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Year : 2018  |  Volume : 2  |  Issue : 3  |  Page : 155-160

A journey from adult to fetal echocardiography

1 Consultant Cardiologist, Prime Diagnostic Centre, Chandigarh, India
2 Medical Student, Govt Medical College and Hospital, Chandigarh, India
3 Consultant Radiologist, Prime Diagnostic Centre, Chandigarh, India

Date of Web Publication10-Dec-2018

Correspondence Address:
Dr. U P Singh
Consultant Cardiologist, Prime Diagnostic Centre, SCO 155, Sector 24 D, Chandigarh - 160 023
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/jiae.jiae_26_18

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As a cardiologist in a group practice or hospital settings, many a times you are requested to comment on fetal Echocardiography performed by radiologist or fetal medicine specialist. With overconfidence, we perform or comment on fetal echocardiography without knowing critical differences between adult and fetal echocardiography. First, fetal heart at 20 weeks of gestation is of the size of an almond. Due to the limitation of resolution of ultrasound machines, small size of fetal heart makes it difficult to visualize many direct signs of congenital heart defects such as total anomalous pulmonary venous connection (TAPVC), transposition of the great arteries (TGA), coarctation, and double outlet right ventricle (RV). Hence, in fetal echo, we use indirect signs and clues to diagnose these disorders. Second, there are two physiological shunts in fetal circulation; fossa ovalis and ductus arteriosus which make its very different from adult circulation. A cardiologist needs to know about indirect signs, special views, peculiar fetal cardiac defects, and hemodynamics of fetal circulation before attempting fetal echocardiography. Many of us have an impression that fetal heart is just a miniature form of adult heart. Fetal echocardiography is a lot different from adult or pediatric echocardiography because there are many structural and functional differences in fetal circulation. Moreover, many congenital heart defects such as TGA, TAPVC, and ventricular septal defect, can present with only subtle findings, so we need to be more vigilant while performing fetal echocardiography.

Keywords: Ductal restriction, fetal echocardiography, prenatal

How to cite this article:
Singh U P, Singh H, Kaur L. A journey from adult to fetal echocardiography. J Indian Acad Echocardiogr Cardiovasc Imaging 2018;2:155-60

How to cite this URL:
Singh U P, Singh H, Kaur L. A journey from adult to fetal echocardiography. J Indian Acad Echocardiogr Cardiovasc Imaging [serial online] 2018 [cited 2020 Aug 11];2:155-60. Available from: http://www.jiaecho.org/text.asp?2018/2/3/155/247028

  Fetal Cardiac Size and Morphology Top

As national rules do not permit termination of pregnancy after 20 weeks, we should perform fetal echocardiography before 20 weeks to rule out significant and complex congenital heart defects which can impact survival and morbidity. In these cases, we also need a margin to perform time-consuming genetic/chromosomal studies before 20 weeks. Hence, the best time to perform fetal echocardiography is between 16 and 18 weeks of gestation. Another aspect to understand is that we screen all fetuses like in preventive health checkup and we would find cardiac abnormality in 1 in 200 fetuses.[1]

At 16–20 weeks of gestation, fetal heart is not bigger than an almond[2] [Figure 1], and it is challenging to see cardiac anatomy and functions in this small size. So, trying to find a heart defect is like looking for a needle in a haystack. Moreover, fetal heart rate at this gestation is about 140–150 beats per min. For this small heart size and high heart rate, ultrasound machine should have high temporal and spatial resolution.
Figure 1: Size of fetal heart at 19 weeks as compared with an almond

