SUN-816 - ST-Segment Elevations without Infarction: A Cardiometabolic Manifestation of Parathyroid Carcinoma

Introduction
Severe hypercalcemia can produce electrocardiographic (ECG) changes including changes that might resemble acute myocardial infarction. Causes of hypercalcemia include hyperparathyroidism, malignancy-related disorders, bone metastases, and parathyroid cancer. Recognizing hypercalcemia secondary to parathyroid malignancy as a potential cause of apparent ischemic changes is crucial to prevent unnecessary interventions and to ensure proper endocrine management.

Case Presentation
We report the case of a 76-year-old previously healthy woman who was referred to the emergency department for new ECG changes showing anterior- lead ST segment elevations and repolarization abnormalities. The patient reported worsening weakness that started a few days prior, denying chest pain or any other symptoms. Vital signs showed a newly elevated blood pressure at 180/57 mmHg and physical examination was insignificant apart from a palpable thyroid mass. Laboratory evaluation revealed a serum calcium of 15.8 mg/dL and parathyroid hormone (PTH) of 663 pg/mL. PTH-rp, vitamin D, TSH, and other electrolytes were within normal limits. Extensive cardiac workup was done and showed stable troponin (29 ng/L), normal echocardiogram with an ejection fraction of 62%, and no ischemic findings. Neck computed tomography revealed a 4 × 3 × 2.5 cm mixed solid and cystic mass posterior to the left thyroid lobe, consistent with a parathyroid versus thyroid lesion. The patient was treated with intravenous fluids, subcutaneous calcitonin, intravenous zoledronate, and cinacalcet 60 mg twice daily; and she was referred for parathyroid gland resection. Post-parathyroidectomy histopathology demonstrated an atypical parathyroid neoplasm with infiltrative growth and fibrosis. Postoperatively, her calcium normalized to 10.5 mg/dL, and ECG changes resolved.

Discussion
Severe hypercalcemia exerts significant electrophysiologic effects on the myocardium by shortening ventricular repolarization and, in severe cases, generating ST-segment elevations and T-wave changes that may resemble acute ischemia. In parathyroid carcinoma, sustained PTH overproduction can result in severe hypercalcemia and a pseudoinfarction ECG pattern. Differentiating metabolic from ischemic etiologies requires a comprehensive assessment.

Conclusion
This case emphasizes that parathyroid malignancy-induced hypercalcemia can produce ECG changes mimicking acute myocardial infarction. Awareness of this rare presentation is essential to avoid misdiagnosis, reduce patient distress, and guide appropriate endocrine and surgical management.

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