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The Journal of Maternal-Fetal & Neonatal Medicine
ISSN: 1476-7058 (Print) 1476-4954 (Online) Journal homepage: https://www.tandfonline.com/loi/ijmf20
Non-compaction cardiomyopathy in pregnancy: a
case report of spongy myocardium in both mother
and foetus and systematic review of literature
Erlisa Bardhi, Ida Faralli, Marianna Deroma, Paola Galoppi, Flavia Ventriglia,
Antonella Giancotti, Giuseppina Perrone & Roberto Brunelli
To cite this article: Erlisa Bardhi, Ida Faralli, Marianna Deroma, Paola Galoppi, Flavia
Ventriglia, Antonella Giancotti, Giuseppina Perrone & Roberto Brunelli (2019): Non-compaction
cardiomyopathy in pregnancy: a case report of spongy myocardium in both mother and foetus
and systematic review of literature, The Journal of Maternal-Fetal & Neonatal Medicine, DOI:
10.1080/14767058.2019.1671337
To link to this article: https://doi.org/10.1080/14767058.2019.1671337
Published online: 01 Oct 2019.
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REVIEW ARTICLE
Non-compaction cardiomyopathy in pregnancy: a case report of spongy
myocardium in both mother and foetus and systematic review of literature
Erlisa Bardhi
a
, Ida Faralli
a
, Marianna Deroma
a
, Paola Galoppi
b
, Flavia Ventriglia
c
, Antonella Giancotti
c
,
Giuseppina Perrone
b
and Roberto Brunelli
b
a
Umberto I Policlinico di Roma, Maternal and Child Health and Urological Sciences, Rome, Italy;
b
Department of Gynecologic,
Obstetric and Urologic Sciences, Sapienza –University, Rome, Italy;
c
Department of Obstetrics and Gynecology, Umberto I Hospital,
“Sapienza”University of Rome, Rome, Italy
ABSTRACT
Purpose: Cardiovascular disease is the main nonobstetric cause of maternal death during preg-
nancy and is present in 0.5–4% of pregnancies in the western world. While hypertensive disor-
ders remain the most frequent events, occurring in 6–8% of all pregnancies, cardiomyopathies
are rare but encompass high complication rates. The aim of this systematic review is to report
all data available up to date regarding pregnancies in patients with left ventricular noncompac-
tion (LVNC) cardiomyopathy.
Methods: PubMed, Medline, Cochrane, Scopus and Embase were searched, up to January 2019,
using combinations of these terms: left ventricular noncompaction, hypertrabeculation cardio-
myopathy, spongy myocardium, spongiform cardiomyopathy and delivery, gestation, pregnancy,
cesarean section (CS). After careful selection, 22 articles, reporting a total of 30 cases, including
our own were included in the review.
Results: Fifteen out of 26 women (58%) were diagnosed with LVNC before pregnancy. Around
56% of women presented with symptoms during pregnancy while 44% were asymptomatic.
Heart failure is by far the most common symptom occurring in almost half the cases.
Uncommon clinical presentations included a heart attack, a stroke, and pulmonary hypertension.
Timing of delivery was reported preterm in 58% of cases and at term in 42%. Eleven women
gave birth through vaginal delivery, while 15 (58%) underwent a CS. Our reported case is the
first case of a pregnancy where both mother and fetus are affected by LVNC and the fetus is
diagnosed prenatally.
Conclusions: LVNC is not a contraindication for pregnancy, but clearly increases the risk of pre-
term birth and the rate of cesarean section. On the other hand, pregnancy in a LVNC patient
exposes her to increased risk of clinical deterioration. Further studies are needed to better char-
acterize the management of pregnancies in women with cardiomyopathies.
