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\begin{document}

\title{Takotsubo Cardiomyopathy in the Setting of Severe Hyponatremia and Beer
Potomania: A Case report and Review of Literature}



\author[1]{Sheriff Dodoo}%
\author[2]{Alicia  Agyemang-Sarpong}%
\author[3]{Taka Nchang}%
\author[4]{Richmond Akatue}%
\author[5]{Marcus Williams}%
\affil[1]{Piedmont Newnan Hospital}%
\affil[2]{Harvard Medical School}%
\affil[3]{WellStar West Georgia Medical Center}%
\affil[4]{Meharry Medical College}%
\affil[5]{Emory University at LaGrange}%


\vspace{-1em}



  
  \date{May 24, 2024}


\begingroup
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\selectlanguage{english}
\begin{abstract}
Takotsubo Cardiomyopathy (TC), an acute cardiac event accounting for
about 1-2\% of all acute coronary syndromes is often associated with
acute emotional stress usually in the setting of the other
cardiovascular risk factors.This case report reviews a trigger of TC
(severe hyponatremia) and the link between them.%
\end{abstract}%



\sloppy


\textbf{Takotsubo Cardiomyopathy in the Setting of Severe}

\textbf{Hyponatremia and Beer Potomania: A Case report and Review of
Literature}

Sheriff N Dodoo, MD\textsuperscript{1~}Alicia Agyemang-Sarpong,
MD\textsuperscript{2} Nchang Taka, MD\textsuperscript{3} Richmond A
Akatue, MD\textsuperscript{4} Marcus L Williams, MD\textsuperscript{5}

1. Piedmont Newnan Hospital

Department of Hospital Medicine

745 Poplar Rd,

Newnan GA 30265

\par\null

2. Harvard Medical School

Postgraduate Medical Education,

4 Blackfan Circle

Boston, MA 02115

\par\null

3. WellStar West Georgia Medical Center

Department of Cardiology

1514 Vernon Rd

LaGrange GA 30240

\par\null

4. Meharry Medical College

Department of Internal Medicine

DB Todd Jr Blvd,

Nashville, TN 37208

\par\null

5. Emory University at LaGrange

Department of Cardiology

303 Smith Street, Fl 2

LaGrange, GA 30240

\par\null

Corresponding Author

Sheriff N Dodoo

Piedmont Newnan Hospital

Department of Hospital Medicine

745 Poplar Rd,

Newnan GA 30265 Mobile 408.391.2050 sheriff.dodoo@gmail.com

\textbf{Abstract}

Takotsubo Cardiomyopathy (TC), an acute cardiac event is often
associated with acute emotional stress, usually in the setting of
cardiovascular risk factors. This case report attempts to review one of
the triggers of TC (severe hyponatremia) as well as imaging findings,
that shows the link between severe hyponatremia and TC.

\textbf{Background}

Takotsubo Cardiomyopathy (TC), first described in Japan in 1990, is an
acute cardiac condition that involves transient systolic dysfunction due
to ballooning of the apex and/or mid segments of the left ventricle.
{[}1{]} TC is also known as ``apical ballooning syndrome'',
``stress-induced cardiomyopathy'', ``broken heart syndrome'', and
``ampulla cardiomyopathy''. The name Takotsubo was derived from the
Japanese word for octopus emblematic of the appearance of the left
ventricle on ventriculography during an acute attack. The typical TC
includes apical ballooning during systole due to hypokinesis or akinesis
of the apex or mid ventricle and hyperkinesis of the basal walls.
Atypical variants of TC include hypokinesis of the mid-ventricle alone
{[}2{]}, hypokinesis of the base, and global hypokinesis. {[}3{]}

TC patients are typically postmenopausal Asian or Caucasian women.
Gianni et al reported that 88.8\% of 286 reported TC patients were
women. The mean age ranges from 61-76 years. {[}4{]} The exact
prevalence of TC is unknown, but researchers have reported that
1.7-2.2\% of suspected ACS patients have TC. {[}5-7{]}

TC is usually but not always brought on by an acute medical illness or
an intense mental or physical stressor. {[}8{]} TC patients typically
present with symptoms similar to ACS, including chest pain with
echocardiographic changes and elevated cardiac markers. However, upon
angiography no significant coronary artery obstruction is appreciated.
Sadamatsu et al reported two cases with apical wall abnormalities and
reduced coronary flow without coronary stenosis. {[}9{]}

We report a case of Takotsubo cardiomyopathy in a patient who initially
presented with severe hyponatremia from beer potomania. This patient did
not present with chest pain however, the apical ballooning and negative
coronary artery disease was discovered on left heart catherization and
ventriculogram.

