research letter

Cardiology Journal

2022, Vol. 29, No. 4, 710–713

DOI: 10.5603/CJ.a2022.0048

Copyright © 2022 Via Medica

ISSN 1897–5593

eISSN 1898018X

Severe hypocalcemia mimicking acute ST-segment elevation myocardial infarction: Paradigmatic case and review of literature

Belén PeiróLuis CerdánJosé Antonio DiarteM. Rosario OrtasCarlos Cortés
Miguel Servet University Hospital, Zaragoza, Spain

Address for correspondence: Carlos Cortés, MD, PhD, FESC, Interventional Cardiologist, Miguel Servet University Hospital, 1-3, Paseo Isabel la Católica, 50009, Zaragoza, Spain, tel: +34 627370498, e-mail:

Received: 6.04.2022 Accepted: 12.05.2022 Early publication date: 24.05.2022

This article is available in open access under Creative Common Attribution-Non-Commercial-No Derivatives 4.0 International (CC BY-NC-ND 4.0) license, allowing to download articles and share them with others as long as they credit the authors and the publisher, but without permission to change them in any way or use them commercially.

A 65-year-old woman with a previous history of hypertension and hypercholesterolemia was admitted to the emergency department due to 2-week asthenia, diarrhoea and dizziness. Electrocardiogram (ECG) at admission showed ST-segment elevation in leads I, avL and V2 and depression in the inferior leads, suggestive of high lateral ST-segment elevation myocardial infarction (STEMI). QTc was 447 ms (Fig. 1A). She did not complain of chest pain or dyspnoea. Serum troponin levels were normal, and echocardiogram showed moderate systolic dysfunction with akinesia of medium segments of all cardiac walls. Laboratory evaluation evidenced severe hypocalcemia (6.1 mg/dL, normal 8.5–10.9 mg/dL) with low ionized calcium, corrected by serum albumin (2.6 mg/dL, normal 4.40–5.30 mg/dL). After calcium replenishment, ECG abnormalities reverted to normal (Fig. 1B) and echocardiogram demonstrated improvement of cardiac contractility. Deferred coronary angiography excluded significant epicardial coronary artery disease (Fig. 1C), as well as absence of endothelial dysfunction evaluated in the left anterior descending artery territory by acetylcholine provocation test and normal coronary flow reserve with mild elevation of the index of microcirculatory resistance (Fig. 1D). The patient was discharged after 1 week of hospitalization.

Figure 1. A. Electrocardiogram (ECG) at admission (25 mm/s): ST-segment elevation in I, aVL and V2 and depression in II, III and aVF. QTc 447 ms (Bazett’s formula); B. ECG after electrolyte restocking, showing resolution of the abnormalities; C. Absence of significant epicardial coronary artery disease (C1 = LCA: RAO Cranial; C2 = LCA: RAO Caudal); D. Coronary physiological assessment: normal coronary flow reserve, mild elevation of index of microcirculatory resistance.

Electrolyte imbalances are a well-known cause of electrocardiographic abnormalities. In hypocalcemia, most frequent findings are ST segment and QTc prolongation, due to a reduction in phase two of the action potential. T wave may be flattened or inverted, but usually maintains its polarity. Although it has rarely been reported, hypocalcemia can induce ST segment elevation.

A literature review in Pubmed and Google Scholar databases regarding hypocalcemia as cause of STEMI was conducted. After evaluation by two independent investigators, 7 case reports were found.

Lehmann et al. [1] presented a case, in the year 2000, of a 24-year-old female presenting to the emergency department for loss of consciousness and seizures in the context of severe hypocalcemia due to hypoparathyroidism. ECG at admission showed ST segment elevation in I and aVL and depression in inferior and precordial leads, as well as QTc prolongation. Coronary angiography showed normal coronary arteries. After electrolyte supplementation, ECG changes reversed.

Similar cases have been reported subsequently and are described in Table 1, with no sex differences and a wide range of ages. In most of the cases (75%) ST-segment elevation is presented at lateral leads. Only Adeel et al. [2] described a case with ST elevation in inferior leads.

Table 1. Summary of case reports about hypocalcemia mimicking ST-elevation.




Clinical presentation

ST segment elevation

T waves

QTc [ms]


Coronary angiography

Other diagnostic tests

Cardiac enzymes

Lechmann et al. 2000



Loss of consciousness, seizures

I, aVL



Moderate LV dysfunction Anterolateral impaired motion

No significant stenosis


Ilveskoski et al. 2012



Dyspnea, chest pain

I, aVL V1–V3



Severe LV dysfunction Global

No significant stenosis No vasospasm

Plateau minimal elevation

Gómez-Domínguez et al. 2013



Fatigue, chest pain, confusional state




Severe LV dysfunction Global

No significant stenosis


Kukla et al. 2016



Chest pain, shortness of breath

I, aVL

Tall and peaked


Not performed

Not performed


Adeel et al. 2018



Lethargy, weakness, diarrhea




Preserved LVEF No RWMA

Not performed

SPECT: absence of perfusion defects


Pervaiz et al. 2019



Clenching of the hands

I, aVL, V2–V6

Shallow inversion


Severe LV dysfunction Apical akinesia LV thrombus

Not performed

SPECT: absence of perfusion defects

Merlo et al. 2021



Diarrhea, vomiting

I, aVL V2



Preserved LVEF No RWMA

No significant stenosis


As it is known, the duration of the ST segment is inversely proportional to the plasmatic calcium concentration [3]. Consistent with that, corrected QT interval was prolonged in most of the patients, except for the one described by Kukla et al. [4], who presented with a shortened QT. Authors suggested the hypothesis of a coronary artery spasm as a possible cause. In the current patient, a vasoreactivity test was performed with increasing doses of acetylcholine, up to 100 µg, with no vasospastic response.