ARTICLE HISTORY
Received 20 June 2019
Revised 28 August 2019
Accepted 19 September 2019
KEYWORDS
Cardiomyopathy; hypertra-
beculation cardiomyopathy;
left ventricular
noncompaction; pregnancy;
spongy myocardium
Introduction
Cardiovascular disease is the main nonobstetric cause
of maternal death during pregnancy and is present in
0.5–4% of pregnancies in the western world. While
hypertensive disorders remain the most frequent
events, occurring in 6–8% of all pregnancies, cardio-
myopathies are rare, but encompass high complication
rates [1]. In case of preexisting cardiomyopathy, the
increased haemodynamic demands from the maternal
cardiovascular system during pregnancy may not be
met by maternal physiological adaptations, thus
exposing both the mother and fetus to higher risks for
complications [2]. Noncompaction cardiomyopathy or
left ventricular noncompaction (LVNC) is a rare
cardiomyopathy also known as “spongy myocardium”,
characterized by numerous, excessively prominent,
ventricular trabeculations and deep intertrabecular
recesses, predominantly found at the apex and mid
ventricular areas of the inferior and lateral wall of the
heart [3]. Recently, there is growing interest regarding
this disease and an increasing number of published
reports. Despite this, data regarding LVNC during
pregnancy is scarce. The aim of this article is to review
all cases reported in literature regarding pregnancies
of women affected by LVNC and to report a case of
successful multidisciplinary management of a preg-
nancy where both the mother and fetus were affected
by the disease.
CONTACT Erlisa Bardhi erlibardhi@gmail.com Umberto I Policlinico di Roma, Maternal and Child Health and Urological Sciences, Rome, Italy
ß2019 Informa UK Limited, trading as Taylor & Francis Group
THE JOURNAL OF MATERNAL-FETAL & NEONATAL MEDICINE
https://doi.org/10.1080/14767058.2019.1671337
Background
LVNC, also known as “spongy myocardium”is a rare
and heterogeneous disorder of myocardial morpho-
genesis characterized by numerous, excessively prom-
inent ventricular trabeculations and deep
intertrabecular recesses, predominantly found at the
apex and mid ventricular areas of the inferior and lat-
eral cardiac wall [3]. The reported prevalence in the
adult population varies from 0.01 to 0.27%, while inci-
dence ranges between 0.05 and 0.25% per year [4].
Etiology is unclear. In early embryonic development,
the myocardium initially presents with a finely trabe-
culated, spongy appearance and deep recesses
between the trabeculae. These become compressed
from the epicardium to the endocardium and from
the base to the apex of the heart, approximately
between the fifth and eighth week of gestation. In iso-
lated LVNC, this process either fails or remains incom-
plete, resulting in the persistence of the embryonic
pattern of trabeculation [5,6]. The cause of the non-
compaction is not yet fully understood, but it is
believed that pressure overload or myocardial ische-
mia play a role in the regression of embryonic sinus-
oids. Other plausible causes include syndromic
disorders, inborn errors of metabolism, and non-syn-
dromic monogenic disorders [7]. Clinical manifesta-
tions vary from lack of symptoms to congestive heart
failure, ventricular arrhythmias, thromboembolism and
sudden cardiac death. Electrocardiographic abnormal-
ities include bundle branch block and arrhythmias,
such as atrial fibrillation and ventricular tachycardia,
particularly in adults [8]. Mortality rate remains rele-
vant, although it has been recently found to be lower
(15%) than previously observed (33%), thus arising the
hypothesis that prognosis of LVNC might be better
than formerly expected [9–12].
LVNC can be an isolated manifestation or associ-
ated with other cardiac and noncardiac anomalies. A
distinctive facial dimorphism has been described
[7,13,14], as well as a frequent association with neuro-
muscular disorders (NMDs), such as Becker muscular
dystrophy, metabolic myopathy, myotonic dystrophy,
Leber’s hereditary optic neuropathy, and Barth syn-
drome [15,16]. Moreover, LVNC has been associated
with variants in mitochondrial, cytoskeletal, Z-line, and
sarcomeric genes [17].
The genetic etiology of LVNC is very heterogeneous
and complex. This disorder is familial in up to two-
thirds of cases (18–64%), but it can also be sporadic
[6]. In the familial form, inheritance can be autosomal
recessive, autosomal dominant or sex linked [7]. In the
sporadic forms, both sexes appear to be affected
equally [18].
Echocardiography is the main preferable diagnostic
tool, although different criteria have been proposed
by different authors and are continuously subject to
updates [3,13,19,20]. Additional imaging such as car-
diac magnetic resonance (MRI) can be used to either
confirm the diagnosis or for differential diagnosis, if
necessary. The ratio of noncompacted myocardium to
compacted myocardium must be greater than 2.3 dur-
ing the diastole (sensitivity of 86% and specificity of
99%) [21]. Differential diagnosis includes mainly other
cardiomyopathies, particularly hypertrophic or dilated
cardiomyopathy [22–24]. Therapy is symptomatic and
aims at alleviating manifestations of heart failure,
arrhythmias and reducing thromboembolic risk.