\textbf{Case presentation}

A 56-year-old African American male with medical history significant for
Hypertension, Hyperlipidemia, and alcohol dependence who presented with
incoherent speech with altered mentation. He reported dyspnea with mild
exertion. He denied chest pain, orthopnea, paroxysmal nocturnal dyspnea,
or pedal swelling. He has been binge drinking several cans of beer,
about 24 of 24 -Oz can, prior to presentation. This was, following, a
sudden incarceration and imprisonment of his wife. Patient had his last
drink 5 hours prior to presentation to the Emergency room.

Examination revealed a disheveled middle age African American male who
was confused and inebriated. His Vital signs revealed blood pressure
129/67mmHg, pulse 73beats/minute, and body temperature 99.4F. He was
somnolent but easily arousable, and oriented to person, place but not to
time or situation. Neurologic examination showed no focal neurological
deficits. The rest of his physical examination yielded no addition
findings.

Laboratory investigations including biochemical and hematologic results
obtained in the ER is listed below (Table 1). This revealed serum sodium
102mmol/L, serum osmolality 245mOsm/L, urine osmolality 44mOsm/L, urine
sodium 7mmol/L, blood alcohol level 221mg/dL, and creatine kinase
7,810units/L. Random urine drug screen was positive for opiates. Initial
electrocardiogram showed normal sinus rhythm (Figure 2). Chest x ray
showed no acute cardiopulmonary process (Figure 1). About 45 minutes
after presentation at the Emergency department, he experienced violent
incessant episodes of generalized clonic-tonic seizure episode involving
all limbs. This was concerning for status epilepticus and required
sedation with phenobarbital and intubation for airway protection at the
medical intensive care unit at our community hospital. Nephrology,
critical care, and neurology consultation was subsequently placed.

Patient was given hypertonic saline with close monitoring of his serum
sodium and electrolytes. The rise in serum sodium was 0.5-1mmol/L/h,
serum sodium gradually improved to 120 over 2 days. The patient's chest
x-ray demonstrated possible right middle lobe pneumonia and he was
started on broad spectrum antibiotics of ceftriaxone and azithromycin
intravenously. The patient continued to be on mechanical ventilation and
multiple attempts at extubating failed.

Over the next 24 to 48 hours, a change was noted on telemetry monitoring
concerning for ST elevation and a 12-lead electrocardiogram showed early
repolarization abnormalities in the left lateral leads (Figure 3).
Follow up cardiac enzymes done showed troponin of 4.30 mg/mL, creatine
kinase- MB 50U/L, creatine kinase 1293U/L.'' The ST elevations did not
qualify for classification as STEMI, however, he required urgent
treatment for NSTE-ACS. The patient was, subsequently transferred to a
neighboring hospital with percutaneous coronary intervention and cardiac
catheterization capability.

He stayed on mechanical ventilation several days. Echocardiogram done
prior to the left heart catherization showed left ventricular ejection
fraction of 30\% with severe mid-distal and apical hypokinesis and
ballooning, relaxation abnormality of left ventricular hypertrophy with
mild concentric left ventricular hypertrophy were also appreciated
(Movie 1). The patient received aspirin, metoprolol and lisinopril
orally with heparin intravenously as medical therapy.

The Left Heart Catheterization (LHC) done, showed no evidence of
obstructive CAD (Figure 4). There was no evidence of coronary vasospasm.
LV angiogram showed apical ballooning and hypokinesis of anteroseptal
Left ventricle concerning for Takotsubo cardiomyopathy (Figure 5). The
patient was monitored closely after the LHC. Troponin peaked at
33.0mg/mL and subsequently trended down 0.04mg/mL, 3 days after the LHC.

