Andersons pediatric cardiology 100
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atrioventricularjunctionsofthenormalheart.22Insomecircumstances,theycan
persistandfunctionassubstratesforventricularpreexcitationinotherwise
normallystructuredhearts.Thesestructuresalsoformtheanomalous
atrioventricularnodesasseeninthesettingofcongenitalmalformationssuchas
congenitallycorrectedtranspositionanddouble-inletleftventricle(seeChapters
39and50).Inthecourseofnormaldevelopment,however,onlythe
atrioventricularconductionaxisderivedfromtheoriginalinterventricularring
providesmuscularcontinuitybetweentheatrialandventricularmusclesmasses.
MyocardialVascularizationand
FormationoftheVentricularWalls
Whentheventricularloopisfirstformed,thereisnoneedforanyparticular
systemforvascularizationofthedevelopingwalls,sincemyocardiumisbroken
upintoamassofindividualtrabeculationslinedbyendocardium,withlittle
formationofacompactlayer.Theintertrabecularspaces,whichreachalmostto
theepicardium,playarolesubsequentlyintheformationofthemyocardial
vascularbed.Thefirstindicationoftheepicardialtrunksthatfeedthemural
vesselsisseenwiththeappearanceofasubepicardialendothelialplexus.This
networksubsequentlyestablishescontinuitywithendothelialsproutsthatgrow
fromthewallsofthedevelopingaorticvalvarsinuses.Itwasinitiallythought
thatmultiplecoronaryarterialorificesarosefromboththedevelopingaorticand
pulmonaryroots.23Wenowknowthattheendothelialsproutsgrowonlyfrom
theaorta,makingcontactwithaperitruncalring,whichinturnuniteswiththe
epicardialandmuralvessels.24
Thecompactlayeroftheventricularwallsbeginstoproliferateconcomitant
withtheestablishmentofnourishmentviathedevelopingcoronaryarterialtree,
asopposedtodirectnourishmentfromtheventricularcavities.Attheinitial
stagesofdirectnourishment,atCarnegiestage18inthehuman,thereisstillan
extensivelayeroftrabecularmyocardium,whichisappreciablythickerthanthe
compactlayer(Fig.3.32,left).Thetrabeculations,however,failtomatchthe
extentofproliferationofthecompactcomponent,sobyCarnegiestage22,the
thicknessofthecompactwallhasexceededthethicknessoftheremaining
trabecularlayer(seeFig.3.32,right).Muchhasbeenwritteninrecentdecades
regardingthesignificanceofso-called“noncompaction.”Thereisnoevidence
ofwhichweareawaretosuggestthatthecompactlayeroftheventricular
myocardiumisproducedbycoalescenceofpreexistingtrabeculations.The
papillarymusclesoftheatrioventricularvalves(seeFig.3.32,right),andthe
trabecularcomponentsoftherightventricle,incontrast,arelikelyproducedby
suchcompaction.Theventricularwalls,nonetheless,areproducedbyongoing
proliferationoftheinitialcompactcomponent.
FIG.3.32 Left,Long-axissectionfromanembryoatCarnegiestage18.
Right,Short-axissectionthroughtheventricularmassofanembryoat
Carnegiestage22.Thereislikelylessthanaweekofdevelopment
betweenthetwostages,butinthatshortperiodthecardiomyocytes
makingupcompactlayerofthewallhaveproliferatedsuchthatits
thicknessequalsorexceedsthatofthetrabecularlayer.Thereisno
evidencetoshowthattheinitialtrabeculationcoalescetoproducethe
compactlayer,althoughasseenintherightpaneltheydocompacttoform
thepapillarymusclesofthemitralvalve.
