Aortic valve calcification: association with bone mineral density and cardiovascular risk factors

Aksoy, Yüksel; Yağmur, Cengiz; Tekin, Gülaçan; Yağmur, Jülide; Topal, Ergün; Kekilli, Ersoy; Turhan, Hasan; Koşar, Feridun; Yetkın, Ertan

doi:10.1097/00019501-200509000-00007

Cited by 52 publications

(33 citation statements)

References 36 publications

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“…This was the first study to report an association between angiographically documented coronary artery disease and low BMD predominantly in women. In a population-based study by van der Klift et al (94), low BMD of the femoral neck but not the spine correlated with the existence of peripheral arterial disease; findings that were also observed by Aksoy et al (95) and Schulz et al (96).…”

Section: Relationship Between Bone Loss and Cvdmentioning

confidence: 58%

Contribution of Bone and Mineral Abnormalities to Cardiovascular Disease in Patients with Chronic Kidney Disease

Raggi¹,

Kleerekoper²

2008

Clinical Journal of the American Society of Nephrology

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1,25-Dihydroxyvitamin D 3 levels begin to drop early in the course of kidney disease, leading to elevated parathyroid hormone levels and disrupted mineral metabolism. Impaired mineral metabolism seems to be associated not only with bone disease but also with vascular calcification. Animal models have identified molecular mechanisms by which high mineral levels and other uremic substances induce vascular smooth muscle cells to undergo phenotypic changes that initiate the calcification process. Moreover, several epidemiologic and clinical studies showed strong associations between bone loss, arterial calcification, and cardiovascular disease in populations with and without kidney disease. This review discusses evidence that two early complications of chronic kidney disease-vitamin D deficiency and secondary hyperparathyroidism-contribute to bone and cardiovascular disease. New treatment strategies aimed at the prevention of bone loss and parathyroid hyperplasia, such as vitamin D receptor ligand therapy, calcimimetic agents, and noncalcifying phosphate binders, are being investigated for their impact on improving overall outcome in dialysis patients.Clin . Nearly 80,000 people receive a diagnosis of CKD annually, with diabetes and hypertension being the most common causes (3). More than 8 million Americans have significant impairment of kidney function, and nearly 400,000 receive maintenance dialysis (4 -7). Two of the early complications of CKD include deficiency of 1,25-dihydroxyvitamin D 3 (1,25-D) and development of secondary hyperparathyroidism (SHPT), complications that lead to bone loss and, likely, cardiovascular disease (CVD) (8 -11). Although bone loss contributes to abnormally high fracture rates in patients with CKD, emerging data also indicate that the disorders of bone metabolism typical of kidney failure contribute to the high rates of CVD observed (12-15). This review identifies recent studies that describe the impact of 1,25-D deficiency, SHPT, and bone metabolism derangements on the development of CVD in patients with CKD and summarizes new treatment strategies that are expected to have a substantial impact on mortality in this patient population. 1,25-D Deficiency in CKDThe progressive effects of CKD lead to a deficiency in serum calcitriol levels, which begin to decline when the GFR drops below 70 ml/min in stage 2 CKD (16). 1,25-D regulates calcium and phosphate levels in the blood by enhancing calcium and phosphate absorption in the intestine, enhancing calcium reabsorption in the kidney tubules, and suppressing parathyroid hormone (PTH) secretion (17,18). Accordingly, 1,25-D-deficient individuals are hypocalcemic and have elevated serum levels of PTH (19,20). Moreover, 1,25-D deficiency is the probable primary initiating event behind the elevated PTH levels seen in the majority of patients with stage 3 CKD. Indeed, serum levels of calcitriol begin to decline when GFR falls below 70 ml/min, corresponding to the point at which elevated PTH levels are usually first noted (16,20). It is not unti...

