Fisiologia Cardiaca Fetal

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DOI: 10.1542/neo.13-10-e5832012;13;e583 Neoreviews

Adrian Dyer and Catherine IkembaCore Concepts : Fetal Cardiac Physiology

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Core Concepts: Fetal Cardiac PhysiologyAdrian Dyer, MD,Catherine Ikemba, MD

Author DisclosureDrs Dyer and Ikembahave disclosed nonancial relationshipsrelevant to this article.This commentary doesnot containa discussion of anunapproved/investigative use of a commercial product/device.

AbstractThe fetal myocardium and circulation differ from that of the adult in many important ways. Postnatal circulation occurs in series with the right ventricle providing a full car-diac output to the pulmonary circulation and the left ventricle delivering that samecardiac output to the body (systemic circulation). In the fetus, however, there is a par-allel circulation in which organs receive blood ow from both ventricles, and the ven-tricular output is described as combined. Due to this arrangement, the fetus has uniquemethods to adapt to intrauterine stressors on the cardiovascular system. There are sev-eral normal physiologic transitions that take place after birth which may be perturbedby a compromised hemodynamic state or the presence of congenital heart disease. Thetransition to an adult circulation is a dynamic process, of which the understanding iscritical to the care of neonates.

Objectives After completing this article, readers should be able to:1. Describe the anatomy and physiology of the fetal cardiovascular system and how it

differs from postnatal circulation.2. Explain the physiologic changes of the fetal circulation that occur when confronted

with stress.3. Describe the physiology of common congenital heart disease in utero.4. List the important steps in the cardiovascular transition from fetus to neonate.5. Recognize the limitations of fetal echocardiography.

Fetal Myocardial Function and Cardiac OutputThe structure of the fetal myocardium is anatomically and functionally different than theadult myocardium. To understand the differences in the way the fetus and adult increasetheir CO, the basic components of CO will be discussed brie y.

CO is the product of heart rate (HR) and stroke volume (SV). CO HR SV. The maindeterminantsof SV (the effective amount of blood volume that is ejected with each heart beat)are preload, afterload, and contractility. Preload is the venous return to the heart or the blood volume that is available to be pumped by the ventricles. Afterload is the arterial pressureagainst which the heart has to contract. Contractility is the intrinsic ability of the myocardiumto contract or the force that can be generated at any given muscle length. The Frank Starlingprinciple states that CO increases with an increase in preload, or in other words, increase

stretch of the muscle, up to a critical atrial pressure/lengthof the muscle ber (ie, up to a certain preload). Past this point,increases in preload do not augment CO and actually are det-rimental, resulting in congestive heart failure.

The adult myocardium follows the Frank Starling princi-ple. Increase in preload is an important method for increas-ing contractility and thus CO in the adult. The fetalmyocardium also follows the Frank Starling law but oper-ates at the upper limit of the atrial pressure/SV curve(Fig 1). In other words, the fetus is unable to increase itsCO by increasing preload/muscle ber length. There area few theories as to why the fetus has a much lower preload

AbbreviationsCO: cardiac output DA: ductus arteriosusDV: ductus venosusHR: heart rateIVC: inferior vena cavaRV: right ventricleSV: stroke volume

University of Texas Southwestern Medical Center, Dallas, TX.

Article cardiovascular

NeoReviews Vol.13 No.10 October 2012 e583

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reserve and limited ability to in-crease its CO. The rst explanationis due to the immaturity of the fetalmyocardium. There is a higher per-centage of noncontractile proteinsin the fetal myocardium, up to60%, compared with 30% in theadult. The result is a stiffer, non-compliant myocardium. This isdemonstrated by the normal Dopp-ler ow signals across the atrioven-tricular valves in the fetal heart obtained on a fetal echocardio-gram. In normal older childrenand adults, there is predominately early passive lling of the ventriclesduring ventricular diastole (larger E wave) and only a small amount of

lling with atrial systole (small A wave) (Fig 2). In contrast, the fetusrelies on atrial systole ( atrial kick )for its preload instead of only pas-sive lling during diastole (ie, a smallE wave and large A wave are normalin the fetus but signi es diastolic dys-function in a child) (Fig 3). When there is diastolic dysfunc-

tion (or tachycardia) in the fetus, the atrioventricular in ow is single peak during atrial contraction (Fig 4).

