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\begin{document}

\title{Left ventricular non-compaction in a case of juvenile systemic lupus
erythematosus and Hashimoto's thyroiditis}



\author[1]{Olfa Jomaa}%
\author[1]{Olfa Berriche}%
\author[1]{Sondess Arfa}%
\author[2]{marwa ben brahim}%
\author[3]{Mabrouk Abdelaaly}%
\author[4]{Mouna Braham}%
\author[1]{Haifa Hachfi}%
\author[1]{Mohamed Younes}%
\author[5]{Sonia Hammemi}%
\affil[1]{Tahar Sfar university Hospital}%
\affil[2]{Endocrinology  and Internal medicine Department, Taher Sfar University Hospital, Mahdia , Tunisia}%
\affil[3]{Department of Medical Imaging, Fattouma Bourguiba University Hospital, Monastir, 5000, Tunisia}%
\affil[4]{Rheumatology Department, Taher Sfar University Hospital Mahdia, Tunisia}%
\affil[5]{Department of Endocrinology and Internal Medicine, Fattouma Bourguiba University Hospital, Monastir, 5000, Tunisia }%


\vspace{-1em}



  
  \date{May 15, 2024}


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\selectlanguage{english}
\begin{abstract}
We reported one of the rare, documented cases of a girl with LVNC
associated jSLE with a past history of Hashimoto's thyroiditis.Thus, the
association between jSLE, and LVNC should be considered, and requires
further research in order to find the probable mechanism joining both
entities.%
\end{abstract}%



\sloppy


Left ventricular non-compaction in a case of juvenile systemic lupus
erythematosus and Hashimoto's thyroiditis

Olfa Jomaa\textsuperscript{2}, Olfa Berriche\textsuperscript{1,3,4},
Sondess Arfa\textsuperscript{1,3}, Marwa Ben
Brahim\textsuperscript{1,3,4}, Mabrouk
Abdeaaly\textsuperscript{3-6},Mouna Brahem\textsuperscript{2,3}, Haifa
Hachfi\textsuperscript{2,3}, Mohamed Younes\textsuperscript{2,3}, Sonia
Hammami\textsuperscript{3-5}

\textsuperscript{1}Endocrinology and Internal medicine Department,Taher
Sfar University Hospital Mahdia, Tunisia

\textsuperscript{2}Rheumatology Department, Taher Sfar University
Hospital Mahdia, Tunisia

\textsuperscript{3}Faculty of Medicine, University of Monastir,
Monastir, 5000, Tunisia

\textsuperscript{4}Biochemistry Laboratory, LR12ES05 LR-NAFS
Nutrition-Functional Food and Vascular Health, Faculty of Medicine,
University ofMonastir, Monastir, 5000, Tunisia

\textsuperscript{5}Department of Endocrinology and Internal Medicine,
Fattouma Bourguiba University Hospital, Monastir, 5000, Tunisia

\textsuperscript{6} Department of Medical Imaging, Fattouma Bourguiba
University Hospital, Monastir, 5000, Tunisia

\textbf{Correspondent Author:}

\textbf{Olfa Jomaa, MD}

\textbf{Medical Doctor}

Endocrinology and Internal medicine Department, TaherSfar University
Hospital

Taher Sfar Street, 5100 Mahdia, Tunisia.

Phone: +216 97~776 378

Mail: \emph{olfajomaa2@gmail.com}

\emph{ORCiD~: 0000-0002-3688-5264}

Consent~: Written informed consent was obtained from the parent of
patient to publish this report in accordance with the journal's patient
consent policy''

\textbf{Clinical message}

Left ventricular non compaction (LVNC) is a structural abnormality of
the left ventricular myocardium of unknown cause. It occurs in isolation
or associated with neuromuscular disorders (NMDs). However, its
association with jSLE was rarely described. Herein, We reported one of
the rare, documented cases of a girl with LVNC associated jSLE with a
past history of Hashimoto's thyroiditis. The association between jSLE,
and LVNC requires further research in order to find the probable
mechanism joining both entities.

