Andersons pediatric cardiology 1080

Somedegreeofhyperemiaofthesevesselsiscommoninnewborninfants.
Thereiscontroversywithregardtothestructureoftheintimallayersduring
fetallife.Eccentricallyplacedintimalcushions,ormoundscomposedofsmooth
muscleandelastictissue,havebeendescribedbymanyauthors,with
suggestionsmadethattheformationofthesemoundsprecedesnormalductal
closuresubsequenttobirth.However,itisquestionablewhethertheintimal
cushionsareproducedduringnormalfetalmaturation.Whenaccountistakenof
thehighflowofbloodthroughthefetalduct,itisdifficulttoconceivethat
prominentprotrusionsofintimaintothelumencouldexistwithoutinducing
turbulentflowandabruit.Nosuchbruitisheardintheundisturbedductsoffetal
lambsatterm.Furthermore,inmanyofthestudiessuggestingthepresenceof
intimalcushions,thetissueshaveusuallybeensubjectedtooneormore
perturbations,suchasrelativelyslowfixation,mechanicalstimulation,or
cessationofcirculationwithlossofintraluminaldistendingpressure.Onthis
basis,theexistenceofintimalcushionsasprenatalstructureshasbeen
challenged.Inaseriesofexperiments,32–36Hornbladandcolleaguesshowed
that,independentofthedegreeofclosure,thelumenoftheductremainedround,
waswithoutdeformation,andshowednoevidenceofformationofmounds.Wall
thicknessincreasedatthetimeofclosure,whiletheinternalelasticlamina
becamecorrugated,especiallyinthemidportionofthevessels.Adecreaseinthe
lumenwasassociatedwithaccumulationofendothelialcellswithinthelumen.
Theyconcludedthatclosurewasaidedbypassivecentraldisplacementof
endothelialandinnermedialcellsbutthatnopartofthemediallayerwas
preparedprenatallyforthisprocess.32–36Thesefindingsendorsedearlierstudies
inthehuman,whichsuggestedthatthecushionsappearedasanormalreparative
reactiontodistendingforcesduringfetallife.37
Atbirth,thevesselunequivocallyconstricts.Theintimalthickenings,or
cushions,becomeirregularridgesprotrudingintothelumen,runningmainly
lengthwise.Bytheirextrusion,theyexerttractiononthemedia,causing
disorganizationandformationofmucoidlakes(seeFig.41.5).Anatomic
obliterationfollowsfunctionalclosure.Theprocessbeginswithnecrosisofthe

innerwall,followedbytheformationofdensefibroustissue.Thelumenis
progressivelyobliteratedbyaprocessoffibrosis,probablyrepresenting
organizationofmuralorocclusivethrombus.Eventually,theductbecomes
convertedintoafibrousstrand,thearterialligament,whichmaybecome
calcified.Anatomicobliterationmaytakeseveralweekstocomplete.
Approximatelytwo-thirdsofductsarenormallyobliteratedbytheageof2


weeks38andalmostallby1year.

PersistentlyPatentArterialDuct
Asstatedearlier,innormalcircumstancesallductsshouldbeconvertedtoan
arterialligamentwithinthefirstyearoflife,withtwo-thirdsclosingintheinitial
2weeks.However,someductsneverclose.Thesearethechannelsbest
describedasshowingpersistentpatency.Gittenberger-de-Groot39foundthe
internalelasticlaminatobeintactinsome,butnotall,ofthepersistentlypatent
ductsstudiedhistologically,alongwithasparsityofintimalcushions(Fig.41.6).
Bakker37hadnotedsimilarfindings,describingthemintermsof“aortification.”

FIG.41.6 Histologicsectionthroughthewallsofapersistentlypatent
arterialduct.Notetheintactinternalelasticlaminaandlackofintimal
mounds.(CourtesyProfessorSiewYenHo,ImperialCollege,London.)

Theduct,ifpersistingasapatentstructure,joinsthepulmonaryarteriestothe
descendingaortainthefashionseenintheneonate(Fig.41.7).Thechannelitself
canvarymarkedlyinitswidth(Fig.41.8).


FIG.41.7 Dissectionshowingthecourseofapersistentlypatentarterial
duct.Asexpected,itfollowsthecourseofthechannelseenatbirth(see

Fig.41.3).