In addition, the fetal myocardium handles calcium inef-ciently compared with the adult myocardium. The sarco-

plasmic reticulum is immature, resulting in a decreased

ability to use calcium. This can also explain the sensitivity

of neonates to calcium-channel blockers and the improve-ment in CO with calcium infusions in critically ill neonates.The other explanation is that the noncompliant fetal myo-cardium is secondary to the extrinsic constraints on thefetalmyocardium by the chest wall, pericardium, and uid- lledlungs. The implication is that to improve CO in the fetus,the predominant mechanism is to increase HR.

Adrenergic innervation of the fetus is also immature,thus HR is predominately dictated by cholinergic in uen-ces. This can explain the progressive decrease in HR that occurs as gestation progresses, as well as the bradycardicresponse to hypoxia that occurs in the fetus. In contrast,

the older infant

s response to hypoxia is typically tachycar-dia. Cortisol and thyroid hormone are important for thematurity of the fetal myocardium and adrenergic response.In the sheep model, it has been shown that thyroid hor-mone is important in late gestation for both the develop-ment of the b -adrenoreceptors and the maturity of themyosin chains in the ventricular myocardium.

Anatomy of the Fetal CirculationDuctus Venosus

The placenta functions as the major organ for gas ex-change in the fetus (Figs 5 and 6). Oxygenated blood

Figure 1. FrankStarling Law in the fetus versus maturemyocardium (see text for details). Increase in ventricular strokevolume (SV) as atrial pressure rises with increasing preload. Thefetal heart cannot increase its SV beyond a small incrementalincrease in atrial pressure, with peak SV occurring at w 4 or 5mm Hg. The mature adult heart can continue to increase its SV as preload increases up to atrial pressure 16 to 18 mm Hg.(Reprinted with permission from Rychik J. Fetal cardiovascularphysiology. Pediatr Cardiol . 2004;25:201209.)

Figure 2. Normal Doppler inow across the tricuspid valve in an adult. Note the prominentE wave representing ventricular diastole and smaller A wave representing atrial systole (seetext for details).

cardiovascular fetal physiology

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travels to the fetus via the umbilical vein. The umbilical

vein enters the fetal abdomen and travels toward the liver. A portion of this blood perfuses the left lobe of the liver.The rest bypasses the liver via the ductus venosus (DV),connecting the left branch of the portal vein to the com-mon hepatic vein where it joins the inferior vena cava(IVC ). In the IVC, the hepatic and systemic venous bloodruns with the DV blood; however, the blood coursingthrough the DV accelerates to pass through this narrow (0.5 2 mm) structure. This kinetic energy is transmittedinto the IVC and right atrium and preferentially propelsthe oxygenated blood from the DV across the foramenovale into the left atrium ( streaming effect ). Oxygenatedblood from the left hepatic vein, which is conveniently po-sitioned under the Eustachian valve, is also directed acrossthe foramen ovale into the left atrium. The importance of this is that highly oxygenated blood is preferentially sup-plied to the organs with the highest oxygen demand:the brain and myocardium (via the coronary circulation).

Ductus Venosus Under Fetal StressThe DV is under tonic adrenergic control and responds tonitric oxide and prostaglandins. It can dilate or constrict depending on systemic in uences. For example, in fetalhypoxemia in sheep, the diameter of the DV can increaseby 60%. Therefore, the DV seems to be important in cases

of fetal stress. In fact, the Dopplerow signal of the DV is very useful

in the overall assessment of fetal wellbeing and is part of the Huhta car-diovascularpro le score, whichis de-scribed below.

Right VentricleThe remaining deoxygenated bloodfrom the IVC, right hepatic vein,and superior vena cava is directedacross the tricuspid valve to theRV. The normal tricuspid valve ap-paratus is extremely competent in

fetal life. Any degree of regurgita-tion is abnormal and is a usefulindicator of either abnormal mor-phology of the valve, right ventric-ular dysfunction, or downstreamobstruction.

