Article, Cardiology

ST elevation due to hypercalcemia

a b s t r a c t

Characteristic ECG changes with hypercalcemia include shortening of the QoT, QaT, and QeT intervals which are measured from the beginning of the QRS complex to the origin (O), apex (A), and end (E) of the T wave respec- tively. At very high serum calcium levels ECG changes include slight prolongation of the PR and QRS intervals, T wave flattening or inversion, and the appearance of a J wave at the end of the QRS complex. We present a case of a 22 year-old male, who had been bedbound for 5 months following a severe motor vehicle collision, presenting with shortening of the QoT and QaT intervals leading to anterior ST elevation mimicking acute myocardial infarc- tion. Cardiac Troponin testing was negative, however, laboratory testing revealed a serum calcium level of 15 mg/dL (normal 7.3-10.5 mg/dL). We review the published literature regarding the link between hypercalce- mia and the appearance of ST elevation.

(C) 2017

  1. Case

A 22 year-old bedbound male presented to the Emergency Depart- ment (ED) with worsening and possibly infected sacral decubiti ulcers. He had been involved in a significant motor vehicle collision five months prior, which had resulted in multiple sacral, pelvic, and femur fractures. Following hospital discharge, the patient remained bedridden at home and was unable to fully participate in home Physical therapy secondary to pain.

On exam, the patient had a BP 144/92 mm Hg, HR 115 bpm, RR 18/ min, T 37.3 ?C, and SpO2 98% on RA. He was 190.5 cm in height and 100 kg in weight with a BMI of 27.5 kg/m2. His exam was notable for multiple sacral and heel decubiti ulcers with serosanguinous drainage. He was unable to walk, sit, roll-over without assistance secondary to pelvic girdle pain. His cardiopulmonary exam was normal with the ex- ception of an elevated heart rate.

In addition to laboratory and radiologic investigations, an ECG was obtained (Fig. 1). This was noted to have a sinus rhythm with concave ST segment elevation in V1-V4, Q waves with ST segment elevation in lead I and aVL, ST segment depressions in lead III and aVF, and biphasic T wave in leads V4-V6. The QT was measured at 324 ms and was calcu- lated to be 422 ms when adjusted for heart rate. The QoTc and QaTC were measured at 80 ms and 160 ms and calculated to be 110 ms and 210 ms when adjusted for heart rate.

A pelvic x-ray demonstrated patchy osteopenia or both hips and pel- vis. This patient’s labs were notable for mild leukocytosis and mildly

* Corresponding author at: Department of Emergency Medicine, Oregon Health & Sciences University, 3181 SW Sam Jackson Park Rd, Portland, OR 97239, United States.

E-mail address: [email protected] (E. Durant).

elevated lactate as a well as serum calcium of 15 mg/dL (normal 7.3- 10.5 mg/dL), magnesium 1.4 mg/dL (normal 1.6-2.6 mg/dL), phospho- rus 1.6 mg/dL (normal 2.3-4.7 mg/dL), and a serum albumin of 3.7 g/dL (normal 3.5-5.0 g/dL). Cardiac troponin I was undetectable (b 0.10 ng/mL).

Given the ECG findings, a cardiology consult was obtained and con- cluded the ST elevations noted on the ECG were most likely due to shortening of the QoT and QaT intervals resulting from hypercalcemia. No additional cardiology testing was recommended and a repeat ECG was not performed after treatment of hypercalcemia. The patient was admitted for wound care/infection and had an unremarkable hospital stay prior to being transferred to an inpatient rehabilitation facility.

  1. Discussion

Calcium ion concentration has long been known to affect the cardiac action potential and surface electrocardiogram. Characteristic ECG changes with hypercalcemia include shortening of the QoT, QaT, and QeT intervals, which are measured from the beginning of the QRS com- plex to the origin (O), apex (A), and end (E) of the T wave respectively. A reduction in the duration of the QoTc and QaTc intervals is considered to be a more accurate reflection of hypercalcemia compared to measure- ments using the overall QTc interval [1-3]. The combination of short QoTc (b 180 ms) and QaTc (b 300 ms) had the highest specificity for hy- percalcemia in one series [3]. In our patient the QTc was normal at 420 ms, however the QoTc and QaTc were both reduced at 110 ms and 210 ms respectively.

