Fetal Echocardiography and Magnetocardiography

Fetal Echocardiography and Magnetocardiography - Medical Clinical Policy Bulletins | Aetna

Fetal Echocardiography and Magnetocardiography

Last Review: 02/24/2021

Effective: 05/08/1996

Next Review: 01/27/2022

Number: 0106

Page 1 of 37

*Please see amendment for Pennsylvania Medicaid

at the end of this CPB.

I. Aetna considers fetal echocardiograms, Doppler and color flow

mapping medically necessary after 12 weeks gestation for any of

the following conditions:

A. A mother with type 1 diabetes or pregestational type 2 diabetes on

insulin during the first trimester; or

B. A mother with systemic lupus erythematosus; or

C. As a screening study in families with a first-degree relative of a fetus with congenital heart disease; or

D. Fetal nuchal translucency measurement of 3.5 mm or greater

in the first trimester; or

E. Following an abnormal or incomplete cardiac evaluation on an

anatomic scan, 4-chamber study

(Note: When the 4-chambered view is adequate and there are

no other indications of a cardiac abnormality, a fetal

echocardiogram is not considered medically necessary); or

F. For ductus arteriosus dependent lesions and/or with other known complex congenital heart disease; or

Fetal Echocardiography and Magnetocardiography - Medical Clinical Policy Bulletins | Aetna Page 2 of 37

G. For pregnancies conceived by in vitro fertilization (IVF) or intracytoplasmic sperm injection (ICSI); or

H. In cases of persistent right umbilical vein; or

I. In cases of single umbilical artery; or

J. In cases of suspected or known fetal chromosomal abnormalities;

or

K. In suspected or documented fetal arrhythmia: to define the rhythm

and its significance, to identify structural heart disease and cardiac

function; or

L. In members with autoimmune antibodies associated with

congenital cardiac anomalies [anti-Ro (SSA)/anti-La (SSB)]; or

M. In members with familial inherited disorders associated with

congenital cardiac abnormalities (e.g., Marfan syndrome); or

N. In cases with monochorionic twins; or

O. In cases of multiple gestation and suspicion of twin-twin

transfusion syndrome; or

P. In members with seizure disorders, even if they are not

presently taking anti-seizure medication; or

Q. In cases with non-immune fetal hydrops or unexplained severe polyhydramnios; or

R. When members' fetuses have been exposed to drugs known to

increase the risk of congenital cardiac abnormalities including

but no t limited to:

Anti-seizure medications; or

Excessive alcohol intake; or

Lithium; or

Paroxetine (Paxil); or

Retinoids; or

S. When other structural abnormalities are found on ultrasound;

or

II. Aetna considers repeat studies of fetal echocardiograms medically

necessary for any of the following:

A. When the initial screening study indicates any of the following:


1. A ductus arteriosus dependent lesion; or

2. Structural heart disease with a suggestion of hemodynamic

compromise; or

3. Tachycardia other than sinus tachycardia or heart block; or

B. Fetal surveillance (e.g., congenital heart block) in mother with

documented diagnosis of Sjögren’s syndrome. Frequency of

testing: Doppler fetal echocardiography may be repeated every

1 to 2 weeks starting at 16 weeks gestation continuing through

28 weeks gestation, then every other week until 32 weeks

gestation to detect fetal (congenital) heartblock.

III. Aetna considers fetal echocardiograms experimental and

investigational for all other indications including the following (not

an all-inclusive list) because their effectiveness for these

indications has not been established.

As a screening test in advanced maternal age; or

Gestational diabetes even if requiring insulin after the first

trimester; or

Pregnantwomenreceivingselective serotoninreuptake

inhibitors (except paroxetine); or

Suspected cystic fibrosis.

IV. Aetna considers fetal magnetocardiography experimental and

investigational because its effectiveness has not been established.

Definition of fetal cardiac structures is currently possible at 12 weeks of

gestation with the use of vaginal probes with high-resolution transducers.

With current technologies, accurate segmental analysis of cardiac

structures and blood flow across valves, shunts, and the ductus

arteriosus is possible with a conventional transabdominal approach by 16

to 18 weeks of gestation.


According to the American Institute for Ultrasound in Medicine (AIUM),

fetal echocardiography is commonly performed between 18 and 22

weeks’ gestational age. Some forms of congenital heart disease may

even be recognized during earlier stages of pregnancy (AIUM, 2013).

Newer technology including endovaginal transducers can obtain images

of the heart as early as 12 weeks gestation (AHA, 2018).

Hutchinson et al. (2017) states that early fetal echocardiography (FE),

performed at 12 to 16 weeks' gestational age (GA), can be used to

screen for fetal heart disease similar to that routinely performed in the

second trimester; however, the efficacy of FE at earlier GAs has not been

as well explored, particularly with recent advances in ultrasound

technology. Pregnant women were prospectively recruited for first-

trimester FE. All underwent two-dimensional (2D) cardiac imaging

combined with color Doppler (CD) assessment, and all were offered

second-trimester fetal echocardiographic evaluations. Fetal cardiac

anatomy was assessed both in real time during FE and additionally offline

by two separate reviewers. Very early FE was performed in 202

pregnancies including a total of 261 fetuses, with 92% (n = 241) being

reassessed at greater than or equal to 18 weeks' GA. Transabdominal

scanning was used in all cases, and transvaginal scanning was used

additionally in most at less than 11 weeks' GA (n = 103 of 117 [88%]).