Ductus ArteriosusThe majority of the blood that ispumped by the RV across the pul-monary valve into the main pulmo-

nary artery is directed across the ductus arteriosus (DA).

The DA is a wide muscular vessel that bypasses the pul-monary circulation and instead connects the pulmonary arterial trunk to the descending aorta. In utero, theDA remains open due to the hypoxic fetal environment,nitric oxide, and high circulating levels of prostaglandins.The direction of ow in the DA is dictated by the balancebetween the resistances of the pulmonary vascular andplacental beds. A majority of blood passing throughthe DA returns to the placenta for gas exchange, whereasthe remainder perfuses the lower body.

Ductus Arteriosus and Fetal Congenital Heart

DiseaseIn the case of critical pulmonary valve stenosis or pulmo-nary atresia, there is very little to no blood ow from theRV into the branch pulmonary arteries. Therefore, pulmo-nary perfusion relies on reversal of the direction of blood

ow in the DA from normal right-to-left to left-to-right ow. Postnatally, if this ductus is not kept open with pros-

taglandin, these infants become profoundly cyanotic.

Foramen OvaleIn utero, the mean right atrial pressure is slightly higherthan the left atrial pressure (4 5 mm Hg versus 2 3mm Hg). This gradient promotes the normal right-to-left

Figure 3. Normal Doppler inow across the tricuspid valve in the fetus. Note theprominent A wave (ie, atrial systole) and smaller E wave (ie, ventricular diastole) (see textfor details).





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blood ow of oxygenated blood across the foramen ovalein the fetus and provides the majority of left ventricular

preload. Around 28 to 30 weeks gestation, the amount of blood crossing the foramen decreases. At the same time,pulmonary blood ow, provided by the right atrium and ventricle, increases. Thus there is increased pulmonary ve-nous return to the left atrium, which keeps left ventricularpreload fairly constant and as it prepares for a postnatalcirculation.

Left Atrium and Left VentriclePulmonary venous return is added to the DV and left he-patic venous blood in the left atrium. Based on sheepstudies, it was initially thought that only a trivial fraction

of the right ventricular output ( < 10%) went to the lungs,and therefore, pulmonary venous return contributed triv-ially to left ventricular preload. Human fetal studies haverevealed that a higher proportion of right ventricular out-put goes to the pulmonary circulation (13% 25%), espe-cially after 32 weeks gestation. From the left atrium,this highly oxygenated blood is pumped by the left ventri-cle to the coronary and cerebral circulations (ie, the organs with the highest oxygen demands).

Aortic Isthmus A trivial portion of the left ventricular CO traverses thedistal aortic arch to get to the descending aorta, lower

body, and placenta. The aortic isth-mus is the segment between the or-igin of the left subclavian artery andthe aortic end of the DA. Normally,the left ventricle causes forward ow in the isthmus. The RV may, undersome conditions, pump blood ret-rograde in the isthmus via the DA.The direction of blood ow in thisregion depends on the relative con-tractility of the left ventricle andRV, as well as the downstream resis-tances of the upper body versus theplacenta. Under normal anatomicand physiologic circumstances, thelow resistance of the placenta resultsin forward ow in the aortic isthmusduring systole and diastole.

Aortic Isthmus and FetalCongenital Heart Disease

This region demonstrates the amaz-ingadaptabilityof thefetal circulation.In the case of decreased effective left

ventricular output (ie, hypoplastic left heart syndrome orcritical aortic stenosis), the ow in the aortic isthmus and of-

ten the entire transverse arch, is retrograde and suppliedfrom the RV via the DA. This ensures cerebral perfusionand allows forcontinued development of the brain in fetuses with left-sided obstructive lesions. However, these patientsare at risk for developmental delay, and there is suspicionthat the abnormal, retrograde ow in the isthmus may con-tribute. Obstructive left-sided heart disease is also an exam-ple of the important exibility of the fetal system due to thefetal circulation being in parallel (interdependent). If theoutput of one ventricle falls, the other ventricle increasesits output to compensate, and therefore, may grow largerin comparison. In fetuses with hypoplastic left heart syn-

drome, for example, the RV is dilated and hypertrophied.Aortic Isthmus During Fetal Stress

The direction of ow in this region also may be retrogradein a fetus with signi cant leftventriculardysfunction. This isanother example of the adaptability of the fetal circulationand the ability to autoregulate. To preserve cerebral perfu-sion in the developing brain, the cerebral resistance de-creases and promotes retrograde blood ow from the RV.

