SAT-763 A Case of Parathyroid Crisis with EKG Changes Mimicking ST Elevation Myocardial Infarct

Abstract Disclosure: I. Muneer: None. R. Tariq: None. S. Elattar: None. J. Mullally: None. A Case of Parathyroid Crisis with EKG Changes Mimicking ST Elevation Myocardial Infarct Background: Electrolyte abnormalities are known to disrupt plasma cell membranes and calcium plays a vital role in the stabilization of cardiac membranes. Hypercalcemia can cause cardiac arrhythmias, hemodynamic instability, and rarely can mimic ST elevation myocardial infarction (STEMI) on EKG. Elevated extracellular calcium levels enhance calcium influx, accelerating potassium efflux during repolarization. Early repolarization shortens the QT interval disproportionately shortening the ST segment with the appearance of an ST elevation which, on EKG, usually indicates myocardial injury necessitating emergent coronary angiography. Failure to recognize ST changes from severe hypercalcemia may result in misdiagnosis of cardiac ischemia. Case Description: A 70-year-old female with a remote history of nephrolithiasis and no recent medical care, presented with acute mental status changes and was found to have hypercalcemia (Ca >20.1 mg/dL), acute kidney injury with Cr 2.9 mg/dL, elevated iPTH 3425 pg/mL and elevated troponin 3794 ng/L. EKG showed a shortened QT interval and non-specific ST segment changes. Transthoracic echo (TTE) was normal. CT neck showed a large left heterogeneous parathyroid mass. Due to worsening mental status, the patient was intubated and treated with IV fluids, calcitonin, cinacalcet, and denosumab 120 mg. She was started on hemodialysis for calcium removal in preparation for parathyroidectomy. Despite this, her calcium remained elevated at 16.5 mg/dL. Her hospital course was complicated by up-trending troponin levels and repeat EKG showed worsening ST elevations in the anterolateral leads. TTE revealed hypokinesis in the apical septum and apical lateral wall, with a preserved ejection fraction. The patient was taken for emergent angiography that revealed normal coronary arteries except for minimal non-obstructive LAD disease. The patient’s clinical status deteriorated with worsening shock, and she was not stable enough to undergo parathyroidectomy. She suffered a cardiac arrest and passed away shortly after family requested comfort care measures. Conclusion: Hypercalcemia producing EKG changes that mimic STEMI is a very rare phenomenon with data limited to a few case reports. One case presented with both ST changes and elevated troponin levels, as in our patient, likely due to demand ischemia. Our case presented a particularly challenging diagnostic dilemma with the cooccurrence of ST elevation, up-trending troponins and new wall motion abnormalities on TTE, which suggested acute MI, but ultimately no culprit lesion was identified on angiography. Hypercalcemia was likely the cause of the ST changes. It is crucial to recognize the many cardiac manifestations of severe hypercalcemia, including, albeit rarely, ST segment changes on EKG mimicking STEMI. Presentation: Saturday, July 12, 2025