,5.28] AU/year) and men (3.59 [95% CI 2.09,5.09] AU/year). Significant effect modification was observed, with more pronounced BMD-related acceleration of AVC and MAC progression in older or white participants of one or both sexes, as well as by estimated glomerular filtration rate, though the latter differed by sex for AVC and MAC. CONCLUSIONS: In this multi-ethnic cohort, low thoracic BMD was significantly, but modestly, associated with increased AVC and MAC progression. This suggests that altered bone mineral metabolism does not have a major impact on calcific valve disease in the general population, but the possibility of a more meaningful influence in higher-risk individuals with osteoporosis will require further investigation.
BACKGROUND AND AIMS: Bone and mineral metabolism has been implicated in the pathophysiology of cardiac valve calcification. Whether bone demineralization, a common aging-related disorder, promotes calcific valve disease remains uncertain. We tested the hypothesis that low bone mineral density (BMD) is associated with greater incidence/progression of cardiac valve calcification in the Multi-Ethnic Study of Atherosclerosis. METHODS: Using linear mixed-effects models, we related baseline measurement of BMD of the thoracic vertebrae by computed tomography (CT) in 6768 participants to serial CT assessments of aortic valve calcification (AVC) and mitral annular calcification (MAC) obtained over a >10-year period. RESULTS: After multivariable adjustment, lower BMD (per SD decrement) was associated with accelerated increase in AVC over time in women (0.76 [95% CI 0.42,1.09] Agatston -units [AU]/year) and men (1.41 [95% CI 0.48,2.33] AU/year), as well as for MAC in women (3.22 [95% CI 1.16,5.28] AU/year) and men (3.59 [95% CI 2.09,5.09] AU/year). Significant effect modification was observed, with more pronounced BMD-related acceleration of AVC and MAC progression in older or white participants of one or both sexes, as well as by estimated glomerular filtration rate, though the latter differed by sex for AVC and MAC. CONCLUSIONS: In this multi-ethnic cohort, low thoracic BMD was significantly, but modestly, associated with increased AVC and MAC progression. This suggests that altered bone mineral metabolism does not have a major impact on calcific valve disease in the general population, but the possibility of a more meaningful influence in higher-risk individuals with osteoporosis will require further investigation.
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