Sai Krishna C Korada1, Di Zhao2, Rebecca F Gottesman3, Eliseo Guallar2, Pamela L Lutsey4, Alvaro Alonso4, A Richey Sharrett2, Wendy S Post5, Jared P Reis6, Thomas H Mosley7, Erin D Michos8. 1. Northeast Ohio Medical University, Rootstown, Ohio. 2. Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland. 3. Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland; Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland. 4. Division of Epidemiology and Community Health, School of Public Health, University of Minnesota, St. Paul, Minnesota. 5. Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland; Division of Cardiology, Johns Hopkins School of Medicine, Baltimore, Maryland. 6. Division of Cardiovascular Sciences, National Heart, Lung, and Blood Institute, Bethesda, Maryland. 7. Department of Medicine, University of Mississippi Medical Center, Jackson, Mississippi. 8. Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland; Division of Cardiology, Johns Hopkins School of Medicine, Baltimore, Maryland. Electronic address: edonnell@jhmi.edu.
Abstract
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 < .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 (β = .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.
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 < .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 (β = .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.
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