Case presentation
A 34-year-old pregnant woman (gravida 2 para 1) was
referred to the “high risk pregnancy”unit of our clinic
at 21 weeks of gestation. She had been diagnosed
with LVNC after her first pregnancy, at the age of 32,
following a screening for palpitations. Her medical and
family history was unremarkable, and she and her hus-
band were nonconsanguineous. Although asymptom-
atic, she was immediately submitted to cardiac
evaluation. An ultrasonographic investigation found a
dilated left ventricle with a reduced contraction cap-
acity and a measured ejection fraction (EF) of 36%
(normal value 55%). Cardiac MRI demonstrated a
thinned ventricular layer, with multiple trabeculae in
the contest of the anterior, lateral and inferior wall of
the left ventricle in the medium-apical region. All find-
ings were compatible with her LVNC diagnosis. A
neurologist excluded the presence of neurologic disor-
ders. Noninvasive prenatal screening during the first-
trimester and second trimester anatomy scan of the
fetus were normal; nuchal translucency (NT) was
1.2 mm. During our obstetric ultrasonographic evalu-
ation at admission, the myocardium of the fetus
appeared hypertrophic, thus cardiac ultrasound was
performed. At 24 weeks þ4 days of gestation, the fetal
heart presented with apical and lateral wall trabecula-
tions of the left ventricle, a myocardial performance
index (MPI) of 0.52 (normal value 0.5) (Figure 1) and
a mild pericardial effusion (PE) of 3 mm, hypothesizing
a diagnosis of LVNC. Fetal MRI showed, in addition to
the heart trabeculae, a uretero-pelvic junction stenosis
of the right kidney that caused a mild hydronephrosis.
Subsequently, the fetus was monitored twice monthly
with cardiac ultrasound (Table 1). In view of the fetal
2 E. BARDHI ET AL.
sonographic findings and the mother’s diagnosis, the
patient was referred to a genetic consult that recom-
mended further genetic investigations through amnio-
centesis, but the patient refused.
At 28 weeks, following palpitations and dyspnea,
the woman was included in our Day Hospital regimen
and closely monitored with cardiologic and obstetric
evaluations, as well as fetal echocardiographs, every
15 days. The cardiologist prescribed beta-blockers and
diuretics that the patient refused, given the possible
consequences for the fetus. At 38 weeks, the patient
presented with uterine contractions. Cesarean section
(CS) was indicated given the high risk of maternal
arrhythmias, thus a female infant weighting 2720
grams (25th percentile) was delivered with an Apgar
score of 8 and 9 at 1 and 5 min respectively. No intra
and post operatory complications occurred, but given
the increased risk for cardiac complications, the
mother was strictly monitored in an Intensive
Cardiologic Care Unit (ICCU) for the first 24 h.
Postnatal cardiac ultrasound of the fetus confirmed
the prenatal diagnosis of LVNC (EF: 45%). A treatment
with angiotensin converting enzyme (ACE) inhibitor
was advised to improve EF. Clinical conditions
remained unstable; nonetheless the infant’s conditions
improved after 4 months. The mother was asymptom-
atic in puerperium.
Review methods
An electronic database search was performed using
PubMed, Medline, Cochrane and Embase, and relevant
citations were extracted to identify pertinent articles
published up to January 2019, using varied combina-
tions of the following search terms: left ventricular
noncompaction, left ventricular noncompaction cardio-
myopathy; hypertrabeculation cardiomyopathy,
spongy myocardium, spongiform cardiomyopathy and
delivery, gestation and/or pregnancy, cesarean section.
Duplicates and nonpertinent articles were excluded
and reference lists were scanned. In the end, a total of
53 full text articles were evaluated for eligibility.
Articles whose full length could not be obtained were
excluded and only published papers that reported
pregnancies of women affected by LVNC were
included in the review, amounting at 22 articles,
reporting a total of 30 cases, including our own
(Figure 2).
Results
Among the published LVNC case reports and series,
30 have been described in pregnant women over the
Table 1. Echocardiographic fetal myocardial indexes.
Gestational age MPI sin MPI dx
Electromechanical
interval (msec) EF %
24 w þ4 d 0.52 0.54 0.127 59
27 w 0.52 0.54 0.128 58
29 w þ2 d 0.60 0.56 0.126 58
31 w 0.54 0.53 0.126 60
32 w þ3 d 0.55 0.60 0.136 57
33 w þ2 d 0.58 0.47 0.131 60
34 w þ3 d 0.63 0.53 0.138 60
36 w þ2 d 0.61–0.66 0.47 0.131 59
37 w þ2 d 0.64 0.69 0.131 60
MPI: Myocardial Performance Index; EF: Ejection Fraction.