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Before we start scanning fetal heart, ultrasound machine settings should be changed to optimize the image. With understanding of ultrasound physics, we know that resolution depends on the width and depth of the scanning sector. Hence, we should keep width and depth to be minimum possible.[3] Best way is to zoom the image. If we zoom the image, only that sector of area of interest is scanned and thus frame rate is high. In contrast, by magnifying the image, we just magnify the image, but resolution does not improve. In fetal echo, it is a must to zoom area of interest to improve resolution. We should also use various tools like speckle reduction to improve gray scale. Most of the ultrasound presets have a high dynamic range, i.e., it can differentiate more shades of gray. This is important when you are scanning structures such as liver where we need tissue characterization. In heart imaging, we need clear demarcation of tissue blood interface. Thus, imaging would be better if dynamic range is kept low [Figure 2].
Figure 2: (a) Fetal echocardiography image of four-chamber view at high dynamic range. (b) Same view of the fetus with low dynamic range. LA: Left atrium, LV: Left ventricle, RA: Right atrium, RV: Right ventricle

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In two-dimensional (2D) imaging, axial resolution is better than lateral one, but azimuthal resolution is worse than axial and lateral resolution [Figure 3] Azimuthal resolution behaves like slice thickness of computed tomography scan or magnetic resonance imaging. Poor azimuthal resolution means that we see thick slice of heart as an image on the screen which would overlap structures present in that slice on each other. Color Doppler azimuthal resolution is worse than 2D resolution meaning color Doppler slice thicker than 2D. Color flow of various structures overlaps on each other. For example, pulmonary artery and aorta color signals can overlap in left ventricular outflow tract (LVOT) view and illusion is produced as if PA is arising from aorta [Figure 4]. Due to this resolution problem, we miss many direct signs of various disorders such as in total anomalous pulmonary venous connection (TAPVC) where pulmonary veins converge into a posterior chamber, but because of poor color Doppler resolution, they falsely appear to open into the left atrium (LA).
Figure 3: Illustration showing ultrasound beam from a probe demonstrating axial, lateral, and azimuthal planes

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Figure 4: Color Doppler image of fetal heart at outflow plane showing the right angle cross of pulmonary artery and aorta. Aorta flow is in red arrow which is in front plane and pulmonary artery flow in white arrow in backplane order. PA: Pulmonary artery, AO: Aorta

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  Fetal Cardiovascular Hemodynamics and Pathophysiology Top

Functionally, also fetal heart is different from adult heart. There are shunts which are not present in adult heart. These are ductus venosus, patent fossa ovalis, and ductus arteriosus [Figure 5]. Abnormal connections or absence of ductus venosus produce alteration in the right and left heart preloads.[4] These situations are peculiar to fetal circulation only as ductus venosus closes when umbilical blood flow stops.
Figure 5: Diagram of fetal circulation showing physiological shunts. Fossa ovalis shunting umbilical flow to left atrium and ductus arteriosus shunting blood from pulmonary artery to descending aorta. AO: Aorta, LV: Left ventricle, RA: Right atrium, RV: Right ventricle, DA: Ductus arteriousus, DV: Ductus venosus, UMV: Umbilical vein

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The presence of fossa ovalis and ductus arteriosus produces a communication between left and right circulations. Hence, if there is any obstruction due to valve abnormality or ventricular hypoplasia blood can flow to other side and maintain entire circulation by these shunts. For example, if there is tricuspid valve atresia, blood can flow to LA, LV, and then to aorta, and right-sided circulation is maintained through retrograde filling of pulmonary artery from aorta through ductus arteriosus. Further, areas of heart with lower flow would lag in growth. In tricuspid valve obstruction, RV and pulmonary arteries would become hypoplastic. Similarly, aortic or mitral stenosis can progress to hypoplastic left heart syndrome as pregnancy advances because blood is shunted to the right side and left side becomes hypoplastic due to low flow.

Second, in fetal circulation, only 12%–20% of right ventricular cardiac output goes to the lungs, and rest is shunted by ductus arteriosus to descending aorta and then placenta. Thus, pulmonary veins have reduced flow affecting their visualization.

Third, heart is surrounded by solid lungs with reduced compliance and behaves like constriction physiology causing ventricular interdependence. Preload changes to one ventricle affect other one also.

Fourth, RV is a dominant ventricle supplying lower half of the body, lungs, and placenta, while left ventricle only caters to upper half of the body.