There was stepwise improvement in image resolution of the fetal heart in

those pregnancies that presented at later gestation for assessment.CD

assisted with definition of cardiac anatomy at all GAs. A four-chambered

heart could be identified in 52% of patients in the eighth week (n = 12 of

23), improving to 80% (n = 36 of 45) in the 10th week and 98% (n = 57 of

58) by the 11th week. The inferior vena cava was visualized by 2D

imaging in only 4% (n = 1 of 23) in the eighth week, increasing to 13% (n

= 6 of 45) by the 10th week and 80% (n = 25 of 31) by the 13th week. CD

improved visualization of the inferior vena cava at earlier GAs to greater

than 80% (n = 37 of 45) from 10 weeks. Pulmonary veins were not

visualized by either 2D imaging or CD until after the 11th week. Both

cardiac outflow tracts could be visualized by 2D imaging in the minority

from 8+0 to 10+6 weeks (n = 18 of 109 [16%]) but were imaged in most

from 11+0 to 13+6 weeks (n = 114 of 144 [79%]). CD imaging improved

visualization of both outflow tracts to 64% (n = 29 of 45) in the 10th week.

On 2D imaging alone, both the aortic and ductal arches were seen in only

29% of patients in the 10th week (n = 13 of 45), increasing to 58% when


CD was used (58% [n = 26 of 45]) and to greater than 80% (n = 47 of 58)

using CD in the 11th week. The authors concluded that very early FE,

from as early as 8 weeks, can be used to assess cardiac structures;

however, the ability to image fetal heart structures between 6 and 8

weeks is currently nondiagnostic. The use of CD significantly increases

the detection of cardiac structures on early FE. The ideal timing of

complete early FE, excluding pulmonary vein assessment, appears to be

after 11 weeks' GA.

Ventriglia et al. (2016) state that there is a growing body of evidence that

most of the major cardiac abnormalities can be diagnosed from 12-16

weeks of gestation (compared with the usual 18-22 weeks). Furthermore,

the reason for performing early fetal echocardiography (EFEC) is that "the

combined EFEC-NT (nuchal translucency) approach (11th-13th week)

gives a 60-70% increase in detection rate for CHD. Combined EFE-NT

analysis is also justified by the high CHD frequency in genetic syndromes

and the similarity of anatomic relations between cardiac structures at 11

13 wks GA and those of the second trimester." "The technical limits of

EFEC are CRL < 50 mm, an increase of maternal Body mass index

(BMI), unfavorable fetal position and a possible progression of cardiac

disease especially in outflow obstructions. This means that the pregnant

women should be informed about the limits of early screening and also

recommended to have a further scan as from 18 weeks for a more

complete diagnosis."

Patients are referred for fetal echocardiography because of an

abnormality of structure or rhythm noted on ultrasound examination or

because the patient is in a high-risk group for fetal heart disease.

Treatment of the patient is facilitated by the early recognition of the exact

nature of the cardiac problem in the fetus. The correct diagnosis may be

difficult because of fetal physiology, the effect on flow across defects and

valves, inability to see the fetus for orientation reference, and inability to

examine the fetus for clinical findings. For these reasons, fetal

echocardiography should be performed only by trained fetal

echocardiographers.

The umbilical cord normally contains two arteries and one vein embedded

in Wharton's jelly. The umbilical cord "achieves its final form by the 12th

week of gestation". Initially during umbilical cord development, there


are two umbilical arteries and two umbilical veins, in which the two veins

(left and right) converge into one. Obliteration of the right umbilical vein by

the end of the 6th week of gestation results in a single persisting left

umbilical vein (Spurway et al, 2012). However, persistence of the right

umbilical vein in the fetus is a variant of the intra-abdominal umbilical

venous connection. The estimated prevalence of an intrahepatic

persistent right umbilical vein is 1 per 786 births; which may be

an underestimated calculation in populations that do not undergo targeted

sonographic examinations. In addition, the variation in anatomy can be

subtle (Lide et al, 2016).

Lide et al (2016) provided a comprehensive review of the current data

surrounding an intra-hepatic persistent right umbilical vein in the fetus,

including associated anomalies and outcomes, to aid practitioners in

counseling and management of affected pregnancies. These

investigators performed a Medline, Embase, Cochrane Central Register

of Controlled Trials, and Northern Light database search for articles

reporting outcomes on prenatally diagnosed cases of a persistent right

umbilical vein. Each article was independently reviewed for eligibility by

the investigators. Thereafter, the data were extracted and validated

independently by 3 investigators. A total of 322 articles were retrieved,

and 16 were included in this systematic review. The overall prevalence of

an intra-hepatic persistent right umbilical vein was found to be 212 per

166,548 (0.13 %). Of the 240 cases of an intra-hepatic persistent right

umbilical vein identified, 183 (76.3 %) were isolated. The remaining

cases had a co-existing abnormality, including 19 (7.9 %) cardiac, 9 (3.8

%) central nervous system, 15 (6.3 %) genito-urinary, 3 (1.3 %) genetic,

and 17 (7 %) placental/cord (predominantly a single umbilical artery).

The authors concluded that a persistent right umbilical vein is commonly

an isolated finding but may be associated with a co-existing cardiac

defect in 8 % of cases. Therefore, consideration should be given to fetal

echocardiography in cases of a persistent right umbilical vein.

