Coronary Calcification Is Reversely Related with Bone and Hair Calcium: The Relationship among Different Calcium Pools in Body

Lee, Sanghoon; Park, Soo-Jung; Kim, Kyunam; Cho, Doo‐Yeoun; Kim, Young-Sang; Kim, Bom-Taeck

doi:10.11005/jbm.2016.23.4.191

Cited by 8 publications

(3 citation statements)

References 37 publications

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“…This is in line with other previous studies which confirm this result with bone density at spine,[24252627] however to date no study evaluated T-score. Choi et al[28] observed an inverse correlation between CACS and BMD at femur which was stronger in women with a longer time since menopause and women with osteoporosis and osteopenia than normal BMD.…”

Section: Discussionsupporting

confidence: 93%

Coronary Artery Calcium Score and Bone Metabolism: A Pilot Study in Postmenopausal Women

et al. 2017

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BackgroundSince 1991 many studies evaluated the link between cardiovascular diseases and osteoporosis, two age-related conditions, but the main common pathologic pathway has not been determined yet. The histological similarity between arterial calcified plaque and bone matrix and involvement of similar cells and mediators provide a special field of research. Therefore in the present study, we aimed to evaluate the relationship between coronary artery calcium score (CACS) as a surrogate marker of atherosclerosis and bone mediators and parameters in postmenopausal women.MethodsEleven postmenopausal women who had CACS higher than 80 were enrolled into the study and underwent bone densitometry. In addition, their serum and urine samples were taken for measuring osteoprotegerin, osteocalcin, and β cross laps. Patients' 10-year probability of fracture was calculated by the World Health Organization fracture-risk assessment tool (FRAX).ResultsThe regression analysis of our results showed the association between CACS and OC (std β=0.66, 95% confidence interval [CI] 5.47-72.27, P=0.027), femoral bone density (std β=−0.6, 95% CI -6864.34-14.27, P=0.05) and T-score (std β=−0.6, 95% CI −773.08-1.28, P=0.05) which remained significant after adjustment for age, weight, years since menopause and body mass index. No association was found between CACS and osteoprotegerin, spinal bone density and FRAX score.ConclusionsIn conclusion, this pilot study with small sample size showed the potential association between CACS and osteocalcin, femoral bone density and T-score. However, the relationship between CACS and osteoprotegerin, receptor activator of nuclear factor-kappa B ligand, FRAX score and other bone parameters remain to be clarified in larger sample size studies.

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Section: Discussionsupporting

confidence: 93%

Coronary Artery Calcium Score and Bone Metabolism: A Pilot Study in Postmenopausal Women

et al. 2017

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“…In theory, both sclerostin and DKK1 could have an effect on bone health and vascular disease, because of their associations with the mineralization process. Previous studies have demonstrated a negative correlation between vascular calcification and osteoporosis by evaluating the BMD of patients with normal kidney function and of those with uremia [34, 35]. However, we found no such correlations with CAC in the present study.…”

Section: Discussioncontrasting

confidence: 90%

Evaluation of the association of Wnt signaling with coronary artery calcification in patients on dialysis with severe secondary hyperparathyroidism

Chen

Hsu

et al. 2019

BMC Nephrol

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Background Patients with end-stage renal disease have a higher risk of death from cardiovascular events, which can be mainly attributed to coronary artery calcification (CAC). Wnt signaling is involved in vascular development and may play a role in vascular calcification. This study aimed to evaluate CAC prevalence in patients on dialysis with severe secondary hyperparathyroidism (SHPT) and identify CAC risk factors. Methods The study is a retrospective analysis of the severe hyperparathyroidism registration study that prospectively recruited patients on dialysis with severe SHPT who were candidates for parathyroidectomy, from October 2013 to May 2015. CAC and bone mineral density (BMD) were measured. Demographic and clinical data including calcium, phosphorus, alkaline phosphatase, intact parathyroid hormone, Dickkopf-related protein 1 (DKK1), and sclerostin levels were analyzed. CAC scores were reported in Agatston units (AU). Results A total of 61 patients were included in this study. No CAC, mild CAC (<100 AU), moderate CAC (>100 AU), and severe CAC (>400 AU) were observed in 4.9%, 11.4%, 14.8%, and 68.9% of patients, respectively. DKK1 and sclerostin were not associated with CAC. In univariate analysis, CAC was significantly correlated with age, sex (male), total cholesterol, and intravenous pulse calcitriol ( p <0.05). CAC was not inversely correlated with the BMD, T scores, or Z scores of the femoral neck ( p >0.05). In multivariate analysis, the stepwise forward multiple linear regression revealed that CAC was associated with age, male sex and intravenous pulse calcitriol ( p <0.05). Furthermore, serum sclerostin was positively correlated with the BMD of the femoral neck but negatively associated with intact parathyroid hormone ( p <0.05). Serum sclerostin was significantly associated with severely low bone mass with Z-scores<-2.5 of the femoral neck, even when adjusted for serum intact parathyroid hormone, vitamin D status, dialysis pattern, sex, and DKK-1 ( p <0.05). Conclusions The patients on dialysis with severe SHPT have a high prevalence of vascular calcification. Although the Wnt signaling pathway could play a role in hyperparathyroid bone disease, CAC may be mainly due to the treatment modality rather than the Wnt signaling pathway associated bone metabolism in patients on dialysis with severe SHPT. Electronic supplementary material The online version of this article (10.1186/s12882-019-1543-3) contains supplementary material, which is available to authorized users.

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“…Arterial calcification plays a crucial role in the development of arterial stiffening [135]. Increased calcium deposits, an element of calcification, are markedly increased in the arterial wall with aging [136, 137]. The morphology of older VSMCs appears osteoblasts-like, producing large amounts of bone-like substrates, such as collagen II [59].…”

Section: Cellular and Matrix Phenotypes In The Aging Arterial Wallmentioning

confidence: 99%

Proinflammatory Arterial Stiffness Syndrome: A Signature of Large Arterial Aging

Wang

Monticone

McGraw³

2018

J Vasc Res

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Age-associated structural and functional remodeling of the arterial wall produces a productive environment for the initiation and progression of hypertension and atherosclerosis. Chronic aging stress induces low-grade proinflammatory signaling and causes cellular proinflammation in arterial walls, which triggers the structural phenotypic shifts characterized by endothelial dysfunction, diffuse intimal-medial thickening, and arterial stiffening. Microscopically, aged arteries exhibit an increase in arterial cell senescence, proliferation, invasion, matrix deposition, elastin fragmentation, calcification, and amyloidosis. These characteristic cellular and matrix alterations not only develop with aging but can also be induced in young animals under experimental proinflammatory stimulation. Interestingly, these changes can also be attenuated in old animals by reducing low-grade inflammatory signaling. Thus, mitigating age-associated proinflammation and arterial phenotype shifts is a potential approach to retard arterial aging and prevent the epidemic of hypertension and atherosclerosis in the elderly.

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Coronary Calcification Is Reversely Related with Bone and Hair Calcium: The Relationship among Different Calcium Pools in Body

Cited by 8 publications

References 37 publications

Coronary Artery Calcium Score and Bone Metabolism: A Pilot Study in Postmenopausal Women

Coronary Artery Calcium Score and Bone Metabolism: A Pilot Study in Postmenopausal Women

Evaluation of the association of Wnt signaling with coronary artery calcification in patients on dialysis with severe secondary hyperparathyroidism

Proinflammatory Arterial Stiffness Syndrome: A Signature of Large Arterial Aging

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