Parathyroid Hormone is Not Independently Associated With Cognitive Decline: 20 Year Follow-up From the Atherosclerosis Risk in Communities (ARIC) Study.
Kim Samuel M; Zhao Di; Schneider Andrea L; Korada Sai Krishna; Lutsey Pamela L; Guallar Eliseo; Alonso Alvaro; Windham B Gwen; Gottesman Rebecca F; Michos Erin D
Circulation
2017
2017-03-08
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Association of parathyroid hormone with 20-year cognitive decline: The ARIC study.
Female; Humans; Male; Middle Aged; Time Factors; Cross-Sectional Studies; Follow-Up Studies; Prospective Studies; Biomarkers/blood; Cognitive Dysfunction/*blood/*epidemiology; Longitudinal Studies; Neuropsychological Tests; Parathyroid Hormone/*blood; Psychological Tests; Human; Cross Sectional Studies; Funding Source; Multicenter Studies; Validation Studies; Comparative Studies; Evaluation Research; Middle Age; Parathyroid Hormones – Blood
OBJECTIVE: We hypothesized that elevated parathyroid hormone (PTH) levels will be independently associated with 20-year cognitive decline in a large population-based cohort. METHODS: We studied 12,964 middle-aged white and black ARIC participants without a history of prior stroke who, in 1990-1992 (baseline), had serum PTH levels measured and cognitive function testing, with repeat cognitive testing performed at up to 2 follow-up visits. Cognitive testing included the Delayed Word Recall, the Digit Symbol Substitution, and the Word Fluency tests, which were summed as a global Z score. Using mixed-effects models, we compared the relative decline in individual and global cognitive scores between each of the top 3 quartiles of PTH levels to the reference bottom quartile. We adjusted for demographic variables, education, vascular risk factors, and levels of calcium, phosphate, and vitamin D. We imputed missing covariate and follow-up cognitive data to account for attrition. RESULTS: The mean (SD) age of our cohort was 57 (6) years, 57% were women, and 24% were black. There was no cross-sectional association of elevated PTH with cognitive global Z score at baseline (p \textgreater 0.05). Over a median of 20.7 years, participants in each PTH quartile showed a decline in cognitive function. However, there was no significant difference in cognitive decline between each of the top 3 quartiles and the lowest reference quartile (p \textgreater 0.05). In a subset, there was also no association of higher mid-life PTH levels with late-life prevalent adjudicated dementia (p \textgreater 0.05). CONCLUSIONS: Our work does not support an independent influence of PTH on cognitive decline in this population-based cohort study.
Kim Samuel M; Zhao Di; Schneider Andrea L C; Korada Sai Krishna; Lutsey Pamela L; Guallar Eliseo; Alonso Alvaro; Windham B Gwen; Gottesman Rebecca F; Michos Erin D
Neurology
2017
2017-08
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
<a href="http://doi.org/10.1212/WNL.0000000000004290" target="_blank" rel="noreferrer noopener">10.1212/WNL.0000000000004290</a>
Parathyroid Hormone and Subclinical Cerebrovascular Disease: The Atherosclerosis Risk in Communities Brain Magnetic Resonance Imaging Study.
*Magnetic Resonance Imaging; Brain; Brain Diseases; Brain Diseases – Complications; brain MRI; Brain/*diagnostic imaging; cerebrovascular disease; Cerebrovascular Disorders; Cerebrovascular Disorders – Blood; Cerebrovascular Disorders/*blood/*diagnostic imaging; Cohort Studies; Computer Assisted; Computer-Assisted; Cross Sectional Studies; Cross-Sectional Studies; Female; Funding Source; Human; Humans; Image Processing; Leukoencephalopathies/complications/diagnostic imaging; Magnetic Resonance Imaging; Male; Middle Age; Middle Aged; Parathyroid hormone; Parathyroid Hormone/*blood; Parathyroid Hormones – Blood; Prospective Studies; subclinical brain infarcts; white matter hyperintensities
BACKGROUND: Elevated parathyroid hormone (PTH) levels have been associated with cardiovascular disease risk factors and events. We hypothesized that elevated PTH levels would also be associated with subclinical cerebrovascular disease. We examined the relationship between elevated PTH level and white matter hyperintensities (WMHs) and subclinical infarcts measured on brain magnetic resonance imaging (MRI). METHODS: PTH was measured at baseline (1993-1994) among participants free of prior clinical stroke who underwent a brain MRI at baseline (n = 1703) and a second brain MRI 10 years later (n = 948). PTH levels of 65 pg/mL or higher were considered elevated (n = 204). Participants who did not return for a follow-up MRI had, at baseline, higher PTH and a greater prevalence of cardiovascular risk factors (P \textless .05 for all); therefore, multiple imputation was used. The cross-sectional and prospective associations of PTH levels with WMH and MRI-defined infarcts (and their progression) were investigated using multivariable regression models. RESULTS: At baseline, the participants had a mean age of 62 years and were 60% female and 49% black. Cross-sectionally, after adjusting for demographic and lifestyle factors, elevated PTH level was associated with higher WMH score (beta = .19, 95% confidence interval [CI] .04-.35) and increased odds of prevalent infarcts (odds ratio 1.56, 95% CI 1.02-2.36). Results were attenuated after adjustment for potential mediators of this association (i.e., hypertension). No prospective associations were found between PTH and incident infarcts or change in estimated WMH volume, although estimates were imprecise. CONCLUSIONS: Although associated cross-sectionally, we did not confirm any association between elevated PTH level and progression of cerebrovascular changes on brain MRIs obtained 10 years apart. The relationship of PTH with subclinical brain disease warrants further study.