Canavan et al (2016) stated that a fetal persistent intrahepatic right

umbilical vein has been linked to anomalies and genetic disorders but can

be a normal variant. These researchers conducted a retrospective review

to determine other sonographic findings that can stratify fetuses for

further evaluation. A total of 313 fetuses had a persistent intra-hepatic

right umbilical vein identified on 17- to 24-week sonography. The


outcome was any major congenital anomaly or an adverse neonatal

outcome, which was defined as aneuploidy, fetal demise, or neonatal

death. A total of 217 patients (69.3 %) had a normal neonatal outcome;

69 patients (22.0 %) were lost to follow-up; 5 fetuses (2.1 %) had

aneuploidy; 4 of the 5 had additional sonographic findings, and 1 had an

isolated persistent intra-hepatic right umbilical vein; 24 fetuses had a

major anomaly in association with the persistent right umbilical vein; 26

additional fetuses had soft sonographic markers associated with

karyotypic abnormalities but were chromosomally normal. Of those with

adverse neonatal outcomes, 12 had a congenital heart defect (57 %). An

additional sonographic finding with a persistent intra-hepatic right

umbilical vein was predictive of a congenital anomaly or an adverse

neonatal outcome (p < 0.001), with a positive predictive value of 44.0 %

(95 % confidence interval[ CI]: 30.0 % to 58.7 %). An isolated persistent

intra-hepatic right umbilical vein had a 0.4 % risk for a congenital anomaly

or an adverse neonatal outcome. The authors concluded that a

persistent intra-hepatic right umbilical vein should prompt an extended

anatomic survey and a fetal cardiac evaluation. If the survey and cardiac

anatomy are reassuring, no further follow-up is needed. If additional

findings are identified, genetic counseling and invasive testing should be

considered.

Kumar et al (2016) appraised the incidence and significance of persistent

right umbilical vein (PRUV), the most common fetal venous aberration.

Based on a South Indian antenatal cohort, these researchers identified 23

cases of PRUV amongst 20,452 fetuses of consecutive pregnancies, from

2009 to 2014, yielding an incidence of 1 in 889 total births (0.11 %). The

median maternal age was 24 (inter-quartile range [IQR], 22 to 26) years,

and median gestational age at diagnosis was 23 (IQR, 22 to 24) weeks.

Intra-hepatic drainage of PRUV was seen in 91.3 % cases. In 3 cases

(13 %), ductus venosus was absent. In 52.2 % of the cases, additional

major abnormalities were observed - predominantly cardiovascular (39.1

%). The common minor marker was single umbilical artery (SUA; 13 %).

The karyotype was found to be normal in 6 cases (26 %) that underwent

invasive testing. When associated anomalies were inconsequential or

absent, the post-natal outcome was good, which reflected in 60.9 % of

these cases. Fetal echocardiography was one of the keywords listed in

this study.


In a prospective, observational study, Hill et al (1994) reviewed their

experience with antenatal detection and subsequent neonatal outcome of

fetuses with a persistent right umbilical vein. A total of 33 cases of

persistent right umbilical vein were detected during 15,237 obstetric

ultrasound examinations performed after 15 weeks' gestation. Persistent

right umbilical vein was detected at a rate of 1 per 476 obstetric

ultrasound examinations; 6 of 33 (18.2 %) fetuses with a persistent right

umbilical vein had additional important congenital malformations. The

authors concluded that careful 2nd- and 3rd-trimester ultrasound

examinations can detect a persistent right umbilical vein. When this

particular anomaly is detected, a thorough fetal anatomic survey,

including echocardiography, should be performed to rule out more serious

congenital malformations.

Wolman et al (2002) conducted a prospective evaluation of the incidence

and neonatal outcome of fetuses with persistent right umbilical vein. This

condition had traditionally been considered to be extremely rare and to be

associated with a very poor neonatal prognosis, but later evidence has

raised some doubts about the veracity of these contentions. Between

August 1995 and November 1998, a total of 8,950 low-risk patients were

prospectively evaluated at 2 medical centers. The sonographic diagnosis

of a persistent right umbilical vein was made in a transverse section of the

fetal abdomen when the portal vein was curved toward the stomach, and

the fetal gall bladder was located medially to the umbilical vein.

Persistent right umbilical vein was detected in 17 fetuses during the

study; 4 of them had additional malformations, of which 3 had been

detected antenatally. The authors established that the incidence of

persistent right umbilical vein in a low-risk population was 1:526. They

believed that the sonographic finding of this anomaly was an indication for

conducting targeted fetal sonography and echocardiography. When the

persistent right umbilical vein was connected to the portal system and

other anomalies were ruled out, the prognosis can generally be expected

to be favorable.

Martínez et al (2012) described the ultrasound findings, maternal and

perinatal variables in cases with a prenatal diagnosis of persistence of

right umbilical vein. This was a descriptive analysis of cases with prenatal

diagnosis of persistence of right umbilical vein in the Fetal Medicine Unit,

Department of Obstetrics and Gynecology, Hospital Universitario Severo


Ochoa. These investigators described ultrasound findings, maternal and

perinatal variables. They examined 9,198 fetuses and 6 cases (0.06 %)

were diagnosis prenatally of persistent right umbilical vein, between 20

and 29 weeks of gestation. The male/female ratio was 1/1. Ductus

venosus was presented in all cases; 2 fetuses (33 %) were proved to

have other structural anomalies and their parents opted for termination of

the pregnancy. All cases had no chromosomal anomaly associated and

after birth, neonatal developments were favorable. The authors

concluded that based on these findings and a literature review, after

prenatal diagnosis of persistent right umbilical vein, an exhaustive

morphological study, which included a fetal echocardiography, is

mandatory in order to rule out other structural malformations. Indication

for fetal karyotype study has to be individualized considering persistence

right umbilical vein type and other ultrasoundfindings.

A single umbilical artery (SUA) is present in 0.2 % to 0.6 % of livebirths,

occurring more frequently in twins and in small for gestational age and

premature infants. In infants with SUA, there is an increased rate of

chromosomal and other congenital anomalies. Studies have shown that

20 % to 30 % of neonates with SUA had major structural anomalies,

frequently involving multiple organs (Palazzi and Brandt, 2009; Thummala

et al, 1998). The most commonly affected organ is the heart. Single

umbilical artery is an isolated finding in the remaining 70 % to 80 % of

infants.