He remained on hypertonic saline with increases of his serum sodium to
123mmol/L. The hypertonic saline was stopped when his serum sodium
increased to 129mmol/L. The sodium remained stable at 128 -- 130mmol/L.
He was successfully extubated, after 4 days of mechanical ventilation.
His mental status slowly improved and began to respond to commands.
Patient made steady improvement in his clinical condition, antibiotics
was discontinued and was discharge after 6 days of hospital stay.

An Echocardiogram done a month post admission during a follow up clinic
visit to our hospital showed left ventricular ejection fraction of 55\%
with resolution of apical hypokinesis and ballooning (Movie 2).

\textbf{Discussion}

The patient's initial presentation of a low serum sodium of 101mmol/L
raised the possibility of number of differential diagnoses including
syndrome of inappropriate anti diuretic hormone (SIADH), dehydration,
congestive heart failure, chronic kidney disease, cerebral- wasting
syndrome, psychogenic polydipsia, and beer potomania. Low urine
osmolarity and low urine sodium levels excluded dehydration, SIADH and
cerebral wasting syndrome as the cause of this patient's hyponatremia
{[}34{]}. The patient's denial of drinking excessive water, also ruled
out psychogenic polydipsia. This patient's noncontributory initial
physical examination, along with chest x-ray without any acute
intrathoracic process with a normal BNP and renal function essentially
ruled out congestive heart failure and renal insufficiency.

His history of alcohol abuse, including clinical presentation of
lethargy and disheveled appearance, along with his laboratory work up of
low serum osmolarity, urine osmolarity and low urine sodium results and
absence of possible explanation, led us to the possibility of beer
potomania accounting for the patient's hyponatremia.

Our eventual working diagnosis of the patient's hyponatremia was likely
related to alcohol, and hence, the patient possibly, had beer potomania
evidenced by low urine sodium and severe hyponatremia. This together led
to the Status epilepticus our patient experienced. We hypothesize that
his severe hyponatremia may have cause the Takotsubo cardiomyopathy
(TC), especially in the context of epileptic seizures. The TC evidenced
by the absence of coronary artery stenosis on LHC and presence of apical
ballooning on ventriculogram and echocardiogram. This was buttressed by
a low left ventricular ejection fraction of 30\% and its eventual
improvement to 55\% over a relatively short period of time of a month.

The pathogenesis of TC is not fully understood but the proposed
mechanisms include endogenous catecholamine excess, multi-vessel
coronary artery vasospasm, and microvascular dysfunction. The most
favored mechanism is endogenous catecholamine excess leading to
microvascular spasm or dysfunction resulting in myocardial stunning
{[}8{]}. Others have also discussed a direct toxicity of cardiomyocyte
from the large amount of circulating catecholamines {[}19{]}.

In support of the endogenous catecholamine excess hypothesis, a mouse
model showed that a high level of epinephrine had negatively inotropic
effect on cardiomyocytes due to a switch from beta-2 adrenoceptor Gs
protein signaling to Gi protein signaling. It is speculated that the
effect is greatest on the apex of the myocardium because of a higher
density of beta-2 adrenoceptors. {[}20{]}

Additionally, Ellison et al found that high doses of isoproterenol cause
diffuse death of myocytes while sparing cardiac stem cells in rats
allowing for rapid recovery of the myocardium. {[}21{]}

Akashi et al in another study, reported that TC patients had an
increased myocardial \textsuperscript{123}I-metaodobenzlguanide
(\textsuperscript{123}I-MBG) washout rate which indicates an increased
norepinephrine release from sympathetic nerve endings or increased
clearance of \textsuperscript{123}I-MBG by extra neural tissues.
Ultimately the increased wash out rate correlated to increased plasma
norepinephrine levels in TC patients. {[}22{]}

There are a few case reports of TC in the setting of moderate to severe
hyponatremia described in the body of literature. {[}10,12,30-33{]}

Hyponatremia has not been thought to be linked to Takotsubo
cardiomyopathy but perhaps may have an indirect causal relationship. The
prevailing theory of this indirect causal relationship is a stress
induced catecholamine storm causing a direct toxic effect on the
myocardium or indirect effect by coronary vasculature constriction. The
mechanistic connection is still not clear; however, it has been
suggested that hyponatremia could interfere with myocardial inotropy by
modifying the cardiomyocytic sodium-calcium exchange pump resulting in
myocardial swelling associated with hypotonicity. {[}10{]}

