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Bone and Mineral Metabolism

SUN-762 - Severe Hypocalcemia Mimicking Acute Coronary Syndrome: A Case Report.

Sunday, June 14, 2026
9:00 AM - 4:00 PM CT
Location: ENDOExpo; Poster Floor


Introduction:
The main causes of hypocalcemia are disorders of parathyroid hormone (PTH) secretion and vitamin D metabolism. Cardiac manifestations are usually associated with severe hypocalcemia and include QT interval prolongation, arrhythmias, and, in rare cases, coronary artery spasm, which may mimic acute coronary syndrome.

Case Report:
A 55-year-old male with a 3-year history of primary hypoparathyroidism and poor treatment adherence presented with recurrent episodes of muscle weakness and paresthesia. Prior to hospitalization, symptoms worsened with the onset of aphonia and precordial chest pain, prompting evaluation in the emergency department. Electrocardiography revealed sinus rhythm with a heart rate of 59 beats per minute, prolonged corrected QT interval (QTc 515 ms), and ST-segment changes suggestive of subepicardial ischemia in leads V3–V6, DII, DIII, and aVF. Cardiac biomarkers showed no troponin elevation. Laboratory tests revealed severe hypocalcemia, with a total serum calcium level of 4.72 mg/dL (corrected calcium 5.0 mg/dL), confirmed by a second measurement of 4.9 mg/dL. Albumin 3.7 g/dL, P 7 mg/dL, MG 1.85 mg/L, and creatinine 1.4 mg/dL. Physical examination demonstrated hyperreflexia and positive Chvostek and Trousseau signs. Antianginal therapy, IV fluids, and calcium gluconate infusion were initiated. Due to persistent chest pain and high-risk features of unstable angina, coronary angiography was performed. No significant obstructive coronary lesions were identified, except for an intramyocardial bridge of the left anterior descending artery (LAD) causing 60% systolic compression (“milking phenomenon”). In the cardiac intensive care unit, intravenous calcium gluconate (1 mg/kg) was continued, and oral calcium carbonate and calcitriol were initiated. Further evaluation showed an intact PTH 6.6 pg/mL and a 24-hour urinary calcium excretion 36.85 mg/day. Thyroid function tests were normal. Transthoracic echocardiography revealed a left ventricular ejection fraction of 52%, with no additional abnormalities. Following correction of hypocalcemia and resolution of acute kidney injury, the patient was discharged with outpatient follow-up.

Discussion:
This case illustrates how severe hypocalcemia can induce coronary artery spasm and in the presence of an intramyocardial bridge in the LAD, produce electrocardiographic changes mimicking subepicardial ischemia. Approximately 2% of patients presenting with acute coronary syndrome have no significant coronary artery lesions, underscoring the importance of considering vasospastic mechanisms.

Conclusion:
This case highlights the importance of considering hypocalcemia in the differential diagnosis of chest pain.

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