An adult or pediatric cardiologist should understand these differences before attempting fetal echocardiography examination or giving expert opinion to a colleague.[5]

  A Special View Exclusive to Fetal Echocardiography Top

Yoo et al. described three-vessel tracheal view, which is a transverse view of the fetal upper mediastinum and is simple to obtain.[6] From four-chamber view, we tilt the probe cranially crossing LVOT and RVOT. Then, we slightly angulate the probe and move cranially to get three-vessel trachea (3VT) view. It demonstrates the main pulmonary artery, arch of aorta in long axis superior vena cava (SVC), and trachea in cross section. Trachea lies posterior to SVC and to the right of aorta. Aorta, ductus arteriosus, and pulmonary artery form two limbs of the V [Figure 6]. Both four-chamber view and 3VT are easily obtained even by a novice and can be used as a good screen tool.[7]
Figure 6: (a) Illustration showing scan plane of 3 vessel and trachea view cutting superior vena cava, aorta, pulmonary artery and ductus arteriosus. (b) Three-vessel and trachea view on color power Doppler showing aorta and pulmonary artery in blue color. (c) Illustration showing various structures and their relationship. SVC: Superior venacava, PA: Pulmonary artery, AO: Aorta, DA: Ductus arteriousus

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3VT view can give important clues to diagnose a condition such as transposition of the great arteries (TGA), pulmonary atresia, aortic atresia, coarctation of aorta, premature ductal restriction, aortic arch abnormalities, persistent left SVC, and more. For example, in hypoplastic left heart syndrome, small aorta is visualized filling retrogradely from ductus arteriosus. In coarctation, aorta is small but maintains forward flow.

  Diagnosis of Valvular Stenosis in Adult Versus Fetal Echocardiography Top

In adult echocardiography, valvular stenosis is diagnosed by thickened and doming valve. In fetal echocardiography done before 20 weeks, normal semilunar valve appears as a thick speck in diastole, but we cannot visualize it in systole as it hugs the arterial wall. With resolution of current ultrasound equipment, we are unable to clearly define doming and thickening of the valve. Hence, we make a diagnosis of stenotic valve if the valve is visible even in systole. Hence, we use this indirect sign to make a diagnosis of stenotic semilunar valve.

Second, in fetal circulation if there is a stenotic lesion or obstruction to blood flow, blood would preferentially flow to the other side through two shunts; fossa ovalis and ductus arteriosus. Hence, we do not get high gradients across stenotic valves like in adult echo. For example, in severe pulmonary stenosis, due to increased resistance across pulmonary valve, blood prefers to flow by shunting toward left side through fossa ovalis, and there is hardly any gradient across pulmonary valve.[8] The diagnosis is made by the presence of small pulmonary artery [Figure 7]. Hence, in fetal echocardiography if we are looking for direct signs of valvular stenosis, like thickened valve leaflets, doming, and gradient across the valve, we would miss majority of patients of valvular stenosis in the prenatal echo. We should look for indirect signs [Figure 8].
Figure 7: Power Doppler image at three-vessel and trachea view showing normal size aorta and small pulmonary artery. PA: Pulmonary artery, AO: Aorta

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Figure 8: Four-chamber view showing bulging of fossa ovalis to the right side (curved arrow). This fetus had mitral stenosis due to Gaucher's disease. Mitral valve did not show signs of doming, but there was mild elevation of inflow velocities. Bulging fossa ovalis was the clue. LA: Left atrium, RV: Right ventricle, LV: Left ventricle

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  Diagnosis of Coarctation of Aorta Top

In adult echocardiography, classic signs of coarctation of aorta are narrow coarctation segment, poststenotic dilatation, high gradient across coarctation segment, and the presence of collaterals. All these signs are not clear in fetal heart. Hence, if you are waiting for these classic signs, you would miss almost all patients of coarctation of aorta.[9]

In normal fetal circulation, isthmus is the narrowest portion of the arch. Further narrowing of this portion is difficult to differentiate from the normal. Instead, the most common finding of coarctation of aorta is dilatation of RA, RV, and PA. Due to obstruction to the left circulation, blood is shunted from LA to right atrium through fossa ovalis.[10] With this increased flow to the right side right atrium, RV and pulmonary artery are dilated.