Very few cases have been reported in the literature hypothesizing a relationship between vasospasm and hypocalcemia [5, 6]. They presented patients with chest pain, ST segment changes and non-obstructive coronary arteries in the context of low calcium levels. Symptoms improved after calcium reposition so an assumption was made that hypocalcemia was related to a possible coronary spasm, however this was not proven with intracoronary physiology studies. Moreover, there is no clear physiopathological mechanism explaining this relationship.

After depolarization, calcium enters smooth muscle cells, triggering the opening of L-channels, promoting calcium interaction with calmodulin and subsequent activation of myosin. This mechanism explains why hypocalcemia can be related with vasodilation and hypotension, more than to vasospasm. It also explains the mechanism of action of calcium antagonists.

Left ventricular dysfunction was found in 4 of the cases. All of them had an angiography or perfusion imaging performed, showing the absence of coronary stenoses or myocardial perfusion defects.

Herein, is no certain explanation for the impairment of ventricular contractility, according to available research, calcium is a fundamental electrolyte participating in the generation of the action potential and cardiac muscle cell contraction. A severe reduction of its levels may have caused abnormalities in both electric and contractile activity, explaining those findings, as well as the absence of a correlation between regional wall motion abnormalities and ECG location of the ST elevation. Experimental studies suggest a correlation between depression of ventricular function and lower calcium concentrations [7]. The entry of calcium in the myocardial cells induces the release of calcium from the sarcoplasmic reticulum (“calcium-induced calcium release”), binds to troponin C and induces actin-myosin interaction. Hence, severe hypocalcemia could be a reversible cause of impaired myocardial contraction and heart failure. This has been described in literature as “hypocalcemic cardiomyopathy” [8]. Accordingly, transient left ventricular dysfunction has been described after blood transfusions with citrate, a calcium binding agent [9]. Other factors may play a physiopathological role, like duration of the electrolyte imbalance or preexisting cardiac conditions.

All patients followed during hospitalization or at discharge showed improvement of ejection fraction after treatment of hypocalcemia. One patient died because of his critical condition at admission.

In conclusion, hypocalcemia can cause a “pseudo-STEMI” pattern, most frequently in lateral leads. Physiopathological mechanism remains unknown but significant coronary disease seems not to be the cause. Although it may present with elevated troponin and regional wall motion abnormalities, electrocardiographic changes and ventricular function may recover after electrolyte correction.

Conflict of interest: None declared


  1. Lehmann G, Deisenhofer I, Ndrepepa G, et al. ECG changes in a 25-year-old woman with hypocalcemia due to hypoparathyroidism. Hypocalcemia mimicking acute myocardial infarction. Chest. 2000; 118(1): 260–262, doi: 10.1378/chest.118.1.260, indexed in Pubmed: 10893393.
  2. Adeel MY, Clarke JRD, Shetty S, et al. Severe hypocalcemia mimicking acute inferior ST-segment elevation myocardial infarction. Oxf Med Case Reports. 2018; 2018(12): omy103, doi: 10.1093/omcr/omy103, indexed in Pubmed: 30487989.
  3. Davis TM, Singh B, Choo KE, et al. Dynamic assessment of the electrocardiographic QT interval during citrate infusion in healthy volunteers. Br Heart J. 1995; 73(6): 523–526, doi: 10.1136/hrt.73.6.523, indexed in Pubmed: 7626350.
  4. Kukla P, Kulik M, Jastrzębski M, et al. Severe hypocalcemia mimicking ST-segment elevation acute myocardial infarction. Ann Noninvasive Electrocardiol. 2017; 22(2), doi: 10.1111/anec.12401, indexed in Pubmed: 27604986.
  5. Magnus PC, Missri J. Hypocalcemia-associated coronary vasospasm. Conn Med. 2005; 69(1): 3–7, indexed in Pubmed: 15736368.
  6. Rasoul S, Dambrink JHE. Recurrent acute coronary syndrome due to coronary artery spasm in different coronary arteries. J Cardiol Cases. 2013; 8(3): 95–98, doi: 10.1016/j.jccase.2013.05.007, indexed in Pubmed: 30546754.
  7. Lang RM, Fellner SK, Neumann A, et al. Left ventricular contractility varies directly with blood ionized calcium. Ann Intern Med. 1988; 108(4): 524–529, doi: 10.7326/0003-4819-108-4-524, indexed in Pubmed: 3248127.
  8. Aguiar P, Cruz D, Ferro Rodrigues R, et al. Hypocalcemic cardiomyopathy. Rev Port Cardiol. 2013; 32(4): 331–335, doi: 10.1016/j.repc.2012.08.008, indexed in Pubmed: 23582987.
  9. Gulati S, Bajpai A, Juneja R, et al. Hypocalcemic heart failure masquerading as dilated cardiomyopathy. Indian J Pediatr. 2001; 68(3): 287–290, doi: 10.1007/BF02723209, indexed in Pubmed: 11338230.


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