Figure 1. Fetal echocardiography: measurement of Tei index or myocardial performance index: 0.52 (0.46 ± 0.08).
THE JOURNAL OF MATERNAL-FETAL & NEONATAL MEDICINE 3
last 20 years, including our case. Clinical characteristics
of patients and pregnancy outcomes are reported in
Table 2 [1,25–45].
Maternal age was reported in 23 out of the 30
cases (76%) with a mean of 28 years (range 14–40).
The timing of diagnosis in relation to the gestation
was reported in 26 out of 30 cases (86%). Fifteen out
of 26 women (58%) were diagnosed with LVNC before
pregnancy; eight during pregnancy; two women mani-
fested symptoms for the first-time during delivery and
one in post-partum. Symptomatology was described
in 27 out of 30 cases (90%). Around 56% of women
presented with symptoms during pregnancy while
44% were asymptomatic. Twelve out of 27 cases pre-
sented with cardiologic symptoms: seven (26%) with
heart failure; three (11%) with dyspnea and two
patients (7%) had both. Heart failure is by far the
most common symptom occurring in almost half the
cases. Uncommon clinical presentations included a
heart attack, a stroke, and pulmonary hypertension.
Maternal ejection fraction (FE) was reported in 19 out
of the 30 cases, ranging from 5 to 57% with a mean
of 32%.
The timing of delivery was reported in 19 out of 30
cases (63%). Of these, 11 out of 19 (58%) were pre-
term deliveries and 8 out of 19 (42%) were at
37 weeks of gestation onwards. Out of the 11 preterm
births, two (18%) were extreme preterm at 24 weeks
of gestation; three (27%) were very preterm from 28
to 32 weeks and the majority (6 out of 11, 55%) were
late preterm from 34 to 37 weeks.
Delivery mode was specified in 26 out of 30 cases
(87%). Eleven women gave birth through vaginal
delivery, while 15 (58%) underwent a cesarean section
(CS). In more than half the cases (53%) the indication
for CS was cardiologic. In two cases the indication was
obstetric (placenta previa and breech presentation)
and in five cases the indication was not specified.
Fetal outcome was indicated in 18 out of the 30
cases. Fifteen fetuses were born alive. There has been
described a fetal demise at 29 weeks and two neonatal
deaths, most probably related to extreme prematurity
Records idenfied through PubMed, Medline,
Cochrane, Scopus and EMBASE searching LVNC,
HTNC, myocardium non compacon, spongy
myocardium and pregnancy and/or gestaon
and/or caesarean secon
(n=89)
Screening
Included Eligibility Idenficaon
Records screened based on tle
and abstract
(n = 53)
Full-text arcles assessed
for eligibility
(
n = 53
)
Arcles included in the review,
including own case
(n = 22)
Full-text arcles excluded
with reason
(n = 31)
Exclusion of duplicates and
non-pernent arcles
(n = 36)
Figure 2. Search strategy and study selection. Moher et al. [50].
4 E. BARDHI ET AL.
(in both cases delivery occurred at 24 weeks of gesta-
tion). The affection of the fetus/neonate by LVNC was
only specified in 5 out of the 30 cases of affected
mothers. In one case it is specified that the fetus was
not affected by the disease. Kitao et al. [26] reported a
diagnosis of fetal LVNC postnatally but the neonate
only survived for 2 days. Munehisa et al. [31] reported
a postnatal suspect of LVNC that remains uncon-
firmed. Lea et al. [33] reported a postnatal diagnosis
of LVNC in the neonate that is alive and well at the
time of publishing. To our knowledge, our reported
case is the first case of a pregnancy where the mother
is affected by LVNC and the fetus is diagnosed in ute-
rus with the same disease, confirmed after birth.
Discussion
The physiological changes that occur during preg-
nancy, labor and delivery may lay ground for cardiac
complications, such as arrhythmias and heart failure,
especially in the presence of preexisting heart disease
[46]. In particular, women affected by cardiomyopa-
thies, are at higher risks for unfavorable pregnancy
outcomes, and if clinical symptoms are severe, often
enough, pregnancy is contraindicated [47]. While it is
still controversial whether LVNC is a distinct disease,
rather than a phenotype of other cardiomyopathies or
even an adaptation of the cardiac muscle, it is a fact
that when symptomatic, LVNC alerts health care
Table 2. Review of literature cases of pregnant patients affected by LVNC.