  Diagnosis of Total Pulmonary Venous Drainage Top

Diagnosis of total pulmonary venous drainage in adult echocardiography is based on visualizing pulmonary veins draining into a confluent chamber posterior to LA and then demonstrating vertical vein or direct drainage into right atrium. There are two problems in the diagnosis of TAPVC in a fetus. First, as compared to adult circulation, only 12%–20% cardiac output goes to the lungs and thus pulmonary venous return is accordingly small. Usual venous flow velocities are below 10 cm/s, and pulmonary veins are small. Due to poor color Doppler resolution, even though pulmonary veins are opening into a posterior chamber, they seem to open into LA and wall of posterior chamber is not visualized. Due to these limitations, in the past, only 2% cases could be detected prenatally. Now, accuracy of diagnosis of TAPVC has improved with the use of indirect signs such as increased gap between descending aorta and posterior wall of LA on four-chamber view [Figure 9]. Other indirect signs are smooth rounded appearance of LA versus straight posterior wall and small twig-like chamber posterior to LA[11] [Figure 10]. Another indirect sign is Coumadin ridge, which is a small ledge between opening of left atrial appendage and left upper pulmonary vein [Figure 11]. In a study, Coumadin ridge was easy to recognize on four-chamber view.[12] The presence of Coumadin ridge indicates left upper pulmonary vein opening into LA, thus ruling out TAPVC.
Figure 9: (a) Four-chamber view showing increased distance between aorta and posterior wall of left atrium (double-sided arrow). (b) Illustration showing increased distance between aorta and posterior wall of left atrium (double-sided arrow). LA: Left atrium, RA: Right atrium

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Figure 10: (a) Four-chamber view showing linear lucent area behind left atrium called “twig sign” (curved arrow). (b) Illustration showing small twig-like structure in total anomalous pulmonary venous connection behind left atrium (curved arrow). LA: Left atrium, RA: Right atrium, Ao: Aorta

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Figure 11: (a) Four-chamber view showing Coumadin ridge (curved arrow). (b) Illustration showing Coumadin ridge (curved arrow). LA: Left atrium, RA: Right atrium, LAA: Left atrial appendage, LUPV: Left upper pulmonary vein

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  Diagnosis of Transposition of the Great Arteries Top

In adult echo, d-TGA is diagnosed by the absence of circle and saucer sign on short axis view and presence of two circles representing aorta and pulmonary arteries. Second, we could demonstrate posterior angulation and bifurcation of artery arising from left ventricle plus nonbifurcating aorta, arising from RV.

On fetal echo, due to small size of cardiac structures, these direct signs are difficult to ascertain, so we rely on indirect signs. In d-TGA, both great vessels show a parallel course instead of crossing each other at right angle in a normal fetus. Second, in D-TGA, both great arteries lie in superior-inferior planes rather than side by side on 3VT view. Hence, on 3VT view, we would see only one artery at one given plane rather than both great arteries and this was described as I sign instead of V sign. These clues help us to suspect TGA.[13]

  Diagnosis of Cardiac Arrhythmia on Fetal Echo Top

Nonavailability of electrocardiography during fetal life makes a diagnosis of arrhythmia more challenging. Hence, we again depend on indirect signs.[14] We use mechanical events to assess electrical activity. For diagnosis of arrhythmias, we use atrial and ventricular activity to be displayed simultaneously.[15] Using M mode cursor line in a plane to transverses one ventricle and one atrium, we visualize both atrial and ventricular contractions. Atrial contraction represents P wave and ventricular QRS complex [Figure 12]. Similarly, we use pulse Doppler at various sites such as LV or RV inflow and outflow signals, renal vein and artery, pulmonary vein and artery,[16] aorta and inferior vena cava (IVC), and aorta and SVC, to get both atrial and ventricular activities. Based on atrial and ventricular activities, we can diagnose almost all arrhythmias. We can also measure PR interval which is time between onset of “a” wave and onset of ejection wave[17] [Figure 13].
Figure 12: M mode of fetal heart showing ventricular contraction (V) and atrial contraction (A). Note atrial rate (white arrows) is faster than ventricular rate and they are dissociated with each other indicating complete heart block