Conception by in vitro fertilization (IVF) or intra-cytoplasmic sperm

injection (ICSI) has been associated with an increased incidence of fetal

heart defects. A meta-analyses on the prevalence of birth defects in

infants conceived following IVF and/or ICSI compared with spontaneously

conceived infants reported a 30 % to 40 % increased risk of birth defects

associated with IVF and/or ICSI (Hansen et al, 2005). Researchers have

reported that infants conceived with the use of IVF and/or ICSI have a 2

to-4-fold increase of heart malformations compared with naturally

conceived infants.

Kurinczuk and Bower (1997) examined the prevalence of birth defects on

420 liveborn infants who were conceived after ICSI in Belgium compared

with 100,454 liveborn infants in Western Australia delivered during the

same period. Infants born after ICSI were twice as likely asWestern


Australian infants to have a major birth defect [odds ratio (OR) 2.03, 95 %

confidence interval (CI): 1.40 to 2.93); p = 0.0002] and nearly 50 % more

likely to have a minor defect (OR 1.49 (0.48 to 4.66); p = 0.49).

Secondary data-led analyses found an excess of major cardiovascular

defects (OR 3.99).

Koivurova et al (2002) evaluated the neonatal outcome and the

prevalence of congenital malformations in children born after IVF in

northern Finland in a population-based study with matched controls.

Children born after IVF (n = 304) in 1990 to1995 were compared with

controls (n = 569), representing the general population in proportion of

multiple births, randomly chosen from the Finnish Medical Birth Register

(FMBR) and matched for sex, year of birth, area of residence, parity,

maternal age and social class. Plurality matched controls were randomly

chosen from the FMBR and analyzed separately. Additionally, IVF

singletons were compared with singleton controls. The prevalence of

heart malformations was four-fold in the IVF population than in the

controls representing the general population (OR 4.0, 95 % CI: 1.4 to

11.7).

Reefhuis et al (2009) analyzed data from the National Birth Defects

Prevention Study, a population-based, multi-center, case-control study of

birth defects. Included were mothers of fetuses or live-born infants with a

major birth defect (case infants) and mothers who had live-born infants

who did not have a major birth defect (control infants), delivered during

the period October 1997 to December 2003. Mothers who reported IVF

or ICSI use were compared with those who had unassisted conceptions.

Among singleton births, IVF or ICSI use was associated with septal heart

defects (adjusted odds ratio [aOR] = 2.1, 95 % CI: 1.1 to 4.0).

As fetal heart disease is typically associated with structural abnormalities

and consequent aberrant blood flow through the heart, it is necessary to

perform Doppler studies and color flow mapping when such abnormalities

are detected with 2D fetal echocardiography.

The American College of Obstetricians and Gynecologists' Committee

Opinion on the treatment with selective serotonin reuptake inhibitors

during pregnancy (ACOG, 2006) noted that paroxetine use among


pregnant women and women planning pregnancy should be avoided, if

possible. Fetal echocardiography should be considered for womenwho

were exposed to paroxetine in early pregnancy.

In a practice bulletin on screening for fetal chromosomal anomalies,

ACOG (2007) has stated that patients who have a fetal nuchal

translucency measurement of 3.5 mm or greater in the first trimester,

despite a negative result on an aneuploidy screen, normal fetal

chromosomes, or both, should be offered a targeted ultrasound

examination, fetal echocardiogram, or both, because such fetuses are at

a significant risk for non-chromosomal anomalies, including congenital

heart defects, abdominal wall defects, diaphragmatic hernias, and genetic

syndromes.

Twin-twin transfusion syndrome (TTTS) is a severe complication of

monochorionic (1 placenta) twin pregnancies, characterized by the

development of unbalanced chronic blood transfer from one twin, defined

as donor twin, to the other, defined as recipient, through placental

anastomoses. If left untreated, TTTS is associated with very high peri

natal mortality and morbidity rates; and fetuses who survive are at risk of

severe cardiac, neurological, and developmentaldisorders.

The American Society of Echocardiography's guidelines and standards

for performance of the fetal echocardiogram (Rychik et al, 2004) stated

that multiple gestation and suspicion of TTTS is an indication of fetal

echocardiography.

Bahtiyar et al (2007) noted that congenital heart defects (CHDs) affect

approximately 0.5 % of all neonates. Recent literature points to a

possible increase in the CHD prevalence among

monochorionic/diamniotic (MC/DA) twin gestations. These researchers

hypothesized that MC/DA twin pregnancy is a risk factor for CHD. A

systematic review of all published English literature was conducted on

MEDLINE (Ovid and PubMed) from January 2000 through April 2007

using the medical subject heading terms "congenital heart defect" and

"monozygotic twins". Four observational studies were included in the

final analysis. Published historical data were used for the population

background risk of CHD. Relative risk (RR) estimates with 95 %

confidence intervals (CIs) were calculated by fixed and random effect


models. These investigators included a total of 40 fetuses with CHDs

among 830 fetuses from MC/DA twin gestations. Compared with the

population, CHDs were significantly more prevalent in MC/DA twins

regardless of the presence of TTTS (RR, 9.18; 95 % CI: 5.51 to 15.29; p

< 0.001). Monochorionic/diamniotic twin gestations affected by TTTS

were more likely to be complicated by CHDs than those that did not have

TTTS (RR, 2.78; 95 % CI: 1.03 to 7.52; p = 0.04). Ventricular septal

defects were the most frequent heart defects. Pulmonary stenosis and

atrial septal defects were significantly more prevalent in pregnancies

complicated with TTTS. The authors concluded that MC/DA twin

gestation appears to be a risk factor for CHDs. Conditions that lead to

abnormal placentation may also contribute to abnormal heart

development, especially in MC/DA twin pregnancies complicated with

TTTS. Fetal echocardiography may be considered for all MC/DA twin

gestations because ventricular septal defects and pulmonary stenosis are

the most common defects.

