Andersons pediatric cardiology 265
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flowalonethroughourcurrentmeansoftraditionalDopplerechocardiography.
FIG.11.2 Placentalweighttobirthweightratioattermgestation(37to40
weeks’gestation).Thenormaldataaredisplayedinredasmeanand
dottedlinesas95%confidenceintervals.Inbluearethevaluesfor120
fetuseswithcomplexcongenitalheartdisease.Thebluelinereflectsthe
meanregressionforthegroupwithcongenitalheartdisease.(Modified
fromAlmogB,ShehataF,AljabriS,etal.Placentaweightpercentilecurves
forsingletonandtwinsdeliveries.Placenta.2011;32:58–62.)
FIG.11.3 Grosspathologyspecimenofplacentafromafull-termnewborn
withhypoplasticleftheartsyndrome.Thearrowpointstoanareaof
infarctionintheperipheralvascularwatershedregionoftheplacenta.
(FromRychikJ,GoffD,McKayE,etal.Characterizationoftheplacentain
thenewbornwithcongenitalheartdisease:distinctionsbasedontypeof
cardiacmalformation.PediatrCardiol.2018.Epubaheadofprint.)
Inutero,invivoassessmentoftheliving,functioningplacentawouldbeof
tremendousvaluebutitisquitechallenging.Variousgroupsareintheprocessof
developingtoolsforimaging-basedassessments.Thisapproachhasgreat
potentialtocontributetoourunderstandingofplacentaldysfunctionandits
influenceonfetaldevelopmentinthosewithCHD.Forexample,recent
investigationusingmagneticresonanceimagingtechniqueshasallowedfor
characterizationofplacentalsizeusingthree-dimensionaltechniques.20Unique
magneticresonanceimagingsequenceslookingatoxygensaturation,showa
significantdecreaseintheoxygencontentofumbilicalvenousbloodinfetuses
withCHD.21Umbilicalvenousbloodshouldbethemosthighlyoxygenatedin
thenormalfetalcirculation.However,inCHD,placentalvasculardysfunction
likelycontributestotherelativedeoxygenationseeninwhatshouldotherwisebe
highlyoxygenatedbloodcontent(seealsoChapter7).
Moreover,thecomplexinterplaybetweenthealteredfetalcirculationinCHD
andplacentalbloodflowisnotwellunderstood.Inthenormalfetalcirculation,
therightheartejectsthemajorityofitsvolumeacrosstheductusarteriosus,
whichjoinstheoutputoftheleftventricleinthedescendingaorta.Together,the
flowfromtherightandleftventricleistermedthecombinedcardiacoutput
(CCO),whichcanbeassessedbyestablishedfetalDopplerechocardiography
techniques.Placentalbloodflownormallycomprisesaboutone-thirdoffetal
CCOinthelatterhalfofpregnancy,decreasingtoone-fifthbytermgestation.
Thisproportionhasbeenshowntobedecreasedinplacentalinsufficiency,while
overallCCOismaintained.22Howplacentalbloodflowanditsrelationshipto
CCOisalteredinthesettingofpossibleplacentalabnormalitiesanddiseasespecificchangestothefetalcirculationisyetunknown.
Summary
Furtherstudyofthepostnatalplacentaandtheplacentainuteroareneeded.
Beyondtheimmediateimpactonfetusandmother,theplacentaplaysarolein
programminglong-termhealth.21Theplacentaactsasthefetus'ssolewindowto
theoutsideworld.Thispictureisfilteredthroughthehealthandmetabolismof
themother.Maternalfactors,suchasnutritionalhistory,bloodpressure,and
evenasthma,affectthemorphologicstructureoftheplacenta,andinturn,
programthefetus’organsandsystemsforlife.23Innormallydevelopingfetuses,
variationsinplacentalmorphologyatbirthareassociatedwitharangeof
disorderssuchashypertension,coronaryarterydisease,type2diabetes,and
colorectalcancer.23Itisnotknownhowabnormalitiesoftheplacentainfetuses
withCHDaffectfetalprogrammingandlong-termoutcomes;however,itis
highlyplausiblethatmanyofthesefactorsinfluenceoutcomesinourpatients
withCHD.Developmentoftoolsthatwillallowustostudyplacentalstructure
andfunctiontoahigherdegreeofaccuracywillallowforbetterunderstanding
offactorsinfluencingpostnataloutcomesinCHD.Thepresenceofplacental
abnormalitiesdetectedafterbirthsuggeststhatstructuralandfunctional
abnormalitiesarepresentduringgestation,manyofwhichmaybemodifiable.
Forexample,thefindingsofthrombosisandinfarctionindicatethepresenceofa
placentalthromboticvasculopathyinCHD.Ifconfirmedinutero,thisfinding
mayultimatelyleadtothedevelopmentoftreatmentstrategiesforplacental
dysfunctioninCHDsimilartothatofferedforotherfetalconditions.24
Whatisnowclearisthatlifebeforebirthplaysacriticalroleinoutcomes
afterbirth.Simplystratifyingpatientsbasedonthepresenceorabsenceofan
alteredmaternal-fetalenvironmentdefinedasthepresenceof(1)preeclampsia,
(2)asmallforgestationalagenewborn,or(3)prematurity,wasrecentlyshown
tohaveanimportantinfluenceonsurgicalsurvivalforCHD(Fig.11.4).25We
cannolongerignorethisimportantandpotentiallymodifiablevariable.Altering
thesubstrateoflifethroughfetaltherapyforplacentaldysfunctioninCHDmay
beawaytoimproveoutcomesinthisfragilepopulation.
