Journal of Cardiology Cases 10 (2014) 190192

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Journal of Cardiology Cases

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Case Report

STEMI complicated with serum sodium of 113 mmol/L from

syndrome of inappropriate antidiuretic hormone secretion:
How worse could it be?
Pongsathorn Kue-A-Pai (MD)a,*, Saranya Buppajarntham (MD)b
a
Bassett Medical Center, Columbia University, Cooperstown, NY, USA
b
Albert Einstein Medical Center, Philadelphia, PA, USA

A R T I C L E I N F O A B S T R A C T

Article history: Hyponatremia commonly occurs in acute coronary syndrome and has been recognized as a worse
Received 28 March 2014 prognostic indicator in patients with ST-segment elevation myocardial infarction (STEMI). However
Received in revised form 23 June 2014 STEMI with preexisting hyponatremia from syndrome of inappropriate antidiuretic hormone secretion
Accepted 11 July 2014
(SIADH) has never been described in the literature.
We describe a case of 59-year-old woman who presented with STEMI and received emergent
Keywords: percutaneous coronary intervention who also had SIADH with the lowest serum sodium measurement of
ST-elevation myocardial infarction
113 mmol/L. Initially, she was treated with hypertonic saline to reduce central nervous system
Syndrome of inappropriate antidiuretic
complications. Then, vasopressin receptor 2 antagonist and demeclocycline were started as well as uid
hormone secretion
Hyponatremia restriction and salt tablet. Her sodium level and clinical symptoms improved. Subsequently, we found
cavitary right upper lung mass and a biopsy report revealed small cell lung cancer as a cause of SIADH.
Severe hyponatremia from SIADH complicated with STEMI could potentially have reduced adverse
outcomes by normalizing sodium level through vasopressin receptor 2 antagonist or demeclocycline.
<Learning objective: Hyponatremia in STEMI from SIADH, prognosis, and treatment options.>
2014 Japanese College of Cardiology. Published by Elsevier Ltd. All rights reserved.

Introduction
Hyponatremia commonly occurs in acute coronary syndrome
(ACS) [1] and has been recognized as a worse prognostic indicator in
patients with ST-segment elevation myocardial infarction (STEMI)
[2]. In addition, hyponatremia is also an independent predictor of
adverse clinical outcomes in hospitalized patients due to decom-
pensated heart failure [3]. However, STEMI with preexisting
hyponatremia from syndrome of inappropriate antidiuretic hor-
mone secretion (SIADH) has never been described in the literature.
We would like to present a case of a woman with STEMI who also had
SIADH with the lowest serum sodium measurement of 113 mmol/L.
Case report
A 59-year-old female who was recently diagnosed with stage 1
breast cancer with ongoing radiation therapy, also had a history of
* Corresponding author at: Internal Medicine Department, 1 Atwell Road,
Medical Education, Cooperstown, NY 13326, USA. Tel.: +1 607 547 3956;
fax: +1 607 547 6612.
E-mail address: pongsathorn.kue-a-pai@bassett.org (P. Kue-A-Pai).
hypertension and 40-pack year smoking. Lisinopril was the only
home medication. She presented to our institution with acute
severe burning sensation in the epigastric area. The physical
examination was remarkable only for mild epigastrium tender-
ness. Laboratory test revealed a troponin of 11.46 ng/mL.
Electrocardiography revealed 3-mm elevation of ST-segment in
V2V5. The patient immediately underwent cardiac catheteriza-
tion with drug-eluting stent placement in proximal left anterior
descending artery without immediate complications. After the
procedure, the patient complained of headache, nausea, and
vomiting. Additionally, the initial electrolyte results revealed
serum sodium of 113 mmol/L with serum osmolality of
244 mOsm/kg. Symptomatic hyponatremia was a concern and
3% NaCl intravenous infusion was initiated. Other countermea-
sures included cessation and withholding of all possible medica-
tions that could cause hyponatremia including lisinopril. Further
laboratory results conrmed the diagnosis of SIADH (urine sodium
62 mmol/L, urine osmolality 547 mOsm/kg, serum glucose
140 mg/dL, serum thyroid stimulating hormone 0.55 mIU/mL,
serum cortisol 15.8 mg/dL, plasma arginine vasopressin 1.8 pg/
mL, and total cholesterol 148 mg/dL.) After her headache and
nausea improved, we stopped 3% NaCl and treated the SIADH with