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Section: Relationship Between Bone Loss and Cvdmentioning

confidence: 58%

Contribution of Bone and Mineral Abnormalities to Cardiovascular Disease in Patients with Chronic Kidney Disease

Raggi¹,

Kleerekoper²

2008

Clinical Journal of the American Society of Nephrology

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“…In contrast, degeneration of heart valve tissue may be caused by mineral metabolism disturbances. The effect of osteoporosis therapy has been investigated because of an association between aortic valve calcification and low skeletal bone mineral density (Aksoy et al, 2005). Several small observational studies demonstrated a possible link between use of bisphosphonates and slowing of AVS progression (Skolnick et al, 2009;Sterbakova et al, 2010;Innasimuthu and Katz, 2011), although such beneficial effects may be not remarkable in older women (Aksoy et al, 2012).…”

Section: Discussionmentioning

confidence: 99%

Mineral metabolism disturbances are associated with the presence and severity of calcific aortic valve disease

Yang

Zhao

Fang

et al. 2015

J. Zhejiang Univ. Sci. B

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Abstract:Objective: We investigated whether disturbance of calcium and phosphate metabolism is associated with the presence and severity of calcific aortic valve disease (CAVD) in patients with normal or mildly impaired renal function. Methods: We measured serum levels of calcium, phosphate, alkaline phosphatase (AKP), intact parathyroid hormone (iPTH), 25-hydroxyvitamin D (25-OHD), and biomarkers of bone turnover in 260 consecutive patients with normal or mildly impaired renal function and aortic valve sclerosis (AVSc) (n=164) or stenosis (AVS) (n=96) and in 164 age-and gender-matched controls. Logistic regression models were used to determine the association of mineral metabolism parameters with the presence and severity of CAVD. Results: Stepwise increases were observed in serum levels of calcium, phosphate, AKP, and iPTH from the control group to patients with AVS, and with reverse changes for 25-OHD levels (all P<0.001). Similarly, osteocalcin, procollagen I N-terminal peptide, and β-isomerized type I collagen C-telopeptide breakdown products were significantly increased stepwise from the control group to patients with AVS (all P<0.001). In patients with AVS, serum levels of iPTH were positively, in contrast 25-OHD levels were negatively, related to trans-aortic peak flow velocity and mean pressure gradient. After adjusting for relevant confounding variables, increased serum levels of calcium, phosphate, AKP, and iPTH and reduced serum levels of 25-OHD were independently associated with the presence and severity of CAVD. Conclusions: This study suggests an association between mineral metabolism disturbance and the presence and severity of CAVD in patients with normal or mildly impaired renal function. Abnormal bone turnover may be a potential mechanism.

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“…Several studies have indicated that skeletal bone metabolism might influence the development of aortic stenosis and vascular calcification, both of which are more prevalent among patients with disorders of calcium metabolism, 30 -32 including osteoporosis. 7,8 Furthermore, common regulatory systems, such as the OPG/RANK/RANKL axis, appear to govern calcification in the valve, vasculature, and skeletal bone. 33 However, our results argue against a fundamental or casual relationship between valvular calcification, vascular calcification, and metabolic bone activity.…”

Section: Discussionmentioning

confidence: 99%

“…2 Furthermore, aortic valve calcification is mediated by many of the processes that drive skeletal bone formation 3 -6 and appears to be accelerated in patients with osteoporosis. 7,8 Osteoblast activity is increased and by the later stages of the disease, lamellar bone, microfractures, and haemopoetic tissue can all be identified within the valve. 4 It has therefore been suggested that the processes underlying aortic stenosis do not occur in isolation within the valve.…”

Section: Introductionmentioning

confidence: 99%

Aortic stenosis, atherosclerosis, and skeletal bone: is there a common link with calcification and inflammation?

Dweck

Khaw

Sng

et al. 2013

European Heart Journal

126

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Aortic valve calcification: association with bone mineral density and cardiovascular risk factors

Cited by 52 publications

References 36 publications

Contribution of Bone and Mineral Abnormalities to Cardiovascular Disease in Patients with Chronic Kidney Disease

Contribution of Bone and Mineral Abnormalities to Cardiovascular Disease in Patients with Chronic Kidney Disease

Mineral metabolism disturbances are associated with the presence and severity of calcific aortic valve disease

Aortic stenosis, atherosclerosis, and skeletal bone: is there a common link with calcification and inflammation?

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