Impact of Parathyroidectomy on Vascular Stiffness: Exploring Pulse Wave Velocity and Renal Resistive Index.

Huber, Aurélie; Pasquier, Théodore; Demarchi, Marco; Sadowski, Samira; Berchtold, Lena; Triponez, Frederic; De Seigneux, Sophie; Ponte, Belén · J Clin Endocrinol Metab · 2025

prospective_cohort · Level II

Where this comes from

Abstract

Primary hyperparathyroidism (PHPT), characterized by elevated parathyroid hormone (PTH) and hypercalcemia, has been implicated in vascular calcification and increased arterial stiffness. Carotid-femoral pulse wave velocity (PWV) is the gold-standard marker of large artery stiffness, while augmentation index (AI), pulse pressure (PP), and renal resistive index (RRI) offer insights into wave reflection and microvascular function. This study aimed to assess the associations between PTH levels and these vascular parameters before and after parathyroidectomy (PTX). In a prospective monocentric cohort study, PHPT patients undergoing elective PTX had vascular assessments at baseline and six months postoperatively. Associations between PTH and vascular markers (PWV, AI, PP, and RRI) were evaluated using Pearson correlations, linear regression and multivariable mixed-effects regression models adjusted for cardiovascular and metabolic covariates. Among 107 patients (80% female, median age of 64), PTH and PWV significantly declined 6 months after PTX, while AI, PP, and RRI remained unchanged. In adjusted models, higher PTH was independently associated with increased PWV (β = 0.10; 95% CI: 0.02-0.18). No significant associations were observed between PTH and AI or PP. At baseline, PTH levels were positively associated with RRI (β = 2.16; 95% CI: 0.19-4.13), but this association did not persist after PTX. Elevated PTH is independently associated with greater large artery stiffness in PHPT, and this effect appears to be at least partially reversible following PTX. However, changes in PTH were not associated with short-term changes in renal microvascular resistance, suggesting a delayed or less reversible impact on renal vasculature.