Status of Bone Mineral Density in Patients Selected for Cardiac Transplantation

Iqbal, Nayyar; Ducharme, J.C.; Desai, Shashank; Chambers, Susan; Terembula, Karen; Chan, Grace W.; Shults, Justine; Leonard, Mary B.; Kumanyika, Shiriki

doi:10.4158/ep.14.6.704

Cited by 11 publications

(4 citation statements)

References 16 publications

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“…Mean serum 25-OH-D concentration was significantly lower in patients with heart failure compared with controls. Similar results or a higher prevalence of suboptimal vitamin D status have been observed in North American, 61 African-American, [62][63][64] Egyptian, 65 and Iranian 66 heart failure populations. Ameri and colleagues 60 measured vitamin D status in 90 patients admitted to the hospital with heart failure and 31 controls without heart disease.…”

Section: Intervention Studiessupporting

confidence: 84%

The Role of Micronutrients in Heart Failure

McKeag

McKinley²,

Woodside³

et al. 2012

Journal of the Academy of Nutrition and Dietetics

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Section: Intervention Studiessupporting

confidence: 84%

The Role of Micronutrients in Heart Failure

McKeag

McKinley²,

Woodside³

et al. 2012

Journal of the Academy of Nutrition and Dietetics

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“…lower prevalence of osteopenia than those previously reported in HF [10,11,[28][29][30]. In all likelihood, the difference arose due to our patient´s older age, long time of treatment, and follow-up as well as the number of comorbidities that is common in HF and possibly caused additional bone damage.…”

Section: Plos Onementioning

confidence: 57%

“…There is little information linking HF and OP in the literature. Between 25% and 60% of patients with severe heart disease evaluated before heart transplantation might present low BMD [10,11], with approximately 1% bone loss per year [2,12]. Patients with HF have lower BMD than non-HF patients, and it has been positively correlated with worse functional capacity, left ventricular ejection fraction, and vitamin D levels.…”

Section: Introductionmentioning

confidence: 99%

Bone quality, mineral density, and fractures in heart failure

Canteri,

Gusmon,

Boguszewski

et al. 2023

PLoS ONE

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Background The trabecular bone score (TBS) indirectly estimates bone quality and predicts low-impact fractures independently of bone mineral density (BMD). However, there is still a paucity of data linking bone and heart diseases, mainly with gaps in the TBS analysis. Methods In this cross-sectional study, we evaluated TBS, BMD, and fractures in patients with heart failure with reduced ejection fraction (HFrEF) and in sex-, BMI- and age-matched controls, and we assessed the fracture probability using the FRAX tool, considering active search for fractures by vertebral fracture assessment (VFA) and the adjustment for the TBS. Results TBS values were 1.296 ± 0.14 in 85 patients (43.5% women; age 65 ± 13 years) and 1.320 ± 0.11 in 142 controls (P = 0.07), being reduced (< 1.31) in 51.8% and 46.1% of them, respectively (P = 0.12). TBS was lower in patients than in the controls when BMD was normal (P = 0.04) and when the BMI was 15–37 kg/m2 (P = 0.03). Age (odds ratio [OR] 1.05; P = 0.026), albumin (OR 0.12; P = 0.046), statin use (OR 0.27; P = 0.03), and energy intake (OR 1.03; P = 0.014) were associated with reduced TBS. Fractures on VFA occurred in 42.4% of the patients, and VFA and TBS adjustment increased the fracture risk by 16%-23%. Conclusion Patients with HFrEF had poor bone quality, with a better discriminating impact of the TBS assessment when BMD was normal, and BMI was suitable for densitometric analysis. Variables related to the prognosis, severity, and treatment of HFrEF were associated with reduced TBS. VFA and TBS adjustment increased fracture risk.

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“…Hepatic congestion and prerenal azotemia may cause mild secondary hyperparathyroidism and further contribute to abnormal mineral metabolism. Although many patients awaiting cardiac transplantation may have normal bone density, approximately 4-10% fulfill World Health Organization (WHO) criteria for osteoporosis (Table 56.3) [19,76,[139][140][141][142], and one study reported a prevalence of 23% [85].…”

Section: Skeletal Status Before Transplantationmentioning

confidence: 99%

Osteoporosis in Organ Transplant Patients

Stein

Shane

2013

Osteoporosis

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As transplantation osteoporosis results from alterations in the bone remodeling system, a review of normal bone remodeling is helpful to understanding the pathogenesis of this disease. The bone remodeling cycle is an orderly progression of events in which old, microdamaged bone is replaced by new, mechanically stronger bone. The complete remodeling cycle at each remodeling site requires approximately 3-6 months. Bone remodeling occurs by two main processes, resorption [1] followed by formation [2], which take place on both cancellous and cortical bone surfaces. Resorption begins with activation of macrophage precursors to form osteoclasts, giant multinucleated cells that excavate a cavity on the bone surface. Osteoclasts express receptors for receptor activator of receptor activator of nuclear factor-kappaB ligand (RANKL), which is produced by osteoblasts and osteocytes, and for calcitonin, prostaglandins (PGs), calcium, and vitronectin (integrin α 1 β 3 ). Approximately 0.05 mm 3 of bone tissue is resorbed by each osteoclast, leaving small resorption pits on the bone surface called Howship's lacunae in a process that takes approximately 2-3 weeks. A brief rest period called the reversal phase follows. Next, local mesenchymal bone marrow stem cells differentiate into osteoblasts that are attracted to the empty resorption pits where they accumulate as clusters of plump cuboidal cells along the bone surface. Osteoblasts produce the collagenous and noncollagenous proteins that constitute the matrix of the newly formed bone and are responsible for mineralization of the matrix or osteoid after a period of maturation that lasts approximately 20 days. Osteoblasts express receptors for several hormones (thyroid and parathyroid hormones, estrogens, vitamin D 3 ), cell adhesion molecules (integrins), and cytokines. RANKL, receptor activator of nuclear factor-kappaB (RANK), and osteoprotegerin (OPG) are three members of the tumor necrosis factor (TNF) ligand and receptor-signaling family that are final mediators of bone resorption [3,4]. RANKL is expressed in osteoblasts, osteocytes, and bone marrow stromal cells. When sufficient concentrations of macrophage colony stimulating factor (M-CSF) are present, RANKL binds to RANK, which is expressed on the surface of osteoclast lineage cells. This binding results in rapid differentiation of osteoclast precursors in bone marrow to mature osteoclasts, increased osteoclast activity, and reduced apoptosis of mature osteoclasts. RANKL is neutralized by binding to OPG, which is secreted by cells of the osteoblast lineage. Competitive binding of RANKL to either RANK or OPG regulates bone remodeling by increasing (RANK) or decreasing (OPG) osteoclastogenesis. Immunosuppressants exert their effects on bone remodeling by interacting with the RANK/RANKL/ OPG system [5].In healthy adults, declines in bone mass as a result of remodeling imbalance occur, but are small. When bone remodeling becomes "uncoupled," such that the rate of resorption exceeds the rate of formation, bone loss will occur...

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Status of Bone Mineral Density in Patients Selected for Cardiac Transplantation

Cited by 11 publications

References 16 publications

The Role of Micronutrients in Heart Failure

The Role of Micronutrients in Heart Failure

Bone quality, mineral density, and fractures in heart failure

Osteoporosis in Organ Transplant Patients

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