http://dx.doi.org/10.1016/j.jccase.2014.07.007
1878-5409/ 2014 Japanese College of Cardiology. Published by Elsevier Ltd. All rights reserved.
 P. Kue-A-Pai, S. Buppajarntham / Journal of Cardiology Cases 10 (2014) 190192
Fig. 1. The serum sodium level during hospitalization.
1 L uid restriction and 6 g per day of salt tablet. As a consequence,
her sodium level was gradually rising but still below 125 mmol/L.
We decided to administer vasopressin receptor 2 antagonist and
demeclocycline to better control her sodium level. Slowly, her
serum sodium was trending up to 126 mmol/L. The trend of serum
sodium level is shown in Fig. 1. The 2D transthoracic echocardiog-
raphy showed reduced left ventricular function to 40% with apical
akinesis and mural thrombus at left ventricular apex. Furthermore,
her chest radiography revealed a cavitary opacity at right upper
lung (Fig. 2) which was conrmed by subsequent computed
tomography of the chest (Fig. 3). The lung biopsy result showed
small cell lung cancer which was likely a primary cause of her
SIADH. At the time magnetic resonance imaging of the brain
revealed no acute intracranial nding and no evidence of
intracranial metastases. The patient was discharged uneventfully
with triple anti-thrombotic therapy, beta blocker, and angiotensin-
converting enzyme inhibitor. Afterward, the patient developed
hemoptysis. She underwent palliative radiation for hemostasis.
Then she had 4 cycles of chemotherapy. The patient passed away 5
months later from brain metastasis.
Chest radiography demonstrated cavitary opacity in the right upper
Fig. 2.
lobe (arrow).
191
Discussion
Over time, more and more data suggested that hyponatremia
could predict worsened short- and long-term outcomes of patients
who had STEMI [2,4]. Additionally, hyponatremia patients who
had ACS were more likely to have a lower ejection fraction,
elevated creatinine on admission, and longer hospitalization
duration [5].
Several mechanisms are known to promote the development of
hyponatremia in heart failure, such as increased production and
release of vasopressin from arterial underlling [6] and upregula-
tion of vasopressin-regulated water channel (AP2) in the collecting
duct [7]. However, the mechanism of hyponatremia in ACS is not
well understood. The proposed mechanism is non-osmotic release
of vasopressin due to the acute development of left ventricular
dysfunction; similar to the response to pain and nausea/vomiting
[810].
Computed tomography of chest with contrast revealed a
4.4 cm  4.2 cm  4.0 cm ill-dened area of consolidation in the right
upper lobe with marked surrounding irregular spiculated densities,
Fig. 3.
airspace opacity, and central cavitation. There is interlobular septal
thickening of the right lung apex which may be due to lymphangitic
spread of malignancy.
192 P. Kue-A-Pai, S. Buppajarntham / Journal of Cardiology Cases 10 (2014) 190192
Recently, Qureshi et al. [5] found that achieving hyponatremia
correction in ACS demonstrated no mortality benet from
hypertonic saline and also increased readmission rates and adverse
cardiac outcomes. However, hyponatremia correction achieved
through vasopressin receptor 2 antagonist use was associated
with a signicant reduction in 30-day mortality when initial
serum sodium levels lay between 115 and 125 mEq/L. This could
be explained by intense neurohormonal activation including
vasopressin in acute phase of myocardial infarction.
Our patient, who had severe symptomatic hyponatremia from
SIADH caused by small lung cancer, was treated with hypertonic
saline, vasopressin receptor 2 antagonist, and demeclocycline
which were necessary to control her symptoms. Per Qureshi et al.,
hypertonic saline would not be the treatment of choice for
achieving hyponatremia correction in ACS, but it is the treatment
of choice for symptomatic hyponatremia. Hence the patient
received it. We hypothesize that hyponatremia from an external
cause, as SIADH from small cell lung cancer as this patient, might
have the same response and outcome as the treatment in ACS-
associated hyponatremia. So in this patient, hypertonic saline
infusion would be less likely to reduce her short- or long-term
complications from a cardiac standpoint but vasopressin receptor
2 antagonist might.
Rarely, angiotensin-converting enzyme inhibitor could cause
drug-induced SIADH. However, in drug-induced hyponatremia,
cessation of the offending agent usually resolves in the normali-
zation of serum sodium. In this case, after cessation of lisinopril,
her sodium was persistently low and we had a more convincing
reason for SIADH. So home lisinopril was resumed when she was
discharged, taking into consideration that the patient also had left
ventricular dysfunction.
Conclusion
We describe an unusual case of severe hyponatremia from SIADH
with STEMI. The knowledge of correcting hyponatremia in this
scenario is not well established. However, we believed that
successfully corrected hyponatremia through vasopressin receptor
2 antagonist or demeclocycline could potentially reduce the adverse
outcomes. Additionally, the treatment of primary lung condition
would be a denite method to normalize the sodium level.
Conict of interest
All authors have no conict of interest and no commercial or
proprietary interest in any drug, device, or equipment mentioned
in the submitted article.
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