Indeed, transient positive inotropic effects on the myocardium were
observed in rat hearts, and the degree of positive inotropy correlated
with the degree of hyponatremia {[}11{]}. There have been cases reported
of Takotsubo cardiomyopathy in the setting of ``isolated hyponatremia''
and it has been suggested that in post-menopausal women presenting with
acute coronary syndrome-like symptoms and hyponatremia, Takotsubo
cardiomyopathy should be considered within the differential diagnoses.
{[}12{]}

Takotsubo cardiomyopathy arising as a direct consequence of hyponatremia
is an unexplored mechanism for this poorly understood disease process.
The prevailing theories for the pathogenesis of TC involves excessive
catecholamine action on the myocardium causing stunning either directly
or through ischemia by causing multi-vessel epicardial or microvascular
spasm. {[}13{]}

There has also been a long-recognized connection between TC and stress,
particularly strong emotional stress, which suggests that there may be a
neurohumoral connection that precipitates TC. Interestingly, TC has been
found in cases of subarachnoid hemorrhage and stroke, and neurologists
have advanced the idea ``neurogenic stunning'' to describe this
reversible cardiomyopathy in the setting of brain injury in the absence
of coronary artery disease {[}13{]} Norepinephrine release in the
myocardium is increased as a result of hypothalamic ischemia from a
subarachnoid hemorrhage, and may be the cause of the myocardial injury
observed {[}14{]}

Furthermore, this neurogenic stunning effect is dampened when there is a
disruption of neural innervation of the myocardium as in diabetes or
heart transplant {[}15{]}. Neurocardiac lesions also occur in
adrenalectomized animals, but to a lesser extent, further strengthening
the neurogenic stunning theory. {[}16{]}

Although ischemia as a direct cause of TC is still being debated, the
dysfunctional myocardium in TC follows a neural rather than vascular
distribution, as there is a much higher concentration of adrenergic
receptors in areas around myocardial arterioles than in areas adjacent
to epicardial coronary arteries. {[}17{]}

\textbf{Conclusions}

TC's preferential effects on the sub-endocardial myocytes manifests as
an increased propensity for arrhythmia; this combined with excessive
catecholamines, which can induce arrhythmia even in healthy myocardium,
may be a major cause of sudden death in neurologic disease including
subarachnoid hemorrhage, stroke, head trauma and increased intracranial
pressure. With the wealth of evidence connecting the brain's effect on
the heart, perhaps hyponatremia indirectly causes TC by first causing
cerebral edema. The resulting neurological disturbance results in
excessive catecholamine action on the myocardium which manifests as TC.

\textbf{Availability of data and materials}

Available on demand

\textbf{Abbreviations}

\textbf{ACS:} Acute coronary syndrome

\textbf{CAD:} Coronary artery disease

\textbf{CK:} Creatine kinase

\textbf{CKMB:} Creatine Kinase Myocardial Band

\textbf{DM:} Diabetes Mellitus

\textbf{EKG:} Electrocardiogram

\textbf{HTN:} Hypertension

\textbf{HLD:} Hyperlipidemia

\textbf{LHC:} Left Heart Catherization

\textbf{LV:} Left Ventricle

\textbf{MI:} Myocardial Infarction

\textbf{NSTE-ACS:} Non ST Elevation Acute Coronary Syndrome

\textbf{PCI:} Percutaneous Coronary Intervention

\textbf{STEMI:} ST Elevation Myocardial Infarction

\textbf{TC:} Takotsubo Cardiomyopathy

\textbf{Authorship List}

1. S.N. Dodoo: Piedmont Newnan Hospital, Department of Hospital
Medicine, 745 Poplar Rd, Newnan GA 30265.

2. A. Agyemang-Sarpong: Harvard Medical School, Postgraduate Medical
Education, 4 Blackfan Circle~{Boston, MA 02115}

3. N. Taka: WellStar West Georgia Medical Center, Department of
Cardiology, 1514 Vernon Rd, LaGrange, GA 30240

4. R.A. Akatue: Meharry Medical College, Department of Internal
Medicine, 1005 DB Todd Jr Blvd, Nashville, TN 37208

5. M.L. Williams: Emory University at LaGrange, Department of
Cardiology, 303 Smith St, LaGrange, GA 30240

\textbf{Author Contributions}

SND conceived the case report, acquired the progress reports, drafted
the initial manuscript, reviewed, and revised the manuscript. SND, AAS,
NT, RAA, MLW reviewed and revised the manuscript. All authors read and
approved the final manuscript.