The Royal College of Obstetricians and Gynaecologists' clinical practice

guidelines on "Management of monochorionic twin pregnancy" (RCOG,

2008) stated that a fetal echocardiographic assessment should be

considered in the assessment of severe TTTS.

Pregnant Women Receiving Selective Serotonin Reuptake Inhibitors

Reefhuis and colleagues (2015) followed up on previously reported

associations between peri-conceptional use of selective serotonin

reuptake inhibitors (SSRIs) and specific birth defects using an expanded

dataset from the National Birth Defects Prevention Study. These

researchers performed a Bayesian analysis combining results from

independent published analyses with data from a multi-center population

based case-control study of birth defects. A total of 17,952 mothers of

infants with birth defects and 9,857 mothers of infants without birth

defects, identified through birth certificates or birth hospitals, with

estimated dates of delivery between 1997 and 2009 were included in this

analysis; exposures were citalopram, escitalopram, fluoxetine, paroxetine,

or sertraline use in the month before through the 3rd month of

pregnancy. Posterior OR estimates were adjusted to account for

maternal race/ethnicity, education, smoking, and pre-pregnancy obesity.

Main outcome measure was 14 birth defects categories that had


associations with SSRIs reported in the literature. Sertraline was the

most commonly reported SSRI, but none of the 5 previously reported birth

defects associations with sertraline was confirmed. For 9 previously

reported associations between maternal SSRI use and birth defect in

infants, findings were consistent with no association. High posterior ORs

excluding the null value were observed for 5 birth defects with paroxetine

(anencephaly 3.2, 95 % CI: 1.6 to 6.2; atrial septal defects 1.8, 95 % CI:

1.1 to 3.0; right ventricular outflow tract obstruction defects 2.4, 95 % CI:

1.4 to 3.9; gastroschisis 2.5, 95 % CI: 1.2 to 4.8; and omphalocele 3.5,95

% CI: 1.3 to 8.0) and for 2 defects with fluoxetine (right ventricular outflow

tract obstruction defects 2.0, 95 % CI: 1.4 to 3.1 and craniosynostosis 1.9,

95 % CI: 1.1 to 3.0). The authors concluded that these data provided

reassuring evidence for some SSRIs; but suggested that some birth

defects occurred 2 to 3.5 times more frequently among the infants of

women treated with paroxetine or fluoxetine early in pregnancy.

A 2015 study by the Centers for Disease Control and Prevention (CDC)

used new data to examine previous reported links between use of specific

SSRIs medications just before or during early pregnancy and the

occurrence of certain birth defects. Researchers looked at links with 5

different SSRI medications: citalopram, escitalopram, fluoxetine,

paroxetine, and sertraline. Although the new data confirmed the risks

seen with paroxetine, it did not appear to suggest that the risk is across

the board with all SSRIs. Therefore, fetal echocardiography is still

recommended for women exposed to paroxetine, but there doesn’t seem

to be enough evidence to recommend coverage of fetal echocardiograms

for all pregnant members receiving any SSRI. The study concluded that

despite the increased risks for certain birth defects from some SSRIs

found in this study, the actual risk for a birth defect among babies born to

women taking one of these medications is still very low. Because these

specific types of birth defects are rare, even doubling the risk still results

in a low absolute risk. For example, the risks for heart defects with

obstruction of the right ventricular outflow tract could increase from 10 per

10,000 births to about 24 per 10,000 births among babies of women who

are treated with paroxetine early in pregnancy.

Fetal Magnetocardiography


Fetal magnetocardiography (fMCG) is a new, non-invasive technique

used to monitor the spontaneous electrophysiological activity of the fetal

heart. Hrtankova and associates (2015) reviewed the evidence on the

clinical value of fMCG. These investigators performed an analysis of the

literature using database search engines PubMed, and SCOPE in field of

fMCG. Compared to cardiotocography and fetal electrocardiography,

fMCG is a more effective method with a higher resolution. The signal

obtained from the fetal heart is sufficiently precise and the quality allows

an assessment of PQRST complex alterations, and to detect fetal

arrhythmia. Thanks to early diagnosis of fetal arrhythmia, there is the

possibility for appropriate therapeutic intervention and the reduction of

unexplained fetal death in late gestation. These investigators also noted

that fMCG with high temporal resolution also increased the level of clinical

trials that recorded fetal heart rate (FHR) variability. According to the

latest theories, FHR variability is a possible indicator of fetal status and

enabled the study of the fetal autonomic nervous system indirectly. The

authors concluded that fMCG is an experimental method that requires

expensive equipment; it has yet to be shown in the future if this method

will get any application in clinical practice.

Eswaran and colleagues (2017) stated that fMCG provides the requisite

precision for diagnostic measurement of electrophysiological events in the

fetal heart. Despite its significant benefits, this technique with current

cryogenic based sensors has been limited to few centers, due to high

cost of maintenance. In this study, these researchers demonstrated that

a less expensive non-cryogenic alternative, optically pumped

magnetometers, can provide similar electrophysiological and quantitative

characteristics when subjected to direct comparison with the current

technology. They concluded that further research can potentially increase

its clinical use for fMCG.

