IHJ Cardiovascular Case Reports (CVCR) 4 (2020) 135e137

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IHJ Cardiovascular Case Reports (CVCR)

journal homepage: www.elsevier.com/locate/ihjccr

Case Report

Hypocalcemia causing acute coronary syndrome*

Ujjawal Kumar a, *, Rupesh George a
a
Department of Cardiology, Amala Institute of Medical Sciences, Thrissur, Kerala, India

a r t i c l e i n f o a b s t r a c t

Article history: Hypocalcemia usually causes heart failure and rarely causes acute coronary syndrome. This is a case
Received 21 November 2019 where hypoparathyroidism and hypocalcemia presented as acute coronary syndrome. A 37 year old
Received in revised form gentleman presented with angina having ST/T changes, elevated troponin levels and wall motion ab-
12 September 2020
normality on echocardiography. He had non-obstructive coronaries. After correction of the calcium his
Accepted 27 September 2020
chest pain subsided. This is a case where hypocalcemia presented as coronary artery spasm and very few
cases have been reported due to it.
Keywords:
© 2020 Cardiological Society of India. Published by Elsevier B.V. This is an open access article under the
Hypocalcemia
Coronary artery spasm
CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
Acute coronary syndrome
Non obstructive coronary artery diasease

Introduction
Calcium plays an essential role in human body especially heart
where it is needed for myocardial contraction. Deficiency of cal-
cium manifests from asymptomatic to severe life-threatening dis-
orders like laryngeal spasm, tetany, and seizures. Common
cardiovascular manifestations of hypocalcemia are prolonged QT
interval, ventricular arrhythmia, and heart failure. However acute
coronary syndrome or coronary artery spasm have been reported
rarely due to hypocalcemia.1,2 2% of patients presenting as acute
coronary syndromes have no obstructive epicardial coronary artery
disease (CAD).3 Coronary artery spasm (CAS) plays an important
role in the pathogenesis of these patients. Here we report a 37 year
old gentleman having hypocalcemia and hypoparathyroidism who
presented with acute coronary syndrome and had non-obstructive
coronaries on angiography. On initiation of calcium supplementa-
tion, his chest pain subsided along with normalization of ECG and
ECHO features.
CASE REPORT
A 37 yr old male presented to our hospital with left-sided non-
radiating chest pain since 2 hours. There was no dyspnea,
* in corona radiation and right cerebellum suggesting typical chronic
Declarations of interest: NONE.
* Corresponding author. Department of Cardiology, Amala Institute of Medical
Sciences, Thrissur, 680555, Kerala, India.
E-mail addresses: u_kumar1@hotmail.com (U. Kumar), rupeshgeorge@gmail.
com (R. George).
palpitation or syncope nor any previous history of CAD. His mother
is suffering from CAD. He is not a smoker and having no other risk
factors. At admission his heart rate was 90 beats per minute, blood
pressure 104/70 mmHg and respiratory rate of 20 cycles per min-
ute. Clinical cardiovascular examination was normal. Other system
examination also was normal. Admission ECG showed sinus
rhythm having T inversions in lateral leads and prolonged QTc
(>460 msecs). Echocardiography showed hypokinesia of lateral and
inferolateral walls with mild LV systolic dysfunction having an
ejection fraction of 50%. His cardiac troponin-I levels were elevated
at 11.24 mg/L (reference range <0.11 m/L). Coronary angiography was
performed which revealed a normal right (RCA) and left circumflex
artery (LCX). A discrete 30% narrowing of mid left descending artery
(LAD) was seen having thrombolysis in myocardial infarction (TIMI)
3 flow. Because of adequate flow and non obstructive lesion,
medical therapy was initiated with intravenous heparin, aspirin,
clopidogrel, beta blocker and a statin. Next day he developed
cramps in his hands. His serum calcium levels was assessed which
was 7.4 mg/dl (reference range 8.62e10.2 mg/dl), ionized calcium
0.89 mmol/L (reference range, 1.13e1.32 mmol/L). Serum phos-
phorus was 3.8 mg/dl (reference range 2.5e4.5 mg/dl), PTH levels
were 14.5 pg/ml (18e88 pg/ml). Other serum electrolytes revealed
no abnormalities. Further he revealed that he underwent a CT brain
one year back due to persistent headache which showed dense
calcifications in B/L basal ganglia and thalamus and faint calcific foci
hypoparathyroidism. He continued to have chest discomfort and
was started on IV 10% calcium gluconate (0.1 g/ml) which was given
for 3 days. He was also given oral calcium supplementation 500mg

https://doi.org/10.1016/j.ihjccr.2020.09.001
2468-600X/© 2020 Cardiological Society of India. Published by Elsevier B.V. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/
licenses/by-nc-nd/4.0/).
U. Kumar and R. George IHJ Cardiovascular Case Reports (CVCR) 4 (2020) 135e137