Fetal Cardiovascular System Under Stress As discussed above, the afterload on a ventricle can bethought of as the pressure that it has to overcome to open

Figure 4. Abnormal Doppler inow across the tricuspid valve in a fetus with hydropsfetalis. Note the single peak inow signal wave (see text for details).





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either the aortic or pulmonary valve. In the fetus, thecombined afterload of the left ventricle (brain, upperbody, and aortic isthmus, which is narrowed even inthe absence of a coarctation) is higher than the right ven-tricular afterload (low resistance DA and placenta in ad-dition to the higher resistance lower body and lung). Theend result is a higher output of the RV compared with theleft (twice as much in fetal sheep). In the human fetus, thebrain is bigger, has a larger vascular surface area, and there-fore offers less resistance, allowing the left ventricular out-put to be more than in sheep but still less than the RV.During stressful situations, autoregulation of blood ow occurs, which alters the afterload of a particular organ thus

preserving blood ow to those organs with the highest oxygen demand. For example, in fetuses with congenitalheart disease consisting of a single ventricle that involvesintracardiac mixing and lower oxygen content to the brain,the relative cerebral hypoxemia stimulates a decrease in ce-rebral vascular resistance resulting in increased diastolicblood ow to the brain. The brain sparing effect may alsobe seen in the case of maternal hypoxia or impaired placen-tal gas exchange in which there is decreased fetal oxygencontent but preservation of blood ow. The fetus is able

to maintain CO by redirecting ow to the organs withthe highest oxygen demands, such as the myocardium, ad-renal glands, and brain, at the expense of the gastrointes-tinal tract, kidneys, lungs, and periphery.

Another interesting example of the interplay betweenafterload and preload in the fetal cardiovascular system isdisplayed in the right ventricular response to stressors. As mentioned earlier, the RV provides more CO thanthe left ventricle, is larger, and has more wall stress (perLaplace s law: wall stress is directly proportional to trans-mural pressure and radius but inversely related to wallthickness). Alterations in preload or afterload affect both ventricles, but the RV is more sensitive to changes. It

Figure 5. Venous ow in the fetus. Diagram showing venousow patterns in the fetal lamb. Umbilical venous blood is

distributed to the left lobe of the liver, through the ductusvenosus (DV), and to the right lobe of the liver. Portal venousblood passes almost exclusively to the right lobe, but a smallproportion enters the DV. DV and left hepatic venous bloodpreferentially pass through the foramen ovale, whereas righthepatic venous and distal inferior vena caval blood arepreferentially directed through the tricuspid valve. Superiorvena caval blood almost all passes through the tricuspid valve.SVC[ superior vena cava; LHV [ left hepatic vein; RHV [ righthepatic vein. (Reprinted with permission from Rudolph AM.Hepatic and ductus venosus blood ows during fetal life.Hepatology . 1983;3:254258.)

Figure 6. Fetal circulation (see text for details). Diagram of the circulation in the normal fetus, showing the patterns of blood ow and the oxygen saturations in the main vessels.Note the higher oxygen saturation in the ascending aortacompared with the descending aorta and the lower saturationin the pulmonary artery. The oxygen saturations shown arederived from fetal lambs in utero. (Reprinted with permissionfrom Rudolph AM. Aortopulmonary transposition in the fetus:speculation on pathophysiology and therapy. Pediatr Res .2007;61[3]:375380.)





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responds with more profound hypertrophy, dilation, and/or dysfunction. Therefore, Doppler assessment of tricuspidin ow, evidence of tricuspid regurgitation, and IVC andDV signals are sensitive indicators of fetal distress. Dopplerassessment has been incorporated in the semiquantitativescoring system developed by Dr James Huhta and col-leagues that has been shown to be predictive of perinataloutcome in congenital heart disease and fetal hydrops.This cardiovascular pro le score includes ve categories:presence/severity of hydrops, umbilical venous and DV Dopplerpattern, heart size, cardiac function, andumbilicalarterial Doppler pattern. Each component is worth twopoints; thus a normal score is 10. Along with the biophys-ical pro le, the cardiovascular pro le score can be used topredict a fetus outcome, with a lower score indicating worseoutcomes.For example, in a hydropic fetus, a cardiovascular pro le score of six or less is associated with higherperinatal mortality.

