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Year : 2021  |  Volume : 9  |  Issue : 2  |  Page : 142-144

Severe hypercalcemia mimicking as ST-segment elevation myocardial infarction

Department of Medicine, All India Institute of Medical Sciences, Rishikesh, Uttarakhand, India

Date of Submission16-May-2021
Date of Decision18-May-2021
Date of Acceptance04-Jul-2021
Date of Web Publication25-Aug-2021

Correspondence Address:
Dr. Ravi Kant
Department of Medicine, Division of Diabetes and Metabolism, All India Institute of Medical Sciences Rishikesh - 249 203, Uttarakhand
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/heartindia.heartindia_82_21

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The identification of ST-segment elevation on the electrocardiogram is an integral part of decision-making in patients who present with suspected ischemia. Unfortunately, ST-segment elevation is nonspecific and may be caused by noncardiac causes such as electrolyte abnormalities. We present a case of a 52-year-old male who presented with ST-segment elevation secondary to hypercalcemia in a patient with hypertension with osteoporotic vertebral collapse.

Keywords: Hypercalcemia, osteoporosis, ST-segment elevation myocardial infarction

How to cite this article:
Pradeep Yadav K L, Tendulkar P, Kant R. Severe hypercalcemia mimicking as ST-segment elevation myocardial infarction. Heart India 2021;9:142-4

How to cite this URL:
Pradeep Yadav K L, Tendulkar P, Kant R. Severe hypercalcemia mimicking as ST-segment elevation myocardial infarction. Heart India [serial online] 2021 [cited 2022 Jan 28];9:142-4. Available from: https://www.heartindia.net/text.asp?2021/9/2/142/324615

  Introduction Top

In cases of suspicion of myocardial ischemia, identification of ST-segment elevation is critical as emergent angiography is indicated for patients with ST-segment elevation myocardial infarction (STEMI).[1] The finding of ST-segment elevation is nonspecific, and approximately 80% of patients who present with chest pain and ST-segment elevation are found to have a coronary lesion with thrombolysis in myocardial infarction Grade Flow of 0–1 at angiography.[2],[3] In addition, approximately 3% of patients with suspected STEMI are found to have angiographically normal coronary arteries.[4] Electrolyte abnormalities including hyperkalemia[5],[6],[7] and hypercalcemia[8] may present with ST-segment elevation and a pseudo-infarction pattern on the electrocardiogram (ECG). In patients presenting with suspected STEMI, the decision to proceed with invasive angiography must often be made before laboratory results are available. In patients at risk for electrolyte abnormalities, clinicians must be aware of the common ECG changes associated with electrolyte abnormalities to avoid unnecessary procedural risks in a potentially unstable patient. The following reviews a patient with osteoporotic vertebral body collapse with hypertension (HTN) who presented with severe hypercalcemia and ST-segment elevation.

  Case Report Top

Clinical history

A 52-year-old male was brought to the emergency department with complaints of generalized malaise, loss of appetite, vomiting, and altered behavior for almost a week's duration; it was associated with low-grade fever for 3 days and nonspecific chest pain. The patient was on injection teriparatide (20 mcg) OD for the past 2 months for osteoporosis and he was on regular antihypertensive medication. There was no history of headache, neck stiffness, and diabetes in the past. His examination revealed altered sensorium in the form of drowsiness and inability to follow verbal commands. His blood pressure (BP) was 180/90 mmHg with the unremarkable systemic examination.

  • 2D ECHO: Concentric Left ventricular hypertrophy (LVH) with normal Left ventricular (LV) function
  • Ultrasonography abdomen: Well-defined lesion in segment seven of the liver (? old abscess)
  • Contrast-enhanced computed tomography thorax/abdomen: Benign lesions in the liver.