Sonada et al., reported several ECG changes with hypercalcemia after performing a case-control study that compared the ECG findings in 89 patients with hypercalcemia to 267 age- and sex-matched controls

http://dx.doi.org/10.1016/j.ajem.2017.02.005

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1033.e4 E. Durant, A. Singh / American Journal of Emergency Medicine 35 (2017) 1033.e31033.e6

Fig. 1.. ECG demonstrating ST segment elevations in leads V1 – V4, I, and avL, ST segment depressions in leads III and avF, and biphasic T waves in leads V4 – V6. QT, QTc, QoTc, ad QaTC are 324 ms, 422 ms, 80 ms, and 160 ms, respectively. Serum calcium was 15 mg/dL.

with normocalcemia [4]. In this series, hypercalcemia was associated with slight prolongation of the PQ interval (160 ms vs. 148 ms, p b 0.001), QRS duration (99 ms vs. 92 ms, p b 0.001), QT interval (354 ms vs. 378 ms, p b 0.001), and QTc (396 ms vs. 406 ms, p = 0.01). ST segment/T wave abnormalities were seen in 33% of patients with hypercalcemia vs. 4% in the control group (p b 0.001). J point ele- vation, identified either as a QRS slurring or a notching >= 0.1 mV in >= 2 consecutive leads, was noted in 30% of patients with hypercalcemia vs. 9% of controls (p b 0.001). Of the patients with J point elevation, over 50% also had ST elevation in two or more anatomic leads.

J point elevation and ST segment abnormalities have been reported in multiple case reports (Table 1) and one case series of patients with moderate/severe hypercalcemia. The majority of these patients

Table 1

Findings from Littmann L, Taylor III L, Brearley Jr. WD. ST-segment elevation: a common

finding in severe hypercalcemia. J Electrocardiol. Vol 40 2007:60-62.

Clinical history

Ca

QTc

ECG

62 yo male

16.5 mg/dL

0.258

STE V3-V4

52 yo male

15.8 mg/dL

0.402

STE V2-V3

49 yo male

17.0 mg/dL

0.420

STE V2-V5, I, aVL

39 yo male

12.9 mg/dL

0.415

STE V2-V6, I, II

23 yo male

14.7 mg/dL

0.418

STE V2-V6

44 yo male

18.5 mg/dL

0.383

STE V2

72 yo male

15.1 mg/dL

0.336

STE V2-V3, II, III, aVF

70 yo female

14.8 mg/dL

0.399

STE V2, I, aVL

45 yo female

20.2 mg/dL

0.326

STE V1-V3

48 yo male

10.9 mg/dL

0.360

STE V2-V5, I, aVL

35 yo male

13.3 mg/dL

0.408

STE V1-V2

43 yo male

11.4 mg/dL

0.382

STE V2-V4

50 yo male

11.1 mg/dL

0.393

STE V2-V5

48 yo female

15.0 mg/dL

0.418

STE V2-V6, II, III, aVF

86 yo male

11.4 mg/dL

0.400

STE V2-V4

36 yo female

10.5 mg/dL

0.352

STE V1-V4

presented with Nonspecific complaints, although several had chest, ab- dominal, back or shoulder pain. ST elevation occurs most often in the anterior leads and can be accompanied by regional ST depression. Serial cardiac enzymes, echocardiography, or cardiac catherization ruled out acute myocardial infarction. Littmann et al. published the largest case series of patients with hypercalcemia and ST elevation [5] (Table 1). Over a period of 14 years, 16 cases of hypercalcemia in which the ECG demonstrated ST-segment elevation that mimicked acute myocardial infarction were reviewed. The authors note ST elevation can occur in any anatomic configuration, but most commonly occurs in the anterior chest leads. The ST segments were reported to have a “scooped” appear- ance and were not followed by distinct T waves. According to Littmann, “ST-segment elevation is not a rare curiosity, but in fact may be the least well documented but most consistent electrocardiographic finding in patients with hypercalcemia.” [5]

Most authors hypothesize that ST elevation occurs as an artifact due to shortening of the interval between the S wave and the end of the T wave. Calcium channels act mainly in Phase 2 of the myocardial action potential. This is the plateau phase, consisting primarily of calcium in- flux and potassium efflux. During phase 3, calcium influx terminates and potassium efflux predominates as the myocyte repolarizes. Thus, the effect of hypercalcemia is confined to the ST segment with very little effect on the T wave (which occurs during phase 3). As the T wave moves closer to the QRS complex, the ST segment that connects the QRS wave to the T wave can appear to be elevated (and scooped) com- pared to the ECG baseline. This process may be accompanied by the ap- pearance of a J wave (Table 2).

Interestingly, Severe hypocalcemia has also been associated with ST elevation that can mimic an acute myocardial infarction [6-10].