\textbf{Corresponding Author}

Correspondence to S.N. Dodoo.

Sheriff.dodoo@gmail.com

\textbf{Acknowledgements}

Not applicable.

\textbf{Funding}

No funding was secured for this study.

\textbf{Ethics approval and consent to participate.}

Not applicable.

\textbf{Consent for publication}

Written informed consent was obtained from the patient for publication
of this case report.

and any accompanying images. A copy of the written consent is available
for review by

the Editor-in-Chief of this journal.

\textbf{Competing interests}

The authors declare that they have no competing interest to disclose.

\textbf{References}

\begin{enumerate}
\tightlist
\item
  Sato H, Tateishi H, Uchida T, et al. Takotsubo type cardiomyopathy due
  to multivessel spasm. In: Kodama K, Haze K, Hon M, eds. \emph{Clinical
  aspect of myocardial injury: from ischemia to heart failure} , Kagaku
  Hyoronsha, Tokyo, 1990, pp. 56--64 {[}in Japanese{]}.
\item
  Eitel, Ingo, et al. ''Clinical characteristics and cardiovascular
  magnetic resonance findings in stress (takotsubo)
  cardiomyopathy.''\emph{Jama} 306.3 (2011): 277-286.
\item
  Win, Cho M., Amit Pathak, and Maya Guglin. ''Not Takotsubo: A
  Different Form of Stress-Induced Cardiomyopathy---A Case
  Series.''\emph{Congestive Heart Failure} 17.1 (2011): 38-41.
\item
  Akashi YJ, Barbaro G, Sakurai T, et al. Cardiac autonomic imbalance in
  patients with reversible ventricular dysfunction Takotsubo
  cardiomyopathy. \emph{Q J Med} . 2007; 100:335-343.
\item
  Bybee KA, Prasad A, Barsness GW, et al. Clinical characteristics and
  thrombolysis in myocardial infarction frame counts in women with
  transient left ventricular apical ballooning syndrome. \emph{Am J
  Cardiol} . 2004; 94:343-346.
\item
  Akashi, Yoshihiro J., et al. ''Takotsubo cardiomyopathy a new form of
  acute, reversible heart failure.'' \emph{Circulation} 118.25 (2008):
  2754-2762.
\item
  Matsuoka K, Okubo S, Fujii E, et al. Evaluation of the
  arrhythmogenecity of stress-induced ``Takotsubo cardiomyopathy'' from
  the time course of the 12-lead surface electrocardiogram. \emph{Am J
  Cardiol} . 2003; 92:230-233.
\item
  Gianni M, Dentali F, Grandi AM, et al. Apical ballooning syndrome or
  Takotsubo cardiomyopathy: a systematic review. \emph{Eur Heart J} .
  2006; 27:1523-1529.
\item
  Sadamatsu K, Tashiro H, Maehira N, et al. Coronary microvascular
  abnormality in the reversible systolic dysfunction observed after
  noncardiac disease. \emph{Jpn Circ J} . 2000; 64:789-792.
\item
  Santos M., Dias V., Meireles A., Gomes C., Luz A., Mendes D., Caiado
  L, Carvalho H, Cabral S, \& Torres S. (2011). Hyponatremia -- an
  unusual trigger of Takotsubo cardiomyopathy. \emph{Revista Portuguesa
  De Cardiologia (English Edition),} \emph{30} (11), 845-848.
  doi:10.1016/ j.repc.2011.09.006
\item
  Kolar F, Cole WC, Ostadal B, \& Dhalla NS. Transient inotropic effects
  of low extracellular sodium in perfused rat heart. \emph{American
  Journal of Physiology -- Heart and Circulatory Physiology, 259} (3)
  H712-H719. Retrieved June 29, 2015, from
  http://ajpheart.physiology.org/content/259/3/H712
\item
  Abouezzeddine O., \& Prasad A. (2010). Apical ballooning syndrome
  precipitated by hyponatremia. \emph{International Journal of
  Cardiology,} \emph{145} (1), E26-E29. Retrieved June 29, 2015, from
  http://www.sciencedirect.com/science/article/pii/S0167527308015234
\item
  Prasad A., Lerman A., \& Rihal C. (2008). Apical ballooning syndrome
  (Tako-Tsubo or stress cardiomyopathy): A mimic of acute myocardial
  infarction. \emph{American Heart Journal,} \emph{155} (3), 408-417.
  Retrieved June 29, 2015, from
  http://www.sciencedirect.com/science/article/pii/S0002870307009143
\item
  Kono T., Morita H., Kuroiwa T., Onaka H., Takatsuka H., \& Fujiwara A.
  Left ventricular wall motion abnormalities in patients with
  subarachnoid hemorrhage: Neurogenic stunned myocardium. \emph{Journal
  of the American College of Cardiology,} \emph{24} (3), 636-640.
  doi:10.1016/0735-1097(94)90008-6
\item
  Samuels M. (2007). The Brain-Heart Connection. \emph{Circulation,2007}
