SUN-817 - CT-Detected Vascular Calcification and Cardiovascular Risk in Primary Hyperparathyroidism

Background
Primary hyperparathyroidism (PHPT) is characterized by chronic elevations in parathyroid hormone (PTH) and serum calcium and has been associated with increased cardiovascular morbidity. Incidental vascular calcification detected on computed tomography (CT) imaging is a recognized surrogate marker of atherosclerotic burden; however, its relationship with biochemical severity of PHPT and major adverse cardiovascular events (MACE) remains incompletely defined.
Objective
To evaluate the prevalence of CT-detected vascular calcification in patients with PHPT and examine its association with subsequent MACE. Secondary exploratory analyses assessed relationships between biochemical disease severity, disease duration, and vascular calcification.
Methods
We performed a retrospective cohort study of 50 adults with biochemically confirmed PHPT who underwent CT imaging of the neck, chest, or abdomen for clinical indications. Vascular calcification was identified from radiology reports. MACE was defined as myocardial infarction, stroke, or transient ischemic attack. Associations were assessed using descriptive statistics, penalized logistic regression, and Fisher’s exact tests.
Results
CT-detected vascular calcification was present in 24 of 50 patients (48%). Increasing age at PHPT diagnosis was associated with vascular calcification (odds ratio 1.18 per year). Peak serum calcium and peak PTH levels were not associated with calcification. Five patients (10%) experienced MACE during follow-up; all events occurred among patients with vascular calcification (20.8% vs 0%, p=0.02). Median time from PHPT diagnosis to MACE was 1450 days, and median time from parathyroidectomy to MACE was 1075 days. Peak serum calcium levels were similar in patients with and without MACE (median 11.7 vs 11.2 mg/dL). Traditional cardiovascular risk factors were more prevalent among patients with MACE.
Conclusion
CT-detected vascular calcification identifies patients with PHPT at increased risk for cardiovascular events, whereas biochemical disease severity and timing of surgical intervention were not associated with MACE. These findings suggest that vascular calcification reflects cumulative cardiovascular risk rather than hypercalcemia or PTH excess alone. Interpretation is limited by the small cohort size and retrospective study design.

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