  1. Conclusion

The ECG changes of hypercalcemia include shortening of the QoTc (b 180 ms) and QaTc (b 300 ms) intervals as well as ST segment/T wave abnormalities that may mimic acute myocardial infarction.

Table 2

E. Durant, A. Singh / American Journal of Emergency Medicine 35 (2017) 1033.e31033.e6

1033.e5

Hypercalcemia and ST elevation case reports.

Year

Author

Title

Journal

Clinical history

Ca

QTc

QoTc

QaTc

ECG

AMI excluded by

Notes

1984

Douglas

Extreme hypercalcemia and electrocardiographic

Am J

44 yo male with weakness,

21.8 mg/dL

0.330

0.140

0.220

STE V1-V5, II, III

Improved with

changes

Cardiol

polyuria, polydipsia for

treatment

3 weeks.

2003

Ashizawa

Hypercalcemia due to vitamin D intoxication with

Intern Med

78 yo male with nausea,

16.2 mg/dL

0.345

0.098

0.234

STE V1-V4; subtle

(-)Cath

clinical features mimicking acute myocardial infarction

fatigue, and anorexia for 10

STD II, III, aVF

days

2003

Topsakal

Electrocardiographic J wave as a result of

Jpn Heart J

67 yo female with nausea,

18.5 mg/dL

NR

STE V3-V6, II, III, aVF;

(-)Echo

hypercalcemia aggravated by Thiazide diuretics in a

vomiting, weakness, and

STD I, aVL, V2

case of primary hyperparathyroidism

constipation

2005

Turhan

ST segment elevation mimicking acute myocardial

Heart J

56 yo male with prolonged

16.2 mg/dL

0.362

STE V1-V6

(-)Enzymes/echo

infarction in hypercalcemia

burning, crushing chest pain

2006

Nishi

Hypercalcemia-induces ST-segment elevation

J

31 yo male with nausea,

17.8 mg/dL

0.415

STE V1-V6

(-)Cath

mimicking acute myocardial infarction

Electrocard

vomiting, lethargy,

abdominal pain radiating to

precordium

2009

Wesson

Severe hypercalcemia mimicking acute myocardial

Clin Med

69 yo female s/p syncopal

20.4 mg/dL

NR

STE V1-V5

(-)Enzymes

infarction

event with vague chest pain

and lethargy

2010

Donovan

Hypercalcemia mimicking STEMI on

Case Report

39 yo male with abdominal

23.0 mg/dL

NR

STE V2-V3, II, aVF

Clinically

2010

electrocardiography

Med

pain, vomiting, and weakness

improved with

supportive care

2010

Madampage

Hypercalcemia due to multiple myeloma with clinical

Chest

54 yo male with shoulder

17.1 mg/dL

“Normal”

STE II, III, aVF

(-)Cath

features mimicking acute myocardial infarction

pain, fatigue, and weight loss

2010

Fang

Acute myocardial infarction mimicking squamous cell

Chin Med J

52 yo male with intermittent

16.0 mg/dL

“Normal”

STE V1-V3

(-)Enzymes/echo

Lung cancer with bone metastases due to

substernal chest pain over

hypercalcemia: A case report

2 weeks

2011

Hajsadeghi

A rare electrocardiographic manifestation of a rare form

Acta

60 yo male with epigastric

20.5 mg/dL

0.310

0.150

0.250

STE aVR, V1, STD II, III,

(-)Echo

*Patient died b24 h

of multiple electrolyte disturbances: Hyperparathyroid

Medica

pain, vomiting, associated

aVF, ??? Precordial

crisis

Iranica

fatigue/weakness for

leads (not included)