Furthermore, an UpToDate review on "Overview of the general approach

to diagnosis and treatment of fetal arrhythmias" (Levine and Alexander,

2017) states that "Magnetocardiography shifts the electrical signals into

an evoked magnetic signal that can be processed to create a beat-to-beat

magnetocardiogram that looks much like a traditional electrocardiogram

(ECG). Continuous recordings can be performed for relatively sustained

periods and have permitted elegant demonstration of arrhythmia


onset/offset and more direct observation of mechanisms. The equipment

is not widely available, requires careful shielding and requires skilled

technical support, so the technology remainsinvestigational".

Fetal Surveillance in Sjögren’s Syndrome

Gupta and Gupta (2017) state that studies show a high incidence of poor

fetal outcomes for women with Sjögren’s syndrome; however pregnancy

outcomes in these women have not been extensively studied. The

authors conducted a literature review to evaluate Sjögren’s syndrome and

pregnancy. Gupta and Gupta found that well-known fetal outcomes in

Sjögren syndrome-complicated pregnancies include neonatal lupus and

congenital heart block (CHB), of which CHB is the most severe fetal

complication. CHB is thought to occur because of damage to the

atrioventricular node by anti-SS-A or anti-SS-B antibodies, or both. The

reported prevalence of CHB in the offspring of an anti-SS-A-positive

woman is 1% to 2%. The recurrence rate in a patient with antibodies, who

has a previous child affected, is approximately 10 times higher. Based on

Gupta’s review, frequent surveillance by serial echocardiograms and

obstetric sonograms between 16 to 20 weeks of gestation and thereafter

is required for at-risk pregnancies, with the goal of early diagnosis and

early treatment of incomplete CHB, thus improving the outcome for the

fetus.

Although there are no formal guidelines for type or frequency of testing to

detect fetal heart block, it is recommended that pregnant women with

Sjögren’s syndrome receive weekly pulsed Doppler fetal

echocardiography from the 18th through the 26th week of pregnancy and

then every other week until 32 weeks. "The most vulnerable period for the

fetus is during the period from 18 to 24 weeks gestation. Normal sinus

rhythm can progress to complete block in seven days during this high-risk

period. New onset of heart block is less likely during the 26th through the

30th week, and it rarely develops after 30 weeks of pregnancy" (eviCore,

2018).

A scientific statement from the American Heart Association by Donofrio et

al. (2014) states that maternal factors of Sjögren’s syndrome are

associated with the absolute risk of 1 to 5 percent of live births that will

have congenital heart block (CHB), risk increases to 11 to 19 percent for


prior affected child with CHB or neonatal lupus. It is recommended that

fetal echocardiography be performed at 16 weeks, then weekly or every

other week to 28 weeks. The authors state that studies have suggested

that high SSA values (≥50 U/mL) correlate with increased fetal risk, and

that concern for late myocardial involvement may justify additional

assessments in the third trimester. In addition to abnormalities in the

conduction system, up to 10% to 15% of SSA-exposed fetuses with

conduction system disease may also develop myocardial inflammation,

endocardial fibroelastosis, or atrioventricular (AV) valve apparatus

dysfunction. "Although the value of serial assessment for the detection of

the progression of myocardial inflammation or conduction system disease

from first-degree block (PR prolongation) to CHB has not been proved,

serial assessment at 1- to 2-week intervals starting at 16 weeks and

continuing through 28 weeks of gestation is reasonable to perform

because the potential benefits outweigh the risks. For women who have

had a previously affected child, more frequent serial assessment, at least

weekly, is recommended."

Fetal Echocardiography for Prediction of Fetal Demise After Laser Coagulation for Twin-Twin Transfusion Syndrome

In a systematic review and meta-analysis, Gijtenbeek and colleagues

(2019) examined the value of echocardiography and Doppler before

fetoscopic laser coagulation for TTTS in the prediction of intra-uterine

fetal demise (IUFD). These investigators compared pre-operative

parameters between fetuses with and without demise following laser

surgery. A total of 18 studies were included. Recipient twins have an

increased risk of demise in case of pre-operative absent/reversed flow

(A/REDF) in the umbilical artery (OR 2.76, 95 % CI: 1.78 to 4.28), absent

or reversed a-wave in the ductus venosus (OR 2.32, 95 % CI: 1.70 to

3.16), or a middle cerebral artery peak systolic velocity of greater than 1.5

multiples of the median (MoM) (OR 7.59, 95 % CI: 2.56 to 22.46). In

donors, only A/REDF in the umbilical artery (OR 3.40, 95 % CI: 2.68 to

4.32) and absent or reversed a-wave in the ductus venosus (OR 1.66, 95

% CI: 1.12 to 2.47) were associated with IUFD. No association was

found between donor-IUFD and pre-operative myocardial performance

index (MPI). Two studies found an association between abnormal MPI

and recipient demise. With this study, these researchers identified a set

of pre-operative Doppler parameters predictive of fetal demise following


laser surgery. The authors concluded that the utility of pre-operative

parameters that reflect cardiac function such as the MPI in predicting

IUFD remains unclear; more research is needed to examine the utility of

pre-operative echocardiographic parameters such as the MPI in

predicting IUFD.

The authors stated that this was the first review and meta‐analysis of pre

operative echocardiography and Doppler in the prediction of IUFD

following fetoscopic laser surgery. To maximize the sample size, these

researchers included all studies that examined fetal demise beforebirth,

not only early‐IUFD (less than 7 days). Other causes of demise such as

placental insufficiency or IUGR could therefore have influenced these

findings, even though the majority of IUFD following laser occurred in the

1st week after laser surgery. Other drawbacks of this study included the

following: Most studies were single-center reports, 50 % of the reports

were retrospective studies. In all but 1 study, selective coagulation was

used for all or for a proportion of cases. It is known that incomplete laser

coagulation is a risk factor for recurrent TTTS or post‐laser twin anemia

polycythemia sequence (TAPS) and therewith for possible subsequent

fetal demise. Finally, these investigators did not include fetal growth

discordance, selective fetal growth restriction (sFGR), or TAPS prior to

laser surgery in this study. They noted that future large‐scale prospective

studies could allow for multi-variate analysis into the interference of sFGR

and TAPS on fetal echocardiography and Doppler parameters for IUFD.