Author
Age
(years)
Diagnosis
(weeks) Symptoms
Time of
delivery
(weeks)
Mode
of delivery
Indication
to CS FE (%) Fetal LVNC Fetal outcome
Williams et al. [25]28 22þ0 Heart failure 36 þ0 CS Cardiologic NA NA Alive
Kitao et al. [26]2324þ0 Heart
failure/dyspnea
24 þ3 CS Cardiologic 52 Yes,
postnatally
Died
Uesugi et al. [27]2320þ0 Heart failure 24 þ0 CS NA NA NA Died
Fernandez Sanchez
et al. [28]
NA During
pregnancy
Stroke NA CS NA NA NA NA
Bahl et al. [29]2336þ0 Dyspnea 40 þ0VD NA19NA NA
Patel et al. [30]2631þ0 Heart failure 37 þ0 VD NA 20 NA Alive
Patel et al. [30]1436þ0 Heart failure 36 þ0 CS Cardiologic 17 NA Alive
Munehisa et al. [31] 24 BP Asymptomatic 31 þ0 CS Cardiologic 45 Not
confirmed
Alive
Fischer et al. [32] 28 During
delivery
Heart failure
and shock
29 þ0 CS Cardiologic 15 NA Intrauterine
demise
at 29 w
Lea et al. [33] 23 During
delivery
Heart failure 40 þ5VD NA15–20 Yes,
postnatally
Alive
Kobza et al. [34] NA BP NA NA CS NA NA NA Alive
Kobza et al. [34] NA BP NA NA CS NA NA NA Alive
Rehfeldt et al. [35] 25 8 weeks
post-partum
Heart attack NA VD NA 5 NA NA
Plastiras et al. [36] 32 BP Asymptomatic NA VD NA NA NA Alive
Panduranga
et al. [37]
30 BP Asymptomatic 37 þ0 NA Cardiologic 35 NA NA
Ba~
nuls Pellicer
et al. [38]
27 BP Asymptomatic 38 þ0 VD NA 40 NA Alive
Kilic et al. [39]1937þ0 Cough/
dyspnea
NA NA NA 20 NA NA
Sawant et al. [40] 37 BP Heart
failure/dyspnea
NA CS Cardiologic 25 NA Alive
Dogan et al. [41] 32 BP Heart failure 35 þ0 CS Cardiologic 25 NA NA
Stollberger et al. [42] NA NA Asymptomatic NA CS Obstetric
(breech
presentation)
NA NA NA
Stollberger et al. [42] NA NA Asymptomatic NA VD NA NA NA NA
Stollberger et al. [42] NA NA Asymptomatic NA VD NA NA NA NA
Stollberger et al. [42] NA NA Asymptomatic NA VD NA NA NA NA
Spitzer et al. [43] 31 BP Dyspnea/
Orthopnea
34 þ0 CS Cardiologic 38 NA Alive
Reuschel et al. [44] 27 BP Asymptomatic 37 þ0 CS NA 38 No Alive
Ueda et al. [45] 36 BP Asymptomatic 37 þ0 VD NA 35 NA Alive
Ueda et al. [45] 31 BP Pulmonary
hypertension
30 þ0 NA NA NA NA Alive
Ueda et al. [45] 40 BP Asymptomatic 36 þ0 CS Obstetric
(placenta
previa)
57 NA Alive
Billebeau et al. [1] 26 BP NA Before 37 w NA NA 45 NA Alive
Own case 32 BP Asymptomatic 38 þ0 CS Cardiologic 36 Yes,
prenatally
Alive
NA: not available; BP: before pregnancy; VD: vaginal delivery; CS: cesarean section.
THE JOURNAL OF MATERNAL-FETAL & NEONATAL MEDICINE 5
providers as an entity with uncertain prognosis, par-
ticularly during pregnancy [48,49].
Literature search resulted in a total of 30 cases of
pregnant women affected by LVNC, including our
own. In the collected data, nearly 60% of women were
diagnosed before the pregnancy, while in the remnant
cases LVNC was diagnosed during pregnancy, delivery
or immediate postpartum, suggesting that in 40% of
cases the pregnancy deteriorated and/or unmasked an
underlying LVNC. In some reported cases, the physi-
cians had advised against the continuation of preg-
nancy [40,43,44].