1 month

2013

Huan

Bones, groans, stones, and STEMI overtones

OHSU

68 yo male with syncopal

17.6 mg/dL

NR

STE V2-V6, subtle

(-)Enzymes/echo

event

STD III, aVF

2013

Cheng

Hypercalcemia-induced new onset left bundle branch

Acta Cardiol

78 yo female with vague

12.8 mg/dL

NR

STE V1-V4

(-)Enzymes/echo

block mimicking acute myocardial infarction in a

Sin

chest pain and lethargy for

patient with primary hyperparathyroidism

3 h

2013

Kukla

Hypercalcemia mimicking acute coronary syndrome

Kardiologia

69 yo female with chest pain

17.9 mg/dL

0.375

0.250

STE V1-V6, I, aVL

(-)Enzymes

*Translated from Polish

Polska

2013

Chhabra

Milk Alkali syndrome: an electrocardiographic

Heart

46 yo male with severe

16.0 mg/dL

0.322

STE V3-V6, I, aVL, II,

(-)Enzymes

masquerader for non-hypothermic Osborn

heartburn/Epigastric pain

III

phenomenon

2014

Schutt

Severe hypercalcemia mimicking ST-segment elevation

Methodist

65 yo female with

N 14 mg/dL

0.420

0.240

STE V1-V3

(-)Enzymes/echo

myocardial infarction

Debakey

near-syncope, vomiting, and

Cardiovasc J

fatigue

2015

Patnaik

Just hypercalcemia or acute ST elevation myocardial

BMJ Case

79 yo male with lethargy and

19.4 mg/dL

NR

0.200

STE V1-V4

(-)Enzymes

infarction – A review of hypercelcemia-related

Rep

confusion for 1 day

electrocardiographic changes

2015

Braun

Suspected hypercalcemia induced ST segment elevation

Mil Med

55 yo male with shortness of

13.0 mg/dL

“Normal”

STE V1-V5

(-)Cath

in a patient with sarcoidosis

breath and fatigue for 6 h

2015

Strand

Not all ST-segment changes are myocardial infarction:

BMJ Case

83 yo male with progressive

14.2 mg/dL

0.418

STE V1-V4, STD

(-)Enzymes/echo

Hypercalcemia-induced ST-segment elevation

Reports

shortness of breath and leg

V5-V6

swelling

2016

Nahass

Hypercalcemia-induced pancreatitis presenting with

Am J Emerg

32 yo male with sharp

17.0 mg/dL

NR

STE V1-V5

(-)Enzymes/echo

acute ST-elevations mimicking a myocardial infarction

Med

epigastric pain radiating to

the back and vomiting for

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1033.e6 E. Durant, A. Singh / American Journal of Emergency Medicine 35 (2017) 1033.e31033.e6

Table 2 (continued)

Year Author

Title

Journal

Clinical history

1 day

51 yo female with epigastric pain and exertional dyspnea for 1 week

Ca

2016 Manne

STriking resemblance: Calcium-alkali syndrome

Am J Med

Excluded 1993 Harris

Non-Hodgkin’s lymphoma – An unusual cause of myocardial infarction and hypercalcemia

Clin Oncology

66 yo male with vomiting, dehydration, and confusion

References

*Patient developed anterior chest pain/dyspnea/sweating

  1. Nierenberg DW, Ransil BJ. Q-aTc interval as a clinical indicator of hypercalcemia. Am

J Cardiol 1979:243-8.

  1. Saikawa T, Tsumabuki S, Nakagawa M, Takakurma T, Tamurama M, Maeda T, et al. QT intervals as an index of high serum calcium in hypercalcemia. Clin Cardiol 1988;11:75-8.

Notes

  1. Ahmed R, Hashiba K. Reliability of QT intervals as indicators of clinical hypercalce- mia. Clin Cardiol 1988;11:395-400.
  2. Sonoda K, Watanabe H, Hisamatsu T, Ashihara T, Ohno S, Hayashi H, et al. High fre- quency of early repolarization and Brugada-type electrocardiograms in hypercalce- mia. Ann Noninvasive Electrocardiol 2016;21:30-40.

AMI excluded by

(-)Enzymes

  1. Littmann L, Taylor III L, Brearley Jr WD. ST-segment elevation: a common finding in severe hypercalcemia. J Electrocardiol 2007;40:60-2.

(+)AMI at

autopsy

  1. Reddy CV, Gould L, Gomprecht RF. Unusual Electrocardiographic manifestations of hypocalcemia. Angiology 1974;25:764-8.
  2. Lehmann G, Deisenhofer I, Ndrepepa G, Schmitt C. ECG changes in a 25-year-old woman with hypocalcemia due to hypoparathyroidism. Hypocalcemia mimicking acute myocardial infarction. Chest 2000;118:260-2.

STE V1-V5,STD II, III,

aVF

  1. Eleftheriadis D, Fourla E, Vrizidis P. Acute myocardial infarction in a young male pa- tient with combined hormonal disorder. Chest 2002:2265-6.

STE V4-V6

  1. Ilveskoski E, Sclarovsky S, Nikus K. Severe hypocalcemia simulating ST-elevation myocardial infarction. Am J Emerg Med 2012;30:256.e253-6.
  2. Gomez-Dominguez R, Hidalgo R, Garcia-Rubira JC. Severe hypocalcemia masquerad- ing as acute coronary syndrome. J Emerg Med 2013;45:715-7.

QTc

QoTc

QaTc

ECG

16.3 mg/dL

0.440

17.5 mg/dL

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