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Generation of Hypoparathyroid Rats via Carbon-Nanoparticle-Assisted Parathyroidectomy
Published on: July 14, 2023
Hemodynamic markers and subclinical atherosclerosis in postmenopausal women with primary hyperparathyroidism
Kimon Stamatelopoulos1, Fani Athanasouli, Theodora Pappa
1Department of Clinical Therapeutics, Alexandra Hospital, Medical School, National and Kapodistrian University of Athens, 11528 Athens, Greece.
Context:
Recent evidence suggests that primary hyperparathyroidism (pHPT) is linked with hypertension and subclinical atherosclerosis. These associations have not been examined in postmenopausal women, in whom cardiovascular risk steeply rises after menopausal transition.
Objective:
The objective of the study was to assess whether pHPT is associated with hemodynamic markers and subclinical atherosclerosis in postmenopausal women under a cross-sectional case-control design.
Methods:
One hundred two postmenopausal women with pHPT and 102 women matched 1:1 for age and menopausal status were consecutively recruited. In all patients, flow-mediated dilatation, carotid-femoral pulse wave velocity, reflected waves, aortic blood pressures (BP), intima-media thickness, and the presence of plaques in the carotid and common femoral arteries were measured.
Results:
Women with pHPT had higher aortic and peripheral BP (P < .05 for all), but no correlation was observed with subclinical atherosclerosis. After adjusting for possible confounders, pHPT was an independent determinant of peripheral and aortic diastolic BP (P < .05 for all). The association with systolic BP was lost after adjusting for C-reactive protein. Further adjustment for PTH and 25-hydroxyvitamin D levels revealed that PTH but not 25-hydroxyvitamin D was an independent determinant of all BP parameters. Both peripheral and aortic BP increased across PTH tertiles as compared with the control group, but this association lost significance after adjustment for C-reactive protein.
Conclusions:
These results suggest that pHPT may increase peripheral and aortic BP through PTH and inflammatory-mediated mechanisms. A direct impact of the disease on the arterial wall cannot be implicated despite the large number of markers of subclinical atherosclerosis measured in this study.
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