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Figure 13: Pulse Doppler tracing of left ventricular inflow and outflow signals taken close to mitral valve opening. It shows left ventricular inflow velocities “e” and “a” and outflow velocity (V). PR interval on electrocardiogram is measured from onset of “a” wave and onset of “v” wave (double-sided arrow)

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  Disorders Exclusive to Fetal Heart Top

There can be situations which can happen only in fetal life like ductal restriction. Ductus arteriosus is important in fetal life as it shunts 80-90% of right ventricular output to descending aorta. Ductal patency is maintained by prostaglandins released from placenta and oxygen saturation. Duct becomes sensitive to prostaglandin inhibition in advanced pregnancy. Restriction of ductus arteriosus can develop due to prostaglandin inhibition by NSAIDs, steroids, flavonoids, and antioxidants in herbal products and food items such as green tea and dark chocolate. Ductal restriction is reversible after removal of the causative agent.[18],[19] However, if restriction continues due to delay in diagnosis, there is increased RV afterload and causes heart failure, hydrops, and even fetal demise. Ductus restriction is diagnosed by increased systolic and diastolic velocities across the ductus in 3VT or sagittal view [Figure 14].
Figure 14: CW at level of ductus arteriosus showing increased systolic and diastolic velocities suggesting ductal restriction. CW: Continuous Doppler

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Another abnormality unique to fetus is abnormal drainage of umbilical vein into IVC, portal sinus, renal vein, and iliac vein due to the absence of ductus venosus. Ductus venosus is a narrow vessel which connects umbilical vein to IVC. By producing increased velocity jet, this vessel diverts oxygenated blood of umbilical vein (UV) selectively to LA. If ductus venosus is absent, entire umbilical blood enters right atrium through IVC or a direct opening of UV into RA causing increased preload and failure[20] [Figure 15].
Figure 15: Power Doppler in glass body mode showing umbilical vein draining directly into the right atrium bypassing liver

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  Conclusion Top

Fetal echocardiography is a separate specialty. There are many differences between adult and fetal echocardiography. Small size of fetal heart challenges the resolution of ultrasound machine. Due to poor color Doppler and azimuthal resolutions, structures overlap creating ambiguity in diagnosis. Understanding of the challenges of small size of the fetal heart and peculiar circulatory differences is mandatory before we attempt fetal echocardiography.

