Key result
Primary hyperparathyroidism shows no significant difference in coronary artery calcium scores compared to controls.
Why the study?
Evidence suggests a potential association between primary hyperparathyroidism and cardiovascular alterations, but data on arterial stiffness are heterogeneous and studies evaluating coronary artery calcium score are limited and conflicting.
Does hypercalcemic primary hyperparathyroidism increase coronary artery calcium score and arterial stiffness compared with controls without primary hyperparathyroidism?
Cross-Sectional (n=45)
No
Does hypercalcemic primary hyperparathyroidism increase coronary artery calcium score and arterial stiffness compared with controls without primary hyperparathyroidism?
Answers are grounded in this paper and cite their sources.
Although coronary artery calcium scores and arterial stiffness parameters did not significantly differ between mild primary hyperparathyroidism patients and controls, a disease-specific positive correlation between CACS and augmentation index was observed exclusively in the PHPT group.
Background Evidence suggests a potential association between primary hyperparathyroidism (PHPT) and cardiovascular alterations. However, data on arterial stiffness in PHPT are heterogeneous, and studies evaluating the coronary artery calcium score (CACS) are limited and report conflicting results. This study compared CACS and arterial stiffness parameters between patients with hypercalcemic PHPT and control subjects and evaluated correlations among these markers and their associations with serum parathyroid hormone (PTH) and calcium levels. Methods This exploratory study included 20 patients with PHPT and 25 control subjects. CACS was evaluated by non-contrast cardiac computed tomography. Arterial stiffness indices— augmentation index (AIx), and pulse wave velocity (PWV)—were estimated using an oscillometric device. Results Forty-five participants were evaluated, with similar age distribution between groups and a predominance of women. No significant differences were observed between PHPT and controls for CACS (median 0.00 [0.00–52.00] vs. 7.00 [0.00–256.50]; P = 0.443), CACS percentile (0.00 [0.00–79.25] vs. 70.00 [0.00–92.00]; P = 0.418), AIx (24.55 ± 11.26 vs. 26.72 ± 10.73; P = 0.513), or PWV (9.13 ± 1.22 vs. 9.07 ± 1.10 m/s; P = 0.868). In PHPT participants with CACS > 0, mean CACS percentile was elevated (77.78 ± 19.27). In PHPT patients, CACS, AIx, and PWV were not correlated with serum PTH or calcium. A positive correlation between CACS and AIx was observed exclusively in the PHPT group (r = 0.472; P = 0.035), with no such association among controls (r = − 0.012; P = 0.956). Conclusions CACS correlated positively with AIx in patients with PHPT but not in controls. This finding may suggest a potential disease-specific interplay between central hemodynamics and subclinical atherosclerosis in the context of primary hyperparathyroidism.
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Siqueira et al. (2026) conducted a cross-sectional in Mild hypercalcemic primary hyperparathyroidism (n=45). Hypercalcemic primary hyperparathyroidism (PHPT) vs. Control subjects without primary hyperparathyroidism was evaluated on Coronary artery calcium score (CACS, median Agatston units) (p=0.443). Primary hyperparathyroidism showed no significant difference in CACS vs controls, though CACS positively correlated with AIx in PHPT.
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