Embryology Cardiovascula rsystem development

7/30/2019 Embryology Cardiovascula rsystem development

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EMBRYOLOGY

BY

Dr. THAAER MOHAMMED DAHER ALSAAD

SPECIALIST IN GENERAL SURGERY

M.B.Ch.B. (MBBS) F.I.B.M.S. (PhD)SENIOR LECTURER

ISM MSU


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Cardiovascular System

Heart development


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Establishment of the Cardiogenic Field 1/2

The vascular system appears in the middle of the third week. Cardiac progenitor cells lie in the ectoderm, immediately

lateral to the primitive streak. Cells destined to form cranial segments of the heart, the outflow

tract, migrate first, and cells forming more caudal portions, rightventricle, left ventricle, and sinus venosus, respectively, migrate in

sequential order. The cells proceed toward the cranium and position themselves

rostral to the buccopharyngeal membrane and neural folds.

The cells reside in the splanchnic layer of the lateral platemesoderm, they are induced by the underlyingpharyngeal endoderm to form cardiac myoblasts


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Dorsal view of a late

presomite embryo(approximately 18 days) after

removal of the amnion.

Prospective myoblasts and

hemangioblasts reside in thesplanchnic mesoderm in

front of the neural plate and

on each side of the embryo.


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Transverse section to show the position of the bloodislands in the splanchnic mesoderm layer.


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Cephalocaudal section through a similarstaged embryo showing the

position of the pericardial cavity and cardiogenic field.


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Formation and Position of the Heart Tube 1/4

Initially, the central portion of the cardiogenic area is anterior to

the buccopharyngeal membrane and the neural plate.

With closure of the neuraltube and formation of the brain

vesicles, however, the central nervous system grows cephalad so

rapidly that it extends over the central cardiogenic area and the

future pericardial cavity.

As a result of growth of the brain and cephalic folding of the

embryo, the buccopharyngeal membrane is pulled forward,

while the heart and pericardial cavity move first to the cervicalregion and finally to the thorax.

As the embryo folds cephalocaudally, it also folds laterally.


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As a result, the crescent part of the horseshoe-shaped area

expands to form the future outflow tract and ventricular regions.

Thus, the heart becomes a continuous expanded tube consisting of

an inner endothelial lining and an outer myocardial layer.

It receives venous drainage at its caudal pole and begins to pump

blood out of the first aortic arch into the dorsal aorta at its cranial

pole.

The developing heart tube bulges more and more into the

pericardial cavity.

Initially, the tube remains attached to the dorsal side of the

pericardial cavity by a fold of mesodermal tissue, the dorsal

mesocardium.

No ventral mesocardium is ever formed



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The dorsal mesocardium disappears, creating the transverse

pericardial sinus, which connects both sides of the pericardial

cavity.

The heart is now suspended in the cavity by blood vessels at its

cranial and caudal poles.

During these events, the myocardium thickens and secretes a thick

layer of extracellular matrix, rich in hyaluronic acid, that separates it

from the endothelium.

In addition, mesothelial cells from the region of the sinus venosus

migrate over the heart to form the epicardium.



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Thus the heart tube consists of three layers:

(a) the endocardium,forming the internalendothelial lining of the heart;

(b) the myocardium, forming the muscularwall; (c) the epicardium or visceral pericardium,

covering the outside ofthe tube.

This outer layer is responsible for formationof the coronary arteries, including theirendothelial lining and smooth muscle.



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The head folds (HF) are expanding and curving over the heart (H)

and pericardial cavity (asterisk).

The intestinal opening (arrow) of the gut into the primitive pharynx

and the endoderm (E ) of the open region of the gut tube are shown.


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Figures showing effects of the rapid growth

of the brain on positioning of the heart.


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20 days


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The following showsTransverse sections through embryos at different

stages of development, showing formation of a

single heart tube from paired primordia.


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Early presomite embryo (17 days)


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Late presomite embryo (18 days)


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Eight-somite stage (22 days).


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Cephalic end of an early somite embryo. The developing endocardial heart tube and its

investing layer bulge into the pericardial cavity. The dorsal mesocardium is breaking down


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Frontal section through the heart

of a 30-day embryo showing the

primary interventricular foramen

and entrance of the atrium into

the primitive left ventricle.

Note the bulboventricularflange.

Arrows, direction of blood flow.


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Formation of the Cardiac Loop 1/4

The heart tube continues to elongate and bend on day 23.

The cephalic portion of the tube bends ventrally, caudally, and to the right.