The patient was having severe hypercalcemia (calcium >14 mg/dl) [Table 1], he was started on isotonic saline at a rate of 200–300 ml/h with strict monitoring on fluid intake and output. Injection teriparatide was stopped and injection zoledronate (4 mg) was given. His antihypertensive medications were continued with strict BP charting. The patient symptomatically improved with correction of serum calcium in form of improvement in sensorium, resolution of ST elevation in 12 lead ECG [Figure 1] and [Figure 2].
Figure 1: Standard 12 lead electrocardiogram suggestive of normal sinus rhythm and normal axis with ST elevation in lead V1, V2, and V3 with T wave inversion in lead V4, V5, V6, and reciprocal T wave inversion in lead I and aVL

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Figure 2: Standard 12 lead electrocardiogram s/o resolution of ST elevation in lead V1, V2, V3 after correction of hypercalcemia

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Table 1: Investigation

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  Discussion Top

This patient presented with hypercalcemia and pseudo-infarction pattern on the ECG and appropriate treatment for hypercalcemia was initiated once laboratory results were obtained, The most commonly recognized manifestations of hypercalcemia on the ECG are shortening of QT interval with upsloping of the T wave On the ECG, the lower limits for the duration of QTc is not well-defined, but it is reasonable to consider a normal QTc interval as between 360 ms and 450 ms in males and 370 ms to 470 ms in females, interestingly, when this patient's serum calcium was 16.5 mg/dl the QTc was actually normal (370 ms) and ECG obtained after correcting hypercalcemia also shows normal QTc (376 ms), this case emphasizes that all ST-segment elevations are not due to myocardial infarction there are other causes which can lead to ST elevation like hypercalcemia.

  Conclusion Top

ST-segment elevation is a known consequence of severe hypercalcemia and clinicians should be aware that high calcium levels may be associated with a pseudo-infarct pattern on the ECG. The possibility of electrolyte-induced ECG changes should be considered when evaluating the ECG for signs of ischemia.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient (s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initial s will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Authors' contributions

Dr Pradeep Yadav K L- manuscript writing -Dr Prakash Tendulkar- manuscript writing -Dr Ravi Kant- Supervision and editing.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

  References Top

O'Gara PT, Kushner FG, Ascheim DD, Casey DE Jr., Chung MK, de Lemos JA, et al. 2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction: Executive summary: A report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation 2013;127:529-55.  Back to cited text no. 1
DeWood MA, Spores J, Notske R, Mouser LT, Burroughs R, Golden MS, et al. Prevalence of total coronary occlusion during the early hours of transmural myocardial infarction. N Engl J Med 1980;303:897-902.  Back to cited text no. 2
Chesebro JH, Knatterud G, Roberts R, Borer J, Cohen LS, Dalen J, et al. Thrombolysis in myocardial infarction (TIMI) trial, Phase I: A comparison between intravenous tissue plasminogen activator and intravenous streptokinase. Clinical findings through hospital discharge. Circulation 1987;76:142-54.  Back to cited text no. 3
Widimsky P, Stellova B, Groch L, Aschermann M, Branny M, Zelizko M, et al. Prevalence of normal coronary angiography in the acute phase of suspected ST-elevation myocardial infarction: Experience from the PRAGUE studies. Can J Cardiol 2006;22:1147-52.  Back to cited text no. 4
Levine HD, Merrill JP, Somerville W. Advanced disturbances of the cardiac mechanism in potassium intoxication in man. Circulation 1951;3:889-905.  Back to cited text no. 5
Levine HD, Wanzer SH, Merrill JP. Dialyzable currents of injury in potassium intoxication resembling acute myocardial infarction or pericarditis. Circulation 1956;13:29-36.  Back to cited text no. 6
Pastor JA, Castellanos A, Moleiro F, Myerburg RJ. Patterns of acute inferior wall myocardial infarction caused by hyperkalemia. J Electrocardiol 2001;34:53-8.  Back to cited text no. 7
Wesson LC, Suresh V, Parry RG. Severe hypercalcaemia mimicking acute myocardial infarction. Clin Med (Lond) 2009;9:186-7.  Back to cited text no. 8


  [Figure 1], [Figure 2]

  [Table 1]


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