A 56 year old man was admitted to our clinic with the diagnosis of ST segment elevation myocardial infarction (MI). He had prolonged burning, crushing type of chest pain, and his ECG showed ST segment elevation in leads V1–V6, I, and II, and small Q waves in leads V2 and V3 (upper panel). Because more than 12 hours had passed since the onset of his chest pain thrombolytic treatment was not given. His troponin T and creatine kinase-MB (CK-MB) values were normal. No evolutive changes typical for MI or pericarditis were seen in his ECG, and echocardiographic examination revealed normal wall motion. Therefore the diagnosis of acute MI was ruled out. His biochemical analysis showed a pronounced increase in serum calcium concentration (4.05 mmol/l) and parathyroid hormone concentration (230.4 pmol/l). Ultrasonographic examination revealed a parathyroid adenoma. Serum calcium concentration returned to normal after saline infusion and administration of furosemide, calcitonin, and pamidronate; the patient then underwent parathyroid adenomectomy. His ECG after the operation was normal (lower panel). His chest pain was attributed to a peptic ulcer resulting from hypercalcaemia, and alleviated with antacid treatment.
In hypercalcaemia ST segment elevation in leads V1–V3 can be seen, but such extensive ST segment elevation along with the transient Q waves as in our case has not been previously reported. Measurement of QTc interval along with lack of evolutive changes may help in the diagnosis. In our patient, in the hypercalcaemic ST elevated phase, the QTc interval was 362 ms and returned to 436 ms after hypercalcaemia was corrected.
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