The atrial (caudal) portion shifts dorsocranially and to the left .

This bending, creates the cardiac loop. It is complete by day 28.

While the cardiac loop is forming, local expansions become visible

throughout the length of the tube.

The atrial portion, initially a paired structure outside the pericardial cavity, forms

a common atrium and is incorporated into the pericardial cavity.

The atrioventricular junction remains narrow and forms the atrioventricularcanal,

Atrioventricular canal connects the common atrium and the early embryonic

ventricle.


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The bulbus cordis is narrow except for its proximal third.This portion will form the trabeculated part of the rightventricle.

The midportion, the conus cordis, will form the outflow

tracts of both ventricles. The distal part of the bulbus, the truncus arteriosus, will

form the roots and proximal portion of the aorta andpulmonary artery.

The junction between the ventricle and the bulbus cordis,externally indicated by the bulboventricular sulcus,remains narrow.

It is called the primary interventricular foramen.



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Thus, the cardiac tube is organized by regions along itscraniocaudal axis from the conotruncus to the rightventricle to the left ventricle to the atrial region,respectively.

Evidence suggests that organization of these segmentsis regulated by homeobox genes in a manner similar tothat for the craniocaudal axis of the embryo.

At the end of loop formation, the smooth-walled heart

tube begins to form primitive trabeculae in two sharplydefined areas just proximal and distal to the primaryinterventricular foramen.



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The bulbus temporarily remains smooth walled.

The primitive ventricle, which is now trabeculated, iscalled the primitive left ventricle.

Likewise, the trabeculated proximal third of the bulbuscordis may be called the primitive right ventricle.

The conotruncal portion of the heart tube, initially on theright side of the pericardial cavity, shifts gradually to amore medial position.

This change in position is the result of formation of twotransverse dilations of the atrium, bulging on each side ofthe bulbus cordis.



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Scanning electron

micrograph of a mouse

embryo equivalent to 19

days in the human,showing coalescence of the

blood islands by

vasculogenesis into a

horseshoeshaped

heart tube (arrows) lying in

the primitive pericardial

cavity under the cranial

neural folds (asterisks).


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Scanning electron micrograph of a

mouse embryo at a stage similar to

that shown in the diagram.

The head folds (HF) are expanding and curvingover the heart (H) and pericardial cavity

(asterisk). The intestinal opening (arrow) of the

gut into the primitive pharynx and the

endoderm (E ) of the open region of the gut

tube are shown.


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The heart tube (arrows)

is horseshoe shaped in

the pericardial cavity

beneath the neural

folds (stars)

11.4


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The crescent portion of the

horseshoe expands to form

the ventricular and outflow

tract regions, while lateral

folding brings the caudal(venous) poles of the

horseshoe together


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The caudal

regions begin

to fuse


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Fusion of the caudal regions is

complete, leaving the caudal poles

embedded in the septumtransversum (arrowheads).

Cardiac looping has also been

initiated.

Asterisk, pericardialcavity; large

arrow, anterior intestinal portal.


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A, primitive atrium;

arrow, Septum transversum;

S, sinus venosus;

V, ventricle.


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Abnormalities of Cardiac Looping 1/2

Dextrocardia, in which the heart lies on the right side ofthe thorax instead of the left, is caused because the heartloops to the left instead of the right.

Dextrocardia may coincide with situs inversus, a complete

reversal of asymmetry in all organs. Situs inversus, which occurs in 1/7000 individuals, usually is

associated with normal physiology, although there is a slightrisk of heart defects.

In other cases sidedness is random, such that some organsare reversed and others are not; this is heterotaxy.

These cases are classified as laterality sequences.


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Molecular Regulation of Cardiac Development skip

Signals from anterior (cranial) endoderm induce a heart-forming region in

overlying splanchnic mesoderm by turning on the transcription factorNKX2.5.

The signals require secretion of bone morphogenetic proteins (BMPs) 2

and 4 and inhibitors (crescent) of WNT genes in the endoderm and lateral

plate mesoderm.

This combination is responsible for inducing expression ofNKX2.5 that

specifies the cardiogenic field and, later, plays a role in septation and in

development of the conduction system.

NKX2.5 contains a homeodomain and is a homologue of the gene tinman,

which regulates heart development in Drosophila.

TBX5 is another transcription factor that contains a DNA-binding motif

known as the T-box.

