The Clinical Picture

Heartburn or heart attack? A mimic of MI

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A 71-year-old man with a history of hypertension, 4 prior myocardial infarctions (MIs), and well-compensated ischemic cardiomyopathy presented to the emergency department after 2 episodes of sharp pain in the left upper abdomen and chest. The episodes lasted 1 to 2 minutes and were not relieved by rest. Their location was similar to that of the pain he experienced with his MIs. He could not identify any exacerbating or ameliorating factors. The pain had resolved without specific therapy before he arrived.

He reported polydipsia and constipation over the past 2 weeks and generalized muscle weakness and acute exacerbations of chronic back pain in the past 2 days. Neither he nor a friend who accompanied him noticed any confusion. He had been taking as many as 15 calcium carbonate tablets a day for 6 weeks to self-treat dyspepsia refractory to once-daily ranitidine, and hydrochlorothiazide for his hypertension for 3 weeks.


On physical examination, he had diffuse weakness, dry mucous membranes, and an irregular heart rhythm.

Electrocardiography at presentation showed a corrected QT interval of 360 msec.

Figure 1. Electrocardiography at presentation showed a corrected QT interval of 360 msec. In addition to ST-segment elevations (blue arrows) and ST-segment depressions (blue diamonds), varying ectopic beats (red arrows) were present that were absent on previous studies.

Electrocardiography (ECG) ( Figure 1 ) showed ST-segment elevation in leads V 1, V 2, V 3, II, III, and aVF and ST-segment depression in leads I and aVL. The corrected QT interval was 360 ms, compared with 426 ms 4 months earlier ( Figure 2 ).

Laboratory testing showed the following:

  • Troponin I 0.11 ng/mL (reference range ≤ 0.04); repeated, it was 0.12 ng/mL
  • Serum creatinine 3.4 mg/dL (0.44–1.27) (9 months earlier it had been 0.99 mg/dL)
  • Serum calcium 17.3 mg/dL (8.6–10.5)
  • Parathyroid hormone 9 pg/mL (12–88)
  • Serum bicarbonate 33 mmol/L (24–32); 2 weeks earlier, it had been 27 mmol/L.
An electrocardiogram 4 months earlier showed no ST-segment elevations or ST-segment depressions.

Figure 2. An electrocardiogram 4 months earlier showed no ST-segment elevations (blue arrows) or ST-segment depressions (blue diamonds).

A cardiology consult was ordered out of concern for ST-elevation MI (STEMI). The cardiology consult team did not recommend coronary angiography because the patient’s chest pain had resolved spontaneously, its presentation was atypical, and the results of laboratory studies indicated acute kidney injury, a relative contraindication to angiography.


The diagnosis, based on the presentation and the results of the workup, was milk-alkali syndrome complicated by recent hydrochlorothiazide use. This syndrome consists of the triad of hypercalcemia, metabolic alkalosis, and acute kidney injury, all due to excessive ingestion of calcium and alkali, usually calcium carbonate.

His hydrochlorothiazide and calcium carbonate were discontinued. He was given intravenous normal saline and subcutaneous calcitonin, and his serum calcium level came down to 11.5 mg/dL within the next 24 hours. His dyspepsia was treated with pantoprazole.

The patient had no further episodes of chest pain, and the cardiology consult team again recommended against coronary angiography. Repeat ECG after the hypercalcemia resolved showed results identical to those 4 months before his admission. Two months later, his serum calcium level was 9.4 mg/dL and his creatinine level was 1.24 mg/dL.

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