Korada Sai Krishna C; Zhao Di; Gottesman Rebecca F; Guallar Eliseo; Lutsey Pamela L; Alonso Alvaro; Sharrett A Richey; Post Wendy S; Reis Jared P; Mosley Thomas H; Michos Erin D
Journal of stroke and cerebrovascular diseases : the official journal of National Stroke Association
2016
2016-04
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
<a href="http://doi.org/10.1016/j.jstrokecerebrovasdis.2015.12.029" target="_blank" rel="noreferrer noopener">10.1016/j.jstrokecerebrovasdis.2015.12.029</a>
Low thigh muscle mass is associated with coronary artery stenosis among
*Computed Tomography Angiography; *Tomography; Aged; Atherosclerotic; Body Composition; Chi-Square Distribution; Coronary Angiography/*methods; Coronary Artery Disease/*diagnostic imaging/epidemiology/pathology; Coronary artery stenosis; Coronary atherosclerosis; Coronary Stenosis/*diagnostic imaging/epidemiology/pathology; Coronary Vessels/*diagnostic imaging/pathology; Cross-Sectional Studies; HIV Infections/diagnosis/*epidemiology; HIV-infection; Humans; Male; Middle Aged; Multivariate Analysis; Muscle; Muscle mass; Odds Ratio; Plaque; Predictive Value of Tests; Prevalence; Prospective Studies; Risk Factors; Sarcopenia; Sarcopenia/*diagnostic imaging/epidemiology/physiopathology; Skeletal/*diagnostic imaging/physiopathology; Thigh; United States/epidemiology; X-Ray Computed
BACKGROUND: HIV-infected individuals are at increased risk for both sarcopenia and cardiovascular disease. Whether an association between low muscle mass and subclinical coronary artery disease (CAD) exists, and if it is modified by HIV serostatus, are unknown. METHODS: We performed cross-sectional analysis of 513 male MACS participants (72% HIV-infected) who underwent mid-thigh computed tomography (CT) and non-contrast cardiac CT for coronary artery calcium (CAC) during 2010-2013. Of these, 379 also underwent coronary CT angiography for non-calcified coronary plaque (NCP) and obstructive coronary stenosis \textgreater/=50%. Multivariable-adjusted Poisson regression was used to estimate prevalence risk ratios of associations between low muscle mass (\textless20th percentile of the
Tibuakuu Martin; Zhao Di; Saxena Ankita; Brown Todd T; Jacobson Lisa P; Palella Frank J Jr; Witt Mallory D; Koletar Susan L; Margolick Joseph B; Guallar Eliseo; Korada Sai Krishna C; Budoff Matthew J; Post Wendy S; Michos Erin D
Journal of cardiovascular computed tomography
2018
2018-04
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
<a href="http://doi.org/10.1016/j.jcct.2018.01.007" target="_blank" rel="noreferrer noopener">10.1016/j.jcct.2018.01.007</a>
The associations of 25-hydroxyvitamin D levels, vitamin D binding protein gene polymorphisms, and race with risk of incident fracture-related hospitalization: Twenty-year follow-up in a bi-ethnic cohort (the ARIC Study).