Expressed later than NKX2.5, it plays a role in septation


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Heart induction. BMPs secreted in the posterior portion of the primitive

streak and periphery of the embryo, in combination with inhibition ofWNT expression

by crescent in the anterior half of the embryo, induce expression of NKX2.5 in the

heart forming region of the lateral plate mesoderm (splanchnic layer).

NKX2.5 is then responsible for heart induction.


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Development of the Sinus Venosus 1/3

In the middle of the fourth week, the sinus venosusreceives venous blood from the right and left sinus horns.

Each horn receives bloodfrom three important veins: (a) the vitelline or omphalomesenteric vein,

(b) the umbilical vein, (c) the common cardinal vein.

At first communication between the sinus and theatrium is wide.

Soon, however, the entrance of the sinus shifts to the right.This shift is caused primarily byleft-to-right shunts of

blood, which occur in the venous system during thefourth and fifth weeks of development.


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Broken line, the entrance of the sinus venosus into atrial cavity


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24 daysACV, anteriorcardinal vein; PCV, posterior cardinal vein; UV,

umbilical vein; VIT V, vitelline vein; CCV, common cardinal vein


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24 days


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35 days


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35 days


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With obliteration of the right umbilical vein and the left vitelline vein

during the fifth week, the left sinus horn rapidly loses its importance.

When the left common cardinal vein is obliterated at 10 weeks, all that

remains of the left sinus horn is the oblique vein of the left atrium and

the coronary sinus.

As a result of left-to-right shunts of blood, the right sinus horn andveins enlarge greatly.

The right horn, which now forms the only communication between the

original sinus venosus and the atrium, is incorporated into the right

atrium to form the smooth-walled part of the right atrium.

Its entrance, the sinuatrial orifice, is flanked on each side by a valvular

fold, the right and left venous valves.

Dorsocranially the valves fuse, forming a ridge known as the septum

spurium.



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5 weeks fetal stage


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fetal stage


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Initially the valves are large, but when the right sinus horn isincorporated into the wall of the atrium, the left venous valve

and the septum spurium fuse with the developing atrial septum.

The superior portion of the right venous valve disappears

entirely.

The inferior portion develops into two parts:

(a) the valve ofthe inferior vena cava,

(b) the valve of the coronary sinus .

The crista terminalis forms the dividing line

between the original trabeculated part of the right

atrium and the smooth-walled part (sinus venarum),

which originates from the right sinus horn.



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Final stage in development of the sinus venosus and great veins


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Scanning electron micrograph of a similar-

staged mouse heart showing initial formation

of the septum primum; septum spurium is not

visible.

Note the atrioventricular canal (arrow

High magnification of the

interatrial septum (arrows) of amouse embryo. The foramen

ovale is notvisible.


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Formation of the Cardiac Septa

A and B. Septum formation by two actively growing . C. Septum formed by a singleti l i ll


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ridges that approach each other until they fuse actively growing cell mass


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Formation of the Cardiac Septa 1/2 The major septa of the heart are formed between the 27th

and 37th days of development, when the embryo grows in length from 5 mm to

approximately 16 to 17 mm.

One method by which a septum may be formed involvestwo actively growing masses of tissue that approach each

other until they fuse, dividing the lumen into two separatecanals.

Such a septum may also be formed by active growth of asingle tissue mass that continues to expand until it reachesthe opposite side of the lumen.

Formation of such tissue masses depends on synthesisand deposition of extracellular matrices and cellproliferation.

The masses, known as endocardial cushions, develop in the

atrioventricular and conotruncal regions.


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In these locations they assist in formation of the atrial and ventricular(membranous portion) septa, the atrioventricular canals and valves, andthe aortic and pulmonary channels.

The other manner in which a septum is formed does not involveendocardial cushions.

If, for example, a narrow strip of tissue in the wall of the atrium orventricle should fail to grow while areas on each side of it expand rapidly,a narrow ridge forms between the two expanding portions.

When growth of the expanding portions continues on either side of thenarrow portion, the two walls approach each other and eventually merge,

forming a septum. Such a septum never completely divides the originallumen but leaves a

narrow communicating canal between the two expanded sections.

It is usually closed secondarily by tissue contributed by neighboringproliferating tissues.

Such a septum partially divides the atria and ventricles.

Formation of the Cardiac Septa 2/2


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C L I N I C A L C O R R E L A T E S

Because of their key location, abnormalities in endocardialcushion formation contribute to many cardiacmalformations,

including atrial and ventricular septal defects and defectsinvolving the great vessels (i.e., transposition of the great

vessels and tetralogy of Fallot). Since cells populating the conotruncal cushions include

neural crest cells and since crest cells also contributeextensively to development of the head and neck,abnormalities in these cells, produced by teratogenic

agents or genetic causes, often produce both heart andcraniofacial defects in the same individual.