Clinical Correlation of Maladaptive Increase inPreload (Fetal Congestive Heart Failure)

Twin-twin transfusion is thought to be due to a placental vasculopathy that occurs in the presence of monochorionictwins. The result is a smaller donor twin and a larger re-cipient twin who is at risk for signi cant cardiac dysfunc-tion and hydrops. The donor twin is volume depleted

and produces hormones in response. These include activa-tion of the renin-angiotensin system (elevated levels of an-giotensin II) and endothelin-1. These hormones adversely affect the vascular compliance of the donor cardiovascularsystem andpredispose thedonors to hypertension andath-erosclerotic disease later in life. More acutely, the net result in the recipient twin is increased volume load and a pro-gressive cardiomyopathy that leads to ventricular dilation,hypertrophy, and dysfunction. In addition, the hormonesthat are secreted in response to hypovolemia by the donortwin are passed to the recipient, which results in further volume retention, vasoconstriction, and ventricular hyper-

trophy in the recipient twin.

Clinical Correlation of Maladaptive Increase inAfterload

Premature constriction of the DA occurs rarely and is dueto either administration of prostaglandin synthesis inhibi-tors (ie, indomethacin, ibuprofen, aspirin, or any cycloox- ygenase enzyme inhibitors), or rarely, naturally occurringconstriction. The result is an acute increase in the afterloadof the RV. This can cause signi cant right ventriculardysfunction. The fetus compensates by increasing theamount of blood that is shunted right-to-left acrossthe foramen ovale, thus preserving combined CO.The left

ventricle can then become dilated. If the offending agent isremoved, as in short-term tocolysis with indomethacin,these fetuses usually improve. Patients who develop hy-drops in response to acute ductal constriction typically have concomitant premature constriction of the foramenovale, which inhibits the compensatory mechanism; com-bined CO is not able to be preserved and results in car-diac dysfunction.

Transitional CirculationThe neonatal myocardium rapidly increases SV after birth.There is both an increase in thyroid hormone productionshortly before birth and a catecholaminergic surge aroundthe time of birth.

Closure of the Foramen Ovale At birth, the onset of respiration in ates the lungs anddrops the pulmonary vascular resistance. Clamping of the umbilical cord removes the low resistance placenta,and the systemic resistance increases at the same time.This changes the competing systemic and pulmonary vas-cular resistances reversing the direction of ow across theDA. The result is increased blood ow in the branch pul-monary arteries and lungs, instead of across the DA tothe lower body, which now has a higher resistance. Asmore blood returns via the pulmonary veins to the left

atrium and less blood returns to the right atrium due toclamping of the umbilical cord, left atrial pressure increasescompared with the right, which closes the ap mechanismof the foramen ovale. Anatomic closure of the foramenovale typically is complete by age 3 years, but in many adults a small shunt persists and is hemodynamically insigni cant.

Closure of the Ductus ArteriosusThe DA functionally typically closes in 24 hours in ahealthy full-term neonate. Closure is mediated by in-creased oxygen tension and a change in circulating prosta-

glandins. Anatomic closure takes longer and is replacedby the ligamentum arteriosum. This process involvesthrombosis, brosis, and muscle contraction and is usu-ally completed by 2 to 3 months in a normal, full-terminfant. Closure of the DA may be delayed in pretermand/or hypoxic neonates.

Closure of the Ductus VenosusFunctional closure of the DV occurs soon after birth.There is decreased blood ow returning to the right atrium after the umbilical cord is clamped, which allowsthe DV to passively collapse. Anatomic closure may takeup to 3 weeks after birth.