Incorporating signs of sFGR or TAPS, and factors such as Quintero

stage, hydrops, and gestational age at TTTS diagnosis, into aprediction

model together with the before‐mentioned Doppler parameters could be

useful in daily clinical care in cases where the risk of fetal demise turns

out to be high, to spend additional counseling time on cord occlusion as a

back‐up plan if laser surgery appears technically challenging. A

prediction model could also be useful in future clinical trials investigating

innovations in treatment of TTTS.

Documentation Requirements for Fetal Echocardiography


According to guidelines from the American Institute for Ultrasound in

Medicine (AIUM), fetal echocardiography should include the following

cardiac images:

Aortic arch;

Ductalarch;

Four-chamber view;

Inferior vena cava;

Left ventricular outflow tract;

Right ventricular outflow tract;

Short-axis views ("low" for ventricles and "high" for outflow tracts);

Superior vena cava; and

Three-vessel and trachea view.

According to the 2013 AIUM's practice parameter for the "Performance of

Fetal Echocardiography", indications for fetal echocardiography are often

based on a variety of parental and fetal risk factors for congenital heart

disease. However, most cases are not associated with known risk

factors. Common indications for a detailed scan of the fetal heart include

but are not limited to:

Maternal Indications Associated with Congenital Heart Disease

Autoimmune antibodies [anti-Ro (SSA)/anti-La (SSB)]

Familial inherited disorders (e.g., 22q11.2 deletion syndrome)

In-vitro fertilization

Metabolicdisease (e.g., diabetesmellitusandphenylketonuria)

Teratogen exposure (e.g., lithium andretinoids)

Fetal Indications

Abnormal cardiac screening examination

Abnormal heart rate or rhythm

Fetal chromosomal anomaly

Extra-cardiac anomaly

First-degree relative of a fetus with congenital heart disease

Hydrops

Increased nuchal translucency

Monochorionic twins


This AIUM (2013) practice parameter was published in conjunction with

the American College of Obstetricians and Gynecologists (ACOG), and

the Society for Maternal-Fetal Medicine (SMFM), and the American

Society of Echocardiography (ASE). Furthermore, this practice

parameter was endorsed by the American College of Radiology (ACR).

Source: AIUM Practice Parameter – Fetal Echocardiography (2013).

Code Code Description

76825 Echocardiography, fetal, cardiovascular system, real

time with image documentation (2D), with or without

M-mode recording;

76826 follow-up or repeat study

76827 Dopplerechocardiography, fetal, cardiovascularsystem,

pulsed wave and/or continuous wave with spectral

display; complete

76828 follow-up or repeat study

+93325 Doppler echocardiography color flow velocity mapping

(List separately in addition to codes for

echocardiography)

0475T Recording of fetal magnetic cardiac signal using at least

3 channels; patient recording and storage, data

scanning with signal extraction, technical analysis and

result, as well as supervision, review, and interpretation

of report by a physician or other qualified health care

professional



0476T patient recording, data scanning, with raw electronic

signal transfer of data and storage

0477T signal extraction, technical analysis, and result

0478T review, interpretation, report by physician or other

qualified health care professional

0541T

0542T

Myocardial imaging by magnetocardiography (MCG) for

detection of cardiac ischemia, by signal acquisition using

minimum 36 channel grid, generation of magnetic-field

time-series images, quantitative analysis of magnetic

dipoles, machine learning–derived clinical scoring, and

automated report generation

Q9950 Injection, sulfur hexafluoride lipid microspheres, per ml

B97.10,

B97.89

Unspecified viral infection

D68.61 Antiphospholipid syndrome

E10.10

E13.9

Diabetes mellitus [do not report for gestational diabetes]

F10.20

F10.29

Alcohol dependence

G40.001

G40.919

Epilepsy and recurrent seizures

I34.0 - I37.9 Mitral valve disorders, aortic valve disorders, tricuspid

valve disorders and pulmonary valve disorders, specified

as nonrheumatic,

I42.3 Endomyocardial (eosinophilic) disease

I42.4 Endocardial fibroelastosis

I42.6 Alcoholic cardiomyopathy



I50.1 - I50.9 Heart failure

I51.7 Cardiomegaly

I78.0 Hereditary hemorrhagic telangectasia

L93.0

L93.2

Lupus erythematosus

M05.40

M06.9

Rheumatoid arthritis

M32.0

M32.9

Systemic lupus erythematosus

M34.0

M34.9

Systemic sclerosis [scleroderma]

M35.00 -

M35.09

Sicca syndrome [Sjögren]

M35.9,

M36.8

Unspecified diffuse connective tissue disease

O24.011 -

O24.019,

O24.111 -

O24.119

O24.311 -

O24.319,

O24.811 -

O24.819

O24.911 -

O24.919

Diabetes mellitus in pregnancy [pre-existing, excludes

gestational diabetes]

O30.001

O30.93

Multiple gestation

O36.8310 -

O36.8399

Maternal care for abnormalities of the fetal heart rate or

rhythm



O98.411 -

O98.419,

O98.511 -

O98.519

Viral hepatitis and other viral diseases complicating

pregnancy

O98.611 -

O98.619,

O98.711 -

O98.719

O98.811 -

O98.819,

O99.830

Other specified infectious and parasitic diseases

complicating pregnancy

O98.911

O98.93

Unspecified maternal infectious and parasitic diseases

complicating pregnancy, childbirth and the puerperium

099.111

O99.119

Other diseases of the blood and blood-forming organs

and certain disorders involving the immune mechanism

complicating pregnancy with brackets stating

[Antiphospholipid syndrome]