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SEPTUM FORMATION IN THE COMMONATRIUM 1/3

At the end of the fourth week, a sickle-shaped crest grows from theroof of the common atrium into the lumen.

This crest is the first portion of the septum primum.

The two limbs of this septum extendtoward the endocardial cushionsin the atrioventricular canal.

The opening between the lower rim of the septum primum and theendocardial cushions is the ostium primum.

With further development, extensions of the superior and inferiorendocardial cushions grow along the edge of the septum primum,closing the ostium primum.

Before closure is complete, however, cell death produces perforationsin the upper portion of the septum primum.

Coalescence of these perforations forms the ostium secundum,ensuring free blood flow from the right to the left primitive atrium.


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When the lumen of the right atrium expands as a result ofincorporation of the sinus horn, a new crescent-shaped foldappears.

This new fold, the septum secundum, never forms acomplete partition in the atrialcavity.

Its anterior limb extends downward to the septum in theatrioventricular canal.

When the left venous valve and the septum spurium fusewith the right side of the septum secundum, the freeconcave edge of the septum secundum begins to overlapthe ostium secundum.

The opening left by the septum secundum is called theoval foramen (foramen ovale).



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When the upper part of the septum primum gradually disappears, theremaining part becomes the valve of the oval foramen.

The passage between the two atrial cavities consists of an obliquelyelongated cleft through which blood from the right atrium flows to theleft side.

After birth, when lung circulation begins and pressure in the left atriumincreases, the valve of the oval foramen is pressed against the septumsecundum, obliterating the oval foramen and separating the right andleft atria.

In about 20% of cases, fusion of the septum primum and septum

secundum is incomplete, and a narrow oblique cleft remains betweenthe two atria.

This condition is called probe patency of the oval foramen; it does notallow intracardiac shunting of blood.



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30 days (6 mm).


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30 days (6 mm).


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33 days (9 mm)


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33 days (9 mm)


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37 days (14 mm)


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Newborn


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The atrial septum from

the right; same stage as

previous picture.


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Further Differentiation of the Atria 1/2

While the primitive right atrium enlarges by incorporationof the right sinus horn, the primitive left atrium is likewiseexpanding. Initially, a single embryonic pulmonary veindevelops as an outgrowth of the posterior left atrial wall,

just to the left of the septum primum.

This vein gains connection with veins of the developinglung buds.

During further development, the pulmonary vein and itsbranches are incorporated into the left atrium, forming thelarge smooth-walled part of the adult atrium.

Although initially one vein enters the left atrium,ultimately four pulmonary veins enter, as the branches areincorporated into the expanding atrial wall.


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In the fully developed heart, the original embryonic leftatrium is represented by little more than the trabeculated

atrial appendage, while the smooth-walled part originates

from the pulmonary veins.

On the right side the original embryonic right atriumbecomes the trabeculated right atrial appendage containing

the pectinate muscles, and the smooth-walled sinus

venarum originates from the right horn of the sinus venosus.

Further Differentiation of the Atria 2/2


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Coronal sections through the heart to show development of the smooth walled

portions of the right and left atrium. Both the wall of the right sinus horn (blue) andthe pulmonary veins (red) are incorporated into the heart to form the smooth-

walledparts of the atria.


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SEPTUM FORMATION IN THE


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ATRIOVENTRICULAR CANAL 1/2

At the end of the fourth week, two mesenchymal cushions,the atrioventricular endocardial cushions, appear at thesuperior and inferior borders of the atrioventricular canal.

Initially the atrioventricular canal gives access only to theprimitive left ventricle and is separated from the bulbus

cordis by the bulbo (cono) ventricular flange. Near the end ofthe fifth week, however, the posterior

extremity of the flange terminates almost midway alongthe base of the superior endocardial cushion and is muchless prominent than before.

Since the atrioventricular canal enlarges to the right, bloodpassing through the atrioventricular orifice now has directaccess to the primitive left as well as the primitive rightventricle.



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In addition to the superior and inferior endocardialcushions, the two lateral atrioventricular cushions

appear on the right and left borders of the canal.

The superior and inferior cushions, in themeantime, project further into the lumen and

fuse,

resulting in a complete division of the canal

into right and left atrioventricular orifices by

the end of the fifth week.