*Polymorphism; African Continental Ancestry Group; Aged; Alleles; Epidemiology; Ethnic Groups; European Continental Ancestry Group; Female; Follow-Up Studies; Fracture; Fracture Healing; Genetic Variation; Genotype; Hip Fractures/blood/*ethnology/*genetics; Hospitalization; Humans; Incidence; Male; Middle Aged; Proportional Hazards Models; Prospective Studies; Race; Risk Factors; Single Nucleotide; Vitamin D; Vitamin D binding protein polymorphisms; Vitamin D-Binding Protein/*genetics; Vitamin D/*analogs & derivatives/blood
BACKGROUND: Deficient levels of 25-hydroxyvitamin D [25(OH)D] have been associated with increased fracture risk. Racial differences in fracture risk may be related to differences in bioavailable vitamin D due to single nucleotide polymorphism (SNP) variations in the vitamin D binding protein (DBP). METHODS: We measured 25(OH)D levels in 12,781 middle-aged White and Black participants [mean age 57 years (SD 5.7), 25% Black] in the ARIC Study who attended the second examination from 1990-1992. Participants were genotyped for two DBP SNPs (rs4588 and rs7041). Incident hospitalized fractures were measured by abstracting hospital records for ICD-9 codes. We used Cox proportional hazards models to evaluate the association between 25(OH)D levels and risk of fracture with adjustment for possible confounders. Interactions were tested by race and DBP genotype. RESULTS: There were 1122 incident fracture-related hospitalizations including 267 hip fractures over a median of 19.6 years of follow-up. Participants with deficient 25(OH)D (\textless20 ng/mL) had a higher risk of any fracture hospitalization [HR=1.21 (95% CI 1.05-1.39)] and hospitalization for hip fracture [HR=1.35 (1.02-1.79)]. No significant racial interaction was noted (p-interaction=0.20 for any fracture; 0.74 for hip fracture). There was no independent association of rs4588 and rs7041 with fracture. However, there was a marginal interaction for 25(OH)D deficiency with rs7041 among Whites (p-interaction=0.065). Whites with both 25(OH)D deficiency and the GG genotype [i.e., with predicted higher levels of DBP and lower bioavailable vitamin D] were at the greatest risk for any fracture [HR=1.48 (1.10-2.00)] compared to Whites with the TT genotype and replete 25(OH)D (reference group). CONCLUSIONS: Deficient 25(OH)D levels are associated with higher incidence of hospitalized fractures. Marginal effects were seen in Whites for the DBP genotype associated with lower bioavailable vitamin D, but result inconclusive. Further investigation is needed to more directly evaluate the association between bioavailable vitamin D and fracture risk.
Takiar Radhika; Lutsey Pamela L; Zhao Di; Guallar Eliseo; Schneider Andrea L C; Grams Morgan E; Appel Lawrence J; Selvin Elizabeth; Michos Erin D
Bone
2015
2015-09
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
<a href="http://doi.org/10.1016/j.bone.2015.04.029" target="_blank" rel="noreferrer noopener">10.1016/j.bone.2015.04.029</a>
Frailty and subclinical coronary atherosclerosis: The Multicenter AIDS Cohort Study (MACS).
Acquired Immunodeficiency Syndrome/diagnosis/*epidemiology; Asymptomatic Diseases; Atherosclerotic; Cardiac CT; Computed Tomography Angiography; Coronary Angiography/methods; Coronary artery calcium; Coronary Artery Disease/diagnostic imaging/*epidemiology; Coronary atherosclerosis; Cross-Sectional Studies; Exercise; Frailty; Frailty/diagnosis/*epidemiology/physiopathology; Health Status; HIV-Infection; Humans; Linear Models; Male; Middle Aged; Multivariate Analysis; Muscle Strength; Muscle Weakness; Plaque; Prevalence; Prognosis; Risk Factors; United States/epidemiology; Vascular Calcification/diagnostic imaging/*epidemiology; Weight Loss
BACKGROUND AND AIMS: Frailty and cardiovascular disease share many risk factors. We evaluated whether frailty is independently associated with subclinical coronary atherosclerosis and whether any relationships differ by HIV-serostatus. METHODS: We studied 976 [62% HIV-infected] male participants of the Multicenter AIDS Cohort Study who underwent assessment of frailty and non-contrast cardiac CT scanning; of these, 747 men also underwent coronary CT angiography (CCTA). Frailty was defined as having \textgreater/=3 of 5 of the following: weakness, slowness, weight loss, exhaustion, and low physical activity. Coronary artery calcium (CAC) was assessed by non-contrast CT, and total plaque score (TPS), mixed plaque score (MPS), and non-calcified plaque score (NCPS) by CCTA. Multivariable-adjusted regression was used to assess the cross-sectional associations between frailty and subclinical coronary atherosclerosis. RESULTS: Mean (SD) age of participants was 54 (7) years; 31% were black. Frailty existed in 7.5% and 14.3% of
Korada Sai Krishna C; Zhao Di; Tibuakuu Martin; Brown Todd T; Jacobson Lisa P; Guallar Eliseo; Bolan Robert K; Palella Frank J; Margolick Joseph B; Martinson Jeremy J; Budoff Matthew J; Post Wendy S; Michos Erin D
Atherosclerosis
2017
2017-11
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
<a href="http://doi.org/10.1016/j.atherosclerosis.2017.08.026" target="_blank" rel="noreferrer noopener">10.1016/j.atherosclerosis.2017.08.026</a>