\textbf{ABSTRACT}

\textbf{Background:} Left ventricular non compaction (LVNC) is a
structural abnormality of the left ventricular myocardium of unknown
cause. Cardiovascular system involvement is an important manifestation,
in juvenile systemic lupus erythematosus (jSLE), considered as a leading
cause of morbidity and mortality. Pericardium, myocardium, endocardium,
heart valves, coronary vessels, and cardiac autonomic functions may be
affected in jSLE patients. LVNC occurs in isolation or associated with
neuromuscular disorders (NMDs). However, its association with jSLE was
rarely described.

Herein, We aimed to present a case of a jSLE patient with
LVNC.\textbf{Case presentation:} According to the SLICC 2012 criteria, a
15-year-old girl was diagnosed with jSLE with a past history of
Hashimoto's thyroiditis presented with paroxysmal chest pain, exertional
dyspnea, headache, and polyarthralgia. Clinical examination revealed a
febrile patient. There was no polypnea, no evidence of right heart
failure, no audible murmur on cardiac auscultation, and no edema of the
lower limbs. The biological analysis revealed a Leucopenia, anemia,
elevated erythrocyte sedimentation rate and C-reactive protein. The
immunological test revealed homogeneous antinuclear antibodies at 1/10
000 with the positivity of both anti-native DNA and anti-SSA antibodies.
The electrocardiogram showed sinus tachycardia and a cardiac magnetic
resonance imaging (CMRI) was performed confirming the non-compaction of
the LV with an hypertrabeculated sub-endocardium. The patient received
high-dose corticosteroids associated with beta-blocker therapy with a
favorable outcome. \textbf{Conclusion:} We reported one of the rare,
documented cases of a girl with LVNC associated jSLE with a past history
of Hashimoto's thyroiditis. Thus, the association between jSLE, and LVNC
should be considered, and requires further research in order to find the
probable mechanism joining both entities.

\textbf{Key words}

Left ventricular non compaction, Juvenile systemic lupus erythematosus,
Left ventricular hypertrabeculation

\textbf{Background}

Left ventricular noncompaction (LVNC) is a rare genetic cardiomyopathy
with a structural abnormality of the left ventricular (LV) myocardium of
unknown cause (1), characterized by excessively prominent trabeculations
and associated deep recesses that communicate with the ventricular
cavity (2). Heart failure, systemic embolism and arrhythmias are
cardinal findings (3). LVNC occurs isolated or in association with
neuromuscular disorders (NMDs) (4).LVNC can rarely be asymptomatic and
manifest later in life following other unrelated conditions that lead to
exacerbation in contractile dysfunction (5). However, its association
with jSLE was rarely described (6,7). jSLE is known to be associated
with a higher incidence of arthritis, nephritis, haematologic and
neurologic manifestations than that seen in adult-onset disease (8). In
particular, adolescent-onset systemic lupus erythematosus is associated
with more aggressive disease (9). Overall, less than 10\% of jSLE
patients have severe cardiovascular system involvement at presentation
(10). It is an important manifestation as it is now considered a leading
cause of morbidity and mortality in jSLE (11). Pericardium, myocardium,
endocardium, heart valves, coronary vessels, and cardiac autonomic
functions may be affected in jSLE patients (12).

\textbf{Case presentation}

According to the SLICC 2012 criteria (13), a 15-year-old girl of African
ethnicity was diagnosed with jSLE with a past history of Hashimoto's
thyroiditis treated by L-thyroxine presented with paroxysmal
constructive chest pain, Exertional dyspnea, headache, and
polyarthralgia. She also reported photosensitivity. On systemic review,
the patient did not report either an upper airways infection preceding
her complaints or any other associated general or specific symptom.
Clinical examination revealed a fever of 39\selectlanguage{ngerman}° C with blood pressure of
100/60 mmHg. There was no polypnea, no evidence of right heart failure,
no audible murmur on cardiac auscultation, and no edema of the lower
limbs. The biological analysis revealed a Leucopenia (3500/mm3), anemia
(10g/dl), elevated erythrocyte sedimentation rate
(ESR\textbackslash{}1st h = 50 mm\textbackslash{}h at the first hour,
C-reactive protein (20 mg/l) and a direct Coombs test that was negative.
Infections were excluded~ with multiple negative blood cultures, as well
as for anti-streptolysin O antibodies.~ The immunological test revealed
homogeneous anti-nuclear antibodies at 1/10,000 with the positivity of
anti-native DNA antibodies (32 IU/ml) and anti-SSA antibodies.
Antiphospholipid antibodies: anti cardiolipin anti beta 2 glycoprotein,
were negative. The electrocardiogram showed sinus tachycardia, and the
chest X-ray was free of cardiomegaly and pleural effusion. However, the
transthoracic echocardiography has objectified a pericardidtis
associated with a non-compacted LV, nodular thickenings of a few
millimeters on the mitral valve with a small pericardial effusion. Thus,
a cardiac magnetic resonance imaging (CMRI) was performed confirming the
non-compaction of the LV with an hypertrabeculated sub-endocardium in
the distal and apical regions (Figure 1, 2, and 3), with foci of
fibrosis at the level of the cryptic fundus and a global hypokinesia of
the LV. The systemic review did not reveal any proteinuria,
hypocomplementemia or cerebral vasculitis on cerebral magnetic resonance
imaging (MRI). Our patient was treated by high doses of corticosteroids
(0,5mg/kg/j) associated with beta-blocker therapy with favourable
outcome. The 2-year follow-up was characterized by a stabilized disease,
without relapses on low dose corticosteroids.