ATRIOVENTRICULAR CANAL 2/2


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Common atrioventricular canalSuperior endocardial cushion Right atrioventricular canal

Lateral cushionInferior endocardial cushion

Left atrioventricular canal

Formation of the septum in

the atrioventricular canal


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Cushions in the truncus and conus are visible.

Note development of the

cushions in the

atrioventricular canal

Frontal section through the heart of a day 35 embryo. At this stage of development blood

from the atrial cavity enters the primitive left ventricle as well as the primitive right ventricle.

Ring, primitive interventricularforamen.

Arrows, blood flow


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Formation of the atrioventricular valves and chordae tendineae.

The valves are hollowed out from the ventricular side but remain

attached to the ventricular wall by the chordae tendineae.

Atrioventricular Valves

l l


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Atrioventricular Valves

After the atrioventricular endocardial cushions fuse, each atrioventricular orifice is surrounded by local proliferations of

mesenchymal tissue.

When the bloodstream hollows out and thins tissue on the ventricularsurface of these proliferations, valves form and remain attached to the

ventricular wall by muscular cords. Finally, muscular tissue in the cords degenerates andis replaced by

dense connective tissue.

The valves then consist of connective tissue covered by endocardium.

They are connected to thick trabeculae in the wall of the ventricle, thepapillary muscles, by means of chordae tendineae.

In this manner two valve leaflets, constituting the bicuspid, ormitral,valve, form in the left atrioventricular canal, and three, constitutingthe tricuspid valve, form on the right side.

C C C O S


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C L I N I C A L C O R R E L A T E S Heart Defects

Heart and vascular abnormalities make up the largest category ofhuman birth defects, accounting for 1% of malformations amonglive-born infants.

The incidence among stillborns is 10 times as high.

It is estimated that 8% of cardiac malformations are due to genetic

factors, 2% are due to environmental agents, and most are due to acomplex interplay between genetic and environmental influences(multifactorial causes).

Classic examples of cardiovacular teratogens include rubella virusand thalidomide.

Others include isotretinoin (vitamin A), alcohol, and many other

compounds. Maternal diseases, such as insulin-dependentdiabetes and hypertension, have also been linked to cardiacdefects.

Chromosomal abnormalities are associated with heartmalformations, with 6 to 10% of newborns with cardiac defectshaving an unbalanced chromosomal abnormality.


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failure of development of the septum secundum


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Common atrium, or cor triloculare biventriculare, resulting from complete

failure of the septum primum and septum secundum to form



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Furthermore, 33% of children withchromosomal abnormalities have a congenital

heart defect, with an incidence of nearly 100%

in children with trisomy 18. Finally, cardiac malformations are associated

with a number of genetic syndromes,

including craniofacial abnormalities, such asDiGeorge, Goldenhar, and Down syndromes.




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Genes regulating cardiac development are being identified andmapped and mutations that result in heart defects are beingdiscovered.

Heart-hand syndromes (Holt-Oram syndrome).

Atrial septal defect (ASD).

cortriloculare biventriculare.

premature closure of the oval foramen.

persistent atrioventricular canal. ostium primum defect.

Tricuspid atresia



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B. Tricuspid atresia. Note the small

right ventricle and the large left

ventricle.A. Normal heart.

A. Persistent common atrioventricular

canal. This abnormality is always


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canal. This abnormality is always

accompanied by a septum defect in the

atrial as well as in the ventricular portion of

the cardiac partitions.

B. Valves in the atrioventricular

orifices under normal conditions

C. Split valves in a persistent

atrioventricular canal.

D and E. Ostium

primum defect caused

by incomplete fusion

of the atrioventricular

endocardial cushions.

SEPTUM FORMATION IN THE TRUNCUS ARTERIOSUS


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AND CONUS CORDIS During the fifth week, pairs of opposing ridges appear in the

truncus. These ridges, the truncus swellings, or cushions, lie on the

right superior wall (rightsuperior truncus swelling) and onthe left inferior wall (left inferior truncus swelling) (Fig.11.17).

The right superior truncus swelling grows distally and to theleft,

and the left inferior truncus swelling grows distally and to theright.

Hence, while growing toward the aortic sac, the swellings

twist around each other, foreshadowing the spiral course ofthe future septum (Figs. 11.22 and 11.23).

After complete fusion, the ridges form the aorticopulmonaryseptum, dividing the truncus into an aortic and a pulmonarychannel.

SEPTUM FORMATION IN THE VENTRICLES


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SEPTUM FORMATION IN THE VENTRICLES

By the end of the fourth week, the two primitive ventricles begin toexpand.