  (116), 77-84. doi:10.1161/CIRCULATIONAHA.106.67899
\item
  Hawkins WE, Clower BR. Myocardial damage after head trauma and
  simulated intracranial haemorrhage in mice: the role of the autonomic
  nervous system. \emph{Cardiovasc Res.} 1971; 5: 524--529
  Doi:http://dx.doi.org/10.1093/cvr/5.4.524
\item
  Murphree, S., \& Saffitz, J. (1987). Quantitative autoradiographic
  delineation of the distribution of beta- adrenergic receptors in
  canine and feline left ventricular myocardium. \emph{Circulation
  Research,} \emph{1987} (60), 568-579. doi: 10.1161/01.RES.60.4.568
\item
  Dote K, Sato H, Tateishi H, Uchida T, and Ishihara M. Myocardial
  stunning due to simultaneous multivessel coronary spasms: a review of
  5 cases. J Cardiol 1991; 21:203--14.
\item
  Nef, Holger M., et al. ''Tako-Tsubo cardiomyopathy: intraindividual
  structural analysis in the acute phase and after functional
  recovery.''\emph{European heart journal} (2007).
\item
  Lyon, Alexander R., et al. ''Stress (Takotsubo) cardiomyopathy---a
  novel pathophysiological hypothesis to explain catecholamine-induced
  acute myocardial stunning.'' \emph{Nature clinical practice
  Cardiovascular medicine} 5.1 (2008): 22-29.
\item
  Ellison GM, Torella D, Karakikes I, et al. Acute \selectlanguage{ngerman}ß-adrenergic overload
  produces myocyte damage through calcium leakage from ryanodine
  receptor 2 but spares cardiac stem cells. \emph{J Biol Chem} . 2007;
  282:11397-11409
\item
  Akashi YJ, Nakazawa K, Sakakibara M, et al. 123I-MIBG myocardial
  scintigraphy in patients with ``Takotsubo'' cardiomyopathy. \emph{J
  Nucl Med} . 2004; 45:1121-1127.
\item
  Rivera~JM1,~Locketz AJ,~Fritz KD,~Horlocker TT,~Lewallen DG,~Prasad
  A,~Bresnahan JF,~Kinney MO Broken heart syndrome'' after separation
  (from OxyContin). Mayo Clin Proc.~2006 Jun;81(6):825-8
\item
  Dib C, Asirvatham S, Elesber A, Rihal C, Friedman P, Prasad a.
  Clinical correlates and prognostic significance of
  electrocardiographic abnormalities in apical ballooning syndrome
  (Takotsubo/stress-induced cardiomyopathy).
\item
  Cocco G, Chu D: Stress-Induced Cardiomyopathy: A Review. Eur J Int
  Med, 2007; 18: 369--79
\item
  Patel HM, Kantharia BK, Morris DL et al: Takotsubo Syndrome in
  African-American Women with Atypical Presentations: A Single-Center
  Experience. Clin Cardiol, 2007; 30: 14--18
\item
  Kurisu S, Sato H, Kawagoe T et al: Tako-Tsubo-Like Left Ventricular
  Dysfunction with ST-Segment Elevation: A Novel Cardiac Syndrome
  Mimicking Acute Myocardial Infarction. Am Heart J, 2002; 143: 448--55
\item
  Ogura R, Hiasa Y, Takahashi T et al: Specific Findings of the Standard
  12-Lead ECG in Patients with ``Takotsubo'' Cardiomyopathy: Comparison
  with the Findings of Acute Anterior Myocardial Infarction. Circ J,
  2003; 67: 687--90
\item
  Segovia Cubero J, Peraira Moral R: Transient apical ballooning
  syndrome: a transition towards adulthood. Rev Esp Cardiol, 2004; 57:
  194-- 97 {[}in Spanish with English abstract{]}
\item
  M.I. Worthley, T.J. Anderson, Transient left ventricular apical
  ballooning syndrome following a hyponatremic seizure, Int. J. Cardiol.
  115 (2007) e102--e104.
\item
  D.M. Lemke, S.I. Hussain, T.J. Wolfe, et al., Takatsubo cardiomyopathy
  associated with seizures, Neurocrit. Care. 9 (2008) 112--117.
\item
  H Kawano, Y. Matsumoto, S. Arakawa, et al., Takatsubo cardiomyopathy
  in a patient with severe hyponatremia associated with syndrome of
  inappropriate antidiuretic hormone, Intern. Med. 50 (2011) 727--732.
\item
  O. Sagiv, S. Vukelic, S. Czak, F. Messineo, Coplan, Apical ballooning
  syndrome associated with isolated severe hyponatremia: case report and
  suggested pathophysiology, Rev. Cardiovasc. Med. 13 (2012) e198--e202
\item
  Nakajima H, Okada H, Hirose K, et al., Cerebral salt-wasting syndrome
  and inappropriate antidiuretic hormone syndrome after subarachnoid
  hemorrhaging.. Intern Med. 2017;56:677--680.
\end{enumerate}\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/Figure-1-Initial-Chest-Xray-showing-no-acute-cardiopulmonary-process/Figure-1-Initial-Chest-Xray-showing-no-acute-cardiopulmonary-process}