Fetal cardiac specialists have developed many indirect signs and tricks to circumvent problems of low resolution, and learning curve of fetal echocardiography is long and challenging.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Abu-Harb M, Hey E, Wren C. Death in infancy from unrecognised congenital heart disease. Arch Dis Child 1994;71:3-7.  Back to cited text no. 1
Picazo-Angelin B, Zabala-Argüelles JI, Anderson RH, Sánchez-Quintana D. Anatomy of the normal fetal heart: The basis for understanding fetal echocardiography. Annals of Pediatric Cardiology. 2018;11:164-73.  Back to cited text no. 2
Young R, O'Leary PW. Principle of cardiovascular ultrasound. In: Eidem BW, Cetta F, O'Leary PW, editors. Echocardiography in Pediatric and Adult Congenital Heart Disease. Philadelphia, PA: Wolters Kluwer, Lippincott Williams & Wilkins Health; 2010. p. 1-9.  Back to cited text no. 3
Mielke G, Benda N. Cardiac output and central distribution of blood flow in the human fetus. Circulation 2001;103:1662-8.  Back to cited text no. 4
Griffin D, Cohen-Overbeek T, Campbell S. Fetal and utero-placental blood flow. Clin Obstet Gynaecol 1983;10:565-602.  Back to cited text no. 5
Yoo SJ, Lee YH, Kim ES, Ryu HM, Kim MY, Choi HK, et al. Three-vessel view of the fetal upper mediastinum: An easy means of detecting abnormalities of the ventricular outflow tracts and great arteries during obstetric screening. Ultrasound Obstet Gynecol 1997;9:173-82.  Back to cited text no. 6
Gardiner H, Chaoui R. The fetal three-vessel and tracheal view revisited. Semin Fetal Neonatal Med 2013;18:261-8.  Back to cited text no. 7
Kaguelidou F, Fermont L, Boudjemline Y, Le Bidois J, Batisse A, Bonnet D, et al. Foetal echocardiographic assessment of tetralogy of fallot and post-natal outcome. Eur Heart J 2008;29:1432-8.  Back to cited text no. 8
Allan LD, Chita SK, Anderson RH, Fagg N, Crawford DC, Tynan MJ, et al. Coarctation of the aorta in prenatal life: An echocardiographic, anatomical, and functional study. Br Heart J 1988;59:356-60.  Back to cited text no. 9
Hornberger LK, Sahn DJ, Kleinman CS, Copel J, Silverman NH. Antenatal diagnosis of coarctation of the aorta: A multicenter experience. J Am Coll Cardiol 1994;23:417-23.  Back to cited text no. 10
Kao CC, Hsieh CC, Cheng PJ, Chiang CH, Huang SY. Total anomalous pulmonary venous connection: From embryology to a prenatal ultrasound diagnostic update. J Med Ultrasound 2017;25:e130-7.  Back to cited text no. 11
Singh U, Preet M, Kaur L. Use of ‘coumadin ridge’: An easy sign to rule out TAPVC. Ultrasound Obstet Gynecol 2017;50 Supp l: 244.  Back to cited text no. 12
Viñals F, Ascenzo R, Poblete P, Comas C, Vargas G, Giuliano A, et al. Simple approach to prenatal diagnosis of transposition of the great arteries. Ultrasound Obstet Gynecol 2006;28:22-5.  Back to cited text no. 13
Kleinman CS, Nehgme RA. Cardiac arrhythmias in the human fetus. Pediatr Cardiol 2004;25:234-51.  Back to cited text no. 14
Strasburger JF. Prenatal diagnosis of fetal arrhythmias. Clin Perinatol 2005;32:891-912, viii.  Back to cited text no. 15
Carvalho JS, Prefumo F, Ciardelli V, Sairam S, Bhide A, Shinebourne EA, et al. Evaluation of fetal arrhythmias from simultaneous pulsed wave Doppler in pulmonary artery and vein. Heart 2007;93:1448-53.  Back to cited text no. 16
Sonesson SE, Salomonsson S, Jacobsson LA, Bremme K, Wahren-Herlenius M. Signs of first-degree heart block occur in one-third of fetuses of pregnant women with anti-SSA/Ro 52-kd antibodies. Arthritis Rheum 2004;50:1253-61.  Back to cited text no. 17
Zielinsky P, Busato S. Prenatal effects of maternal consumption of polyphenol-rich foods in late pregnancy upon fetal ductus arteriosus. Birth Defects Res C Embryo Today 2013;99:256-74.  Back to cited text no. 18
Singh U, Kaur M, Kaur L. A caution for use of herbal products and flavonoids during pregnancy: Uncommon causes of ductal restriction. Ultrasound Obstet Gynecol 2016;48 Suppl 1:296.  Back to cited text no. 19
Berg C, Kamil D, Geipel A, Kohl T, Knöpfle G, Hansmann M, et al. Absence of ductus venosus-importance of umbilical venous drainage site. Ultrasound Obstet Gynecol 2006;28:275-81.  Back to cited text no. 20


  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8], [Figure 9], [Figure 10], [Figure 11], [Figure 12], [Figure 13], [Figure 14], [Figure 15]


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