This is accomplished by continuous growth of the myocardium on theoutside and continuous diverticulation and trabecula formation on theinside.

The medial walls of the expanding ventricles become apposed and

gradually merge, forming the muscular interventricular septum. The interventricular foramen, above the muscular portion of the

interventricular septum, shrinks on completion of the conus septum.

During further development, outgrowth of tissue from the inferiorendocardial cushion along the top of the muscular interventricular septumcloses the foramen.

This tissue fuses with the abutting parts of the conus septum. Complete closure of the interventricular foramen forms the membranous

part of the interventricular septum.


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Frontal

section


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section

through

the heartof a 7-

week

embryo.

Note theconus

septum

and

position ofthe

pulmonary

valves


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Frontal section through the heart of an embryo at the end of the seventh week.

The conus septum is complete, and blood from the left ventricle enters the aorta.

Note the septum in the atrial region


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6 weeks

(12 mm).

Beginning of the seventh week (14.5 mm).


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Development of the conotruncal ridges

(cushions) and closure of the

interventricularforamen. Proliferations of the right and

left conus cushions, combined

with proliferation of the inferior

endocardial cushion, close the

interventricular foramen

and form the membranous portion ofthe interventricular septum.


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End of the seventh week (20 mm).

Semilunar Valves


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Semilunar Valves

When partitioning of the truncus is almost complete, primordia ofthe semilunar valves become visible as small tubercles found on

the main truncus swellings.

One of each pair is assigned to the pulmonary and aortic channels,

respectively A third tubercle appears in both channels opposite the fused

truncus swellings.

Gradually the tubercles hollow out at their upper surface, forming

the semilunar valves. Recent evidence shows that neural crest cells contribute to

formation of these valves.


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Longitudinal sections through the semilunar valves

6th week 7th week 9th week



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Ventricular septal defect (VSD).

Tetralogy of Fallot. (a) a narrow rightventricular outflow region, a pulmonary

infundibular stenosis.

(b) a large defect of the interventricular septum;

(c) an overriding aorta that arises directlyabove the septal defect; (d) hypertrophy of the right ventricularwall because of higher

pressure on the right side..

Ectopia cordis.

Persistent truncus arteriosus.

Transposition of the great vessels.

Valvular stenosis; aortic valvular stenosis /atresia.


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Normal heart.

Isolated defect in the

membranous portion of theinterventricular septum. Blood

from the left ventricle flows to the

right through the

interventricular foramen (arrows).

the most frequently occurring abnormality of the conotruncal region


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Tetralogy of Fallot. A. Surface view. B. The four components of the

defect: pulmonary stenosis, overriding aorta, interventricular septal

defect, and hypertrophy of the right ventricle.

A

B

Tetralogy of Fallot.


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The only access route to the lungs is by

way of a patent ductus arteriosus.

B. Pulmonary valvular atresia

with a normal aortic rootA. Transposition of the great vessels

Arrow in the arch of the aorta indicates

direction of blood flow. The coronary arteries

li d b hi fl N h ll


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Atresia of aortic valves

Patent ductus arteriosus

Patent oval foramen

Stenosis of

aortic valves

are supplied by this retroflux. Note the small

left ventricle and the large right ventricle.

A. Aortic valvular stenosis.

B. Aortic valvular atresia.

Formation of the Conducting System of


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the Heart

Initially the pacemaker for the heart lies in the caudal part of theleft cardiac tube.

Later the sinus venosus assumes this function, and as the sinus isincorporated into the right atrium,

pacemaker tissue lies near the opening of the superior vena cava.Thus, the sinuatrial node is formed.

The atrioventricular node and bundle (bundle of His) are derivedfrom two sources:

(a) cells in the left wall of the sinus venosus,

(b) cells from the atrioventricular canal.

Once the sinus venosus is incorporated into theright atrium, these cells lie in their final positionat the base of the interatrial septum.

Vascular Development


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NEXT LECTURE

Vascular Development


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19 days


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19-20 days


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20 days


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21 days


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22days


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23-29 days


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30 days


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5

th

week


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5

th

6

th

week


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7th week-neonatal


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7th week-neonatal


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7th week-neonatal


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7th week-neonatal


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Main intraembryonic and extraembryonic arteries (red) and veins (blue) in a 4-mm embryo

(end of the fourth week). Only the vessels on the left side of the embryo are shown


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Documents

Embryology Cardiovascula rsystem development