\textbf{Discussion}LVNC, also known as hypertrabeculation
cardiomyopathy, or spongy myocardium, is currently a rare disease listed
as an unclassified cardiomyopathy (CM) by the World Health Organization
(WHO) (14) and the European Society of Cardiology (ESC) (15), and
classified as a genetic CM by the American Heart Association (AHA) (16).
The other proposed mechanism for the development of LVNC was acquired
microcirculatory dysfunction leading to microinfarcts and
hypertrabeculation. In addition, patients with chronically high preload
or afterload, have a high prevalence of trabeculations and may also
fulfill the criteria for LVNC (5,17).The reported incidence of LVNC is
0.05\%, its prevalence is often underestimated and appears to be
significantly higher in children than in adults (18). Cardiac
involvement is certainly not uncommon in jSLE (19), with a prevalence of
50\% (20). All three layers of the heart-pericardium, myocardium, and
endocardium-can be affected by jSLE. Pericarditis is the most common
cardiac manifestation of jSLE, occurring in up to 25\% of patients (21).
Clinical detection of myocarditis, which is the most characteristic
feature of myocardial involvement in jSLE, ranges from 3\% to 15\% (22).
In a study of children with primary CM of all types, LVNC was present in
9.2\% of cases, making it the third most common type of primary CM after
dilated CM and hypertrophic CM (23). LVNC is due to the failure of
condensation of the myocardial spongy meshwork of fibers and
intertrabecular recesses during intrauterine life leading to the
persistence of ventricular trabeculations (24). Trabecular compaction
occurs between 12 and 18 weeks of gestation, beginning at the base of
the heart and progressing toward the apex (25). For unknown reasons, in
patients with LVNC, this transition does not occur, resulting in the
development of a thickened, noncompacted endomyocardial layer with
prominent trabeculations that are continuous with the LV cavity and do
not communicate with the epicardial circulation, deep recesses, and a
thin, compacted epicardial layer (25). Approximately two-thirds of
patients with LVNC may have NMDs (4), including myotonic dystrophies,
dystrophinopathies, Charcot-Marie-Tooth disease, Barth syndrome,
Friedreich's ataxia, and Pompe disease (26). Thus, Patients with such
NMDs should be screened promptly for CM (27). Men are more frequently
affected by LVNC than women (28). LVNC is more prevalent in blacks (29)
and that was the case of our patient who is a black ethnic background
girl. This CM can occur at any age, ranging from early infancy to late
adulthood or even remain completely asymptomatic, as shown by cases
discovered accidentally (30). Median age at diagnosis is 40- 50 years in
adults, and 5-7 years in pediatric patients (28, 31). The age at
diagnosis in our patient was 15 years. The clinical presentation is
highly variable, LVHT is usually diagnosed when the condition becomes
symptomatic or when complications occur (32). Reasons for consultation
include often unexplained heart failure, palpitations or exertional
dyspnea, chest pain, or syncope (33). Such was the case with our
patient, whose reason for consultation was chest pain with exertional
dyspnea. Meanwhile, the classical triad of heart failure (HF),
ventricular arrhythmias, and systemic embolism constitute typical
complications of this disease (33). No electrical signs are specific for
LVNC, but electrocardiograms (ECG) should be performed routinely in LVNC
cases, as they can show rhythm and conduction disorders of varying
severity, signs of myocardial hypertrophy, ST segment changes, bundle
branch blocks or ventricular extrasystoles (34). The frequency of ECG
abnormalities is high: 88\% in pediatric patients (35). A sinus
tachycardia was noted in our patient. Echocardiography, and CMRI are the
gold standard tests for LVNC diagnosis (36). Transthoracic
echocardiography (TTE), because of its simplicity, is the most commonly
used technique. It shows the presence of criteria leading to the LVNC
suspicion (37) such us: presence of multiple left ventricular