O99.350

O99.353

Diseases of the nervous system complicating pregnancy

[epilepsy]

O99.411

O99.419

Diseases of the circulatory system complicating

pregnancy

O99.89 Other specified diseases and conditions complicating

pregnancy, childbirth and the puerperium [Systemic

lupus erythematosus (SLE)]

Q20.0

Q28.9

Congenital malformations of the circulatory system

Q79.6 Ehlers-Danlos syndrome

Q87.40

Q87.43

Marfan's syndrome

Q89.3 Situs inversus



Q89.7 Multiple congenital malformations, not elsewhere

classified

Q90.0

Q90.9

Down syndrome

Q91.0

Q91.3

Trisomy 18 [Edward's syndrome]

R56.1 Post traumatic seizures

R56.9 Unspecified convulsions [seizure disorder NOS]

R93.1,

R93.8

Abnormal findings on diagnostic imaging of heart and

coronary circulation and other body structures

T42.1x5+,

T42.5x5+

T42.6x5+,

T42.75x+

Adverse effects of other and unspecified anticonvulsants

Z3A.13

Z34.49

13 - 49 Weeks of gestation of pregnancy

Z82.79 Family history of other congenital malformations,

deformations and chromosomalabnormalities

Z98.89 Other specified postprocedural states

O09.811

O09.819

Supervision of pregnancy resulting from assisted

reproductive technology

O33.6xx0

O33.6xx9

Maternal care for disproportion due to hydrocephalic

fetus

O35.0xx0

O35.0xx9

Maternal care for (suspected) central nervous system

malformation in fetus

O35.1xx0

O35.1xx9

Maternal care for (suspected) chromosomal abnormality

in fetus


O35.2xx0

O35.2xx9

Maternal care for (suspected) hereditary disease in fetus

O35.3xx0

O35.3xx9

Maternal care for (suspected) damage to fetus from viral

disease in mother

O35.4xx0

O35.4xx9

Maternal care for (suspected) damage to fetus from

alcohol

O35.5xx0

O35.5xx9


drugs

O35.8xx0

O35.8xx9

Maternal care for (suspected) fetal abnormality and

damage

O35.9xx0

O35.9xx9


damage, unspecified

O36.0110

O36.0999

Maternal care for rhesus isoimmunization

O36.1110

O36.1999

Maternal care for other isoimmunization

O36.20x0

O36.23x9

Maternal care for hydrops fetalis

O36.8310

O03.8399

Maternal care for abnormalities of the fetal heart rate or

rhythm

O40.1XX0

O40.3XX9

Polyhydramnios

O43.011

O43.029

Placenta transfusion syndromes

Q27.0 Congenital absence and hypoplasia of umbilical artery

O09.811

O09.819

Supervision of pregnancy resulting from assisted

reproductive technology



O24.011 -

O24.019,

O24.111 -

O24.119

O24.311 -

O24.319,

O24.811 -

O24.819

O24.911 -

O24.919

Diabetes mellitus in pregnancy [pre-existing, excludes

gestational diabetes]

O33.6xx0

O33.6xx9

Maternal care for disproportion due to hydrocephalic

fetus

O35.0xx0

O35.0xx9

Maternal care for (suspected) central nervous system

malformation in fetus

O35.1xx0

O35.1xx9

Maternal care for (suspected) chromosomal abnormality

in fetus

O35.2xx0

O35.2xx9

Maternal care for (suspected) hereditary disease in fetus

O35.3xx0

O35.3xx9

Maternal care for (suspected) damage to fetus from viral

disease in mother

O35.4xx0

O35.4xx9


alcohol

O35.5xx0

O35.5xx9


drugs

O35.8xx0

O35.8xx9


damage

O35.9xx0

O35.9xx9


damage, unspecified

O36.0110

O36.0999

Maternal care for rhesus isoimmunization



O36.1110

O36.1999

Maternal care for other isoimmunization

O40.1xx0 -

O40.1xx9

Polyhydramnios

O43.011

O43.029

Placenta transfusion syndromes

O76 Abnormality in fetal heart rate and rhythm complicating

labor and delivery

O98.411 -

O98.419,

O98.511 -

O98.519

Viral hepatitis and other viral diseases complicating

pregnancy

O98.611 -

O98.619,

O98.711 -

O98.719

O98.811 -

O98.819,

O99.830

Other specified infectious and parasitic diseases


O98.911

O98.919

Unspecified maternal infectiousandparasiticdiseases


O99.411

O99.419

Diseases of the circulatory system complicating

pregnancy

Q27.0 Congenital absence and hypoplasia of umbilical artery

O09.511

O09.519

Supervision of elderly primigravida

O09.521

O09.529

Supervision of elderly multigravida




O24.410

O24.419

Gestational diabetes mellitus in pregnancy [not covered

even if requiring insulin after the first trimester]

O99.810

O99.815

Abnormal glucose complicating pregnancy, childbirth

and the puerperium

Z13.228 Encounter for screening for other metabolic disorders

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AETNA BETTER HEALTH® OF PENNSYLVANIA

Amendment to Aetna Clinical Policy Bulletin Number: 0106 Fetal

Echocardiography and Magnetocardiography

There are no amendments for Medicaid.

revised 02/24/2021

Date post:	02-Apr-2022
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Fetal Echocardiography and Magnetocardiography

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