\end{center}
\end{figure}\selectlanguage{english}
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\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/Figure-2-Initial-Electrocardiogram-showing-normal-sinus-rhythm/Figure-2-Initial-Electrocardiogram-showing-normal-sinus-rhythm}

\end{center}
\end{figure}\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/Figure-3-EKG-showed-early-repolarization-abnormality-in-the-left-lateral-leads/Figure-3-EKG-showed-early-repolarization-abnormality-in-the-left-lateral-leads}

\end{center}
\end{figure}\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/Fig-4-Heart-Catheterization/Fig-4-Heart-Catheterization}

\end{center}
\end{figure}\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/Figure-5-Left-Ventriculogram-showing-apical-ballooning/Figure-5-Left-Ventriculogram-showing-apical-ballooning}

\end{center}
\end{figure}

\textbf{Hosted file}

\verb`Table 1- Laboratory investigations.docx`  available at \url{https://authorea.com/users/501217/articles/581819-takotsubo-cardiomyopathy-in-the-setting-of-severe-hyponatremia-and-beer-potomania-a-case-report-and-review-of-literature}

\textbf{Hosted file}

\verb`Movie 1-Echo  apical ballooning consistent with TC (1).mp4`  available at \url{https://authorea.com/users/501217/articles/581819-takotsubo-cardiomyopathy-in-the-setting-of-severe-hyponatremia-and-beer-potomania-a-case-report-and-review-of-literature}

\textbf{Hosted file}

\verb`Movie 2-  follow up Echo  resolution of apical ballooning.mp4`  available at \url{https://authorea.com/users/501217/articles/581819-takotsubo-cardiomyopathy-in-the-setting-of-severe-hyponatremia-and-beer-potomania-a-case-report-and-review-of-literature}

\selectlanguage{english}
\FloatBarrier
\end{document}