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Limitations of Fetal Echocardiography Although fetal echocardiography is a powerful tool re-ported to identify 80% of signi cant congenital heart dis-ease, the unique features of fetal cardiovascular anatomy and physiology described earlier in this article lead to sev-eral important limitations to this test. There is a normalinteratrial communication in the fetus, the foramen ovale,thus secundum atrial septal defects cannot be detected inutero. There is limited pulmonary blood ow to the lungsof a fetus, and there is limited pulmonary venous returnsuch that pulmonary venous anatomy is often dif cult todelineate. The aortic isthmus is normally small in the fetus,and coarctation of the aorta often does not manifest untilthe DA closes in postnatal life. Finally, the pressure differ-ences between the right and left ventricle are small, thusa ventricular septal defect may not be detected in uterodue to minimal shunting across such a defect. These lim-itations are important for the neonatologist to keep inmind when evaluating a newborn who may have hada fetal echocardiogram.

ConclusionsThe fetal cardiovascular system has the unique capability of allowing the fetus to develop normally but also adapt tostressors encountered in utero, including signi cant con-genital heart disease. Echocardiography is a powerful non-invasive tool to evaluate the overall health of the fetalcardiovascular system. Understanding fetal anatomy andthe complex transitions that must take place to achieve nor-mal adult cardiac physiology is helpful in caring for normalneonates, as well as infants with congenital heart disease.

Suggested ReadingDonofrio MT, Bremer YA, Schieken RM, et al. Autoregulation of

cerebral blood ow in fetuses with congenital heart disease: thebrain sparing effect. Pediatr Cardiol . 2003;24(5):436 443

Falkensammer CB, Paul J, Huhta JC. Fetal congestive heart failure:correlation of Tei-index and Cardiovascular-score. J Perinat Med . 2001;29(5):390 398

Faye-Petersen OM, Crombleholme TM. Twin-to-twin transfusionsyndrome: Part I. Types and pathogenesis. NeoReviews . 2008;9(9):e370 e379

Friedman WF. The intrinsic physiologic properties of the developing heart. Prog Cardiovasc Dis . 1972;15(1):87 111

Ho SW, Angelini A, Moscoso G. Developmental cardiac anatomy.In: Long WA, ed. Fetal and Neonatal Cardiology . Philadelphia,PA: WB Saunders Company; 1990:3 15

Huhta JC. Right ventricular function in the human fetus. J Perinat Med . 2001;29(5):381 389

Kiserud T, Acharya G. The fetal circulation. [Review] Prenat Diagn .2004;24(13):1049 1059

Kovalchin JP, Silverman NH. The impact of fetal echocardiogra-phy. Pediatr Cardiol . 2004;25(3):299 306

Parellada J, Gest A. Fetal circulation and changes occurring at birth.In: Garson A Jr, Bricker JT, Fisher DJ, Neish SR, eds. The Science and Practice of Pediatric Cardiology , 2nd ed. Baltimore,MD: Williams and Wilkins; 1998:349 358

Robinson JN, Simpson LL, Abuhamad AZ. Screening for fetal heart disease with ultrasound. Clin Obstet Gynecol . 2003;46(4):890 896

Rudolph AM. Aortopulmonary transposition in the fetus: specula-tion on pathophysiology and therapy. Pediatr Res . 2007;61(3):375 380

Rudolph AM. Distribution and regulation of blood ow in the fetaland neonatal lamb. Circ Res . 1985;57(6):811 821

Rudolph AM. Hepatic and ductus venosus blood ows during fetallife. Hepatology . 1983;3(2):254 258

Rychik J. Fetal cardiovascular physiology. Pediatr Cardiol . 2004;25(3):201 209

American Board of Pediatrics Neonatal-PerinatalContent Specications

Know the factors affecting and regulatingmyocardial performance and function inthe fetus and newborn infant and duringthe transitional period.

Know the factors affecting and regulatingthe systemic circulation in the fetus(including umbilical vessels) and newborn infant during thetransitional period.

Know the appropriate techniques to assess cardiovascularfunction in the fetus and newborn infant.

Know the physiology of the ductus arteriosus.





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DOI: 10.1542/neo.13-10-e5832012;13;e583 Neoreviews

Adrian Dyer and Catherine IkembaCore Concepts : Fetal Cardiac Physiology

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