trabeculations, presence of deep intertrabecular recesses, color doppler
flow within the recesses and in communication with the LV cavity.
Classically, when the ratio of non-compacted area to compacted area is
greater than 2, LVNC diagnosis is made (38). In doubtful cases, CMRI
provides similar diagnostic elements, allowing perfect visualization of
the trabeculations and recesses as well as their localization ( 39). It
confirm echographic findings, detect subtle patterns, assess myocardial
damage level, obtain data on myocardial perfusion, assess myocardial
fibrosis, identify ventricular thrombi, and distinguish between LVNC and
other potential diagnoses (39). Real-time 3D echocardiography is another
newly introduced method, which allows a more accurate quantification of
the number of trabeculations and left ventricular mass (40). Our patient
had both TTE and CMRI, and was diagnosed with LVNC by both methods. At
present, no consensus for the diagnostic criteria for LVNC and the best
diagnostic methods (32). Pathoanatomical findings currently seem to be
the gold standard for diagnosing LVHT (41). Currently, there is no
specific option for the LVNC treatment, which is the same as for HF (
42). There are three main goals of treatment: treatment of HF,
antiarrhythmic therapy, and antithrombotic therapy to prevent systemic
embolism in patients with impaired LV function ( 33). The prognosis for
patients with LVNC is extremely variable, ranging from a prolonged
asymptomatic course to rapidly progressive HF, which may lead to heart
transplantation or death. More recent publications, report a mortality
rate ranging from 2\% to 15\% (3) with the highest risk of death
associated with ventricular arrhythmias and HF (24). In 2007, a LVNC was
reported in a patient with Behçet's disease with multiple thrombus
formations (43). Another patient with ankylosing spondylitis also had
features of LVNC (44). Recently, a CM strongly resembling LVNC was
described in a patient with proliferative lupus nephritis (45). Also,
When reviewing literature, there are reports on association of LVNC
with, endocrine abnormalities including hypothyroidism (46)\emph{.} The
current case describes the features of LVNC in a patient with jSLE and
Hashimoto's thyroiditis. LVNC might represent more a morphologic
expression of different underlying morbidities than a distinct CM,
according to some group of authors (47). If these underlying disorders
include jSLE and other connective tissue disorders, it is an open
question.

\textbf{Conclusion}

Currently, we reported one of the rare, documented cases of a girl with
LVNC in a case of jSLE and Hashimoto's thyroiditis. Thus, The
association between jSLE and LVNC may not be coincidental given the
multiplicity of cases reporting such an association. Therefore, it is
necessary to consider this association, which probably requires further
research to find the plausible mechanism joining both entities.

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\includegraphics[width=0.70\columnwidth]{figures/image1/image1}

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Figure 1\selectlanguage{english}
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\includegraphics[width=0.70\columnwidth]{figures/image2/image2}

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Figure 2\selectlanguage{english}
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\includegraphics[width=0.70\columnwidth]{figures/image3/image3}

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Figure 3

Cardiac magnetic resonance imaging, short-axis (Figure 1,2) and 4-cavity
(Figure 3) sections~ showing~ hypertrabeculation of the left ventricular
wall, particularly in the inferior and lateral walls, with thinning of
the compacted outer layer.

\textbf{Funding statement}

`No specific funding was received from any bodies in the public,
commercial or not-for-profit sectors to carry out the work described in
this article.'

\textbf{Acknowledgments:}

No Acknowledgments

\textbf{Disclosure of interest:}

The authors declare no conflicts of interest.

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