Almost all symptomatic patients presented with car-
diac symptoms; with heart failure being by far the pre-
dominant manifestation occurring in three quarters of
cases. Heart failure could determine a placental hypo-
perfusion and consequently fetal distress or growth
restriction, but such issues were not addressed in the
collected data. In one case, clinical deteriorating of the
mother required a heart transplant in the postpartum
[33], and in another case a wearable defibrillator was
necessary [44].
Other severe clinical presentations included stroke,
heart attack and pulmonary hypertension, greatly
increasing the risk of untimely birth. Indeed, nearly
60% of all reported deliveries were preterm, and
among these, almost half the cases were very preterm.
Furthermore, nearly 60% of deliveries occurred through
CS. The indication to CS was not always described, but,
when specified, in 80% of cases it was cardiologic.
Presently, there is no consenting opinion, nor
guidelines regarding the medical therapy in LVNC. In
our collected cases, medical therapy prescribed during
pregnancy was detailed only by three authors and it
mainly consisted on beta-blockers, diuretics, aspirin
and unfractionated heparin [39,40,45]. Since preg-
nancy is a hypercoagulable state, anticoagulation
seems reasonable and may prevent further embolic
events. In the postpartum, many authors prescribed
anticoagulation, particularly with heparin and war-
farin [26,31,37,45].
Regrettably, fetal outcomes in terms of growth
restriction, fetal distress or other fetal complications
were not mentioned by any authors. Most pregnancies
ended in a live birth, although 60% were preterm.
However, a fetal demise at 29 weeks was reported,
and other two neonatal deaths, most probably related
to extreme prematurity (in both cases delivery
occurred at 24 weeks of gestation). Neonatal LVNC
was reported in three cases, while we report the first
case of a pregnancy where the mother is affected by
LVNC and the fetus is diagnosed in uterus with the
same disease, confirmed after birth. Prenatal diagnosis
of LVNC allows the neonatologist to be prepared for
specialized assistance, thus increasing the quality of
the help.
Among the present literature there is no data
regarding LVNC and breastfeeding, although, in one
reported case, it appeared to exacerbate the preexist-
ing heart failure symptoms, thus bromocriptine was
administered to arrest lactation [40].
The overall small number of cases represents a limi-
tation of this review. Additionally, the retrospective
nature of reviews accounts for the lack of some useful
data and warrants cautious interpretation of results.
Nonetheless, given the scarcity of information regard-
ing LVNC and pregnancy, great benefit can be drawn
from the gathering of all available evidence in order
to better council and manage patients.
We describe the case of a pregnant woman with
LVNC, whose child was prenatally diagnosed with the
same disease. Delivery occurred at full term of gesta-
tional age, with successful outcomes for both the
mother and the newborn. In our experience, in such
cases, strict maternal surveillance is mandatory: clinical
symptoms and signs were investigated daily; holter-
ecg was performed monthly, cardiac ultrasonography
was performed every 2 months and the patient was
observed by a multidisciplinary team (cardiologist,
obstetrician, anesthetist, Intensive Care Unit specialists,
and neonatologist). Additional attention ought to be
addressed in distinguishing the fetuses at higher risk
for complications, in order to establish early treatment
and improve prognosis after birth. In our case fetal
surveillance consisted of monthly obstetric ultrasound
and fetal echocardiography twice a month. If available,
genetic testing and consultation would evaluate the
risk of recurrence in the family, while neurological
consultation would evaluate the association with
NMDs. Thromboprophylaxis with either low-molecular-
weight heparin or aspirin should be considered
although there is no evidence to guide treatment regi-
ments currently. Postpartum anticoagulation should
continue for 6 weeks, and based on clinical status
heart failure therapy started as soon as possible [6].
Conclusion
This systematic review gathers all evidence available
up to date on pregnancies of women with LVNC.
Based on data so far, this disease increases the risk of
preterm birth and the rate of CS. On the other hand,
pregnancy in a LVNC patient exposes her to increased
risk of clinical deterioration. LVNC appears to be no
6 E. BARDHI ET AL.
absolute contraindication for pregnancy, although
there might be significant complications.
Disclosure statement
No potential conflict of interest was reported by the authors.
ORCID
Erlisa Bardhi http://orcid.org/0000-0001-6534-0063
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