Fig. 1. ECG at admission (before calcium correction).

three times a day along with vitamin D3 60,000U once a week
orally. Following calcium supplementation, his serum calcium
values on day 2 was 8.4 mg/dl which further improved on day
3e8.3 mg/dl and on day 4 at discharge it raised to 8.6 mg/dl. He had
improved symptomatically as well, with no chest pain or dyspnea
complaints following calcium and vitamin D supplementation.
ECHO at discharge showed no RWMA and normal LV systolic
function and T inversion on ECG had reverted to normal. The pa-
tient was continued oral supplementation with calcium and
vitamin D3 for 6 months. Thereafter, his serum calcium and levels
were normal and he remained asymptomatic after a year of follow-
up, with no further changes seen on ECG and ECHO Figs. 1e3.
Discussion
Calcium is important for normal functioning of heart and blood
vessels. It is essential for myocardial excitation-contraction
coupling. Depolarization of the sarcolemma results in calcium

Fig. 2. CT brain (plain) showing dense calcifications of thalamus and basal ganglia.

136
U. Kumar and R. George
Fig. 3. ECG after calcium correction (at discharge).
influx which induces release of calcium from the sarcoplasmic re-
ticulum, raising the concentration of intracellular calcium which
then binds to troponin C. This leads to actin-myosin interaction and
hence myocyte contraction. Similarly calcium also affects contrac-
tion of blood vessels by regulating smooth muscle cells.4 Release of
calcium from intracellular stores leads to increased calcium within
the cell, which binds to calmodulin and that causes activation of
myosin light chain kinase (MLCK). Activation of MLCK causes
smooth muscle contraction which leads to contraction of blood
vessels. Possible mechanisms of coronary artery spasm due to
hypocalcaemia causing ischemia can be due to demand-supply
mismatch. Myocardial perfusion through coronary blood flow oc-
curs during diastole, coronary artery spasm can cause ischemia if
coronary diastolic flow is reduced below a critical level leading to a
demand-supply mismatch.6 Myocardial bridging another anatomic
variant seen especially in mid-LAD can also cause ischemia by
direct compression. This compression of LAD can lead to retrograde
flow of blood in systole and increased flow velocity during early
diastole and delayed diastolic relaxation of the bridged segment
causing myocardial ischemia.7 Myocardial bridge during acute hy-
pocalcemic event can cause occlusion of the artery and lead to
ischemia.
Common cardiovascular manifestations of hypocalcemia are
long QT interval on the ECG and congestive heart failure, which are
usually reversible following correction. Acute coronary syndrome
and ST/T wave changes on ECG are rare due to hypocalcemia. Cor-
onary artery spasm occurring due to hypocalcemia is even rarer.
Here we have a case of hypoparathyroidism causing hypocal-
cemia having family history of coronary artery disease and no other
cardiac risk factors presented with acute coronary syndrome whose
coronary angiography revealed minor non obstructive disease.
Following correction of calcium levels his angina subsided along
with normalization of ECG and echocardiography. Magnus PC and
Missri J reported a case of hypocalcemia associated coronary spasm
in a 52-year-old woman who presented acute coronary syndrome
in which hypocalcemia looked the only possible explanation for the
137
IHJ Cardiovascular Case Reports (CVCR) 4 (2020) 135e137
spasm.5 Rasoul S and Dambrink reported a 42 year old lady with
recurrent acute coronary syndrome without cardiac risk factors
caused by coronary spasms, alternatively occurring in all three
major coronary arteries. This lady had bleached her hair with a
cream containing etidronate, a bisphosphonate used in hypercal-
cemia.3 They attributed hypocalcemia in causing coronary spasm.
In both the cases the patient had improved following initiation of
calcium supplementation.
Thus in our case this gentleman had non obstructive coronaries
in combination with hypocalcemia, elevated troponin I levels,
prolonged QTC and ST/T changes on ECG, wall motion abnormality
on echocardiography in the absence of other risk factors for CAD.
After starting treatment of hypocalcemia he improved symptom-
atically as well as normalization of ECG and ECHO features, this
supports the assumption of hypocalcemia related coronary spasm
more likely.
Appendix A. Supplementary data
Supplementary data to this article can be found online at
https://doi.org/10.1016/j.ihjccr.2020.09.001.
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