Development of the heart and vascular system begins very early in
mesoderm both within (embryonic) and outside (extra embryonic, yolk sac
and placental) the embryo. Vascular development therefore occurs in
many places, the most obvious though is the early forming heart, which
grows rapidly creating an externally obvious cardiac "bulge" on the early
embryo.
The heart forms initially in the embryonic disc as a simple paired tube
inside the forming pericardial cavity, which when the disc folds, gets
carried into the correct anatomical position in the chest cavity.
Throughout the mesoderm, small regions differentiate into "blood islands"
which contribute both blood vessels (walls) and fetal red blood cells.
These "islands" connect together to form the first vessels which connect
with the heart tube.
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Forms initially in splanchnic mesoderm of prechordal plate region
- cardiogenic region
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Day 22 - 23, begins to beat in humans
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heart tube connects to blood vessels forming in splanchnic and
extraembryonic mesoderm
Week 2 - 3 pair of thin-walled tubes
Week 3 paired heart tubes fuse, truncus arteriosus outflow, heart
contracting
Week 4 heart tube continues to elongate, curving to form S shape
Week 5 Septation starts]], atrial and ventricular
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growth and folding of the embryo moves heart ventrally and downward
into anatomical position
Septation continues, atrial septa remains open, foramen ovale
Week 37-38 At birth, pressure difference closes foramen ovale
leaving a fossa ovalis
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Myocardium: forms from splanchnic mesoderm
surrounding the pericardial coelom. Additional
myocardial cells are added to the outflow tract
during heart looping.
Cardiac Jelly: gelatinous connective
tissue separating the myocardium and heart
tube endothelium.
Endocardium: forms from the endothelium of the
heart tube.
Epicardium: develops from mesothelial cells
arising from the sinus venosus which spread
cranially over the myocardium.
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The heart primordium arises predominantly
from splanchnic mesoderm in the cardiogenic
region of the trilaminar embryo. The
cardiogenic region can be thought of
as bilateral fields that merge cranially to form a
horseshoe-shaped field. During the third week
of development (approximately day
18) angioblastic cords develop in this
cardiogenic mesoderm and canalise to form
bilateralendocardial heart tubes.
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The sinus venosus is also divided into two
parts: the right horn of the sinus venosus and
the left horn of the sinus venosus.
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By day 22, coordinated contractions of the
heart tube are present and push blood cranially
from the sinus venosus.
As the embryo folds, the cranial ends of the
dorsal aortae are pulled ventrally until they
form a dorsoventral loop: the first aortic arch
arteries
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The steps in looping can be summarised as:
The straight heart tube begins to elongate with
simultaneous growth in the bulbus
cordis and primitive ventricle.
This forces the heart to bend ventrally and rotate to
the right, forming a C-shaped loop with convex
side situated on the right.
The ventricular bend moves caudally and the
distance between the outflow and inflow tracts
diminishes.
The atrial and outflow poles converge and
myocardial cells are added, forming the truncus
arteriosus.
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Two endocardial cushions form on the dorsal and
ventral surfaces of the AV canal, referred to as the
superior and inferior cushions respectively. The
cardiac jelly in this region expands while
mesenchymal cells from the endocardium invade
the cushions, allowing them to grow and fuse. This
fusion divides the common AV canal into the right
and left canals, hence partially separating the
primitive atrium and ventricle. Two smaller
endocardial cushions also form on the lateral walls
of the AV canal, which later help to form
the mitral and tricuspid heart valves.
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Membranous tissue forming the septum
primum grows from the roof of the atrium,
dividing it into left and right halves
Blood flows from the right atrium through the
foramen ovale and foramen secundum to
the left atrium, forming a right-to-left shunt.
The remaining portion of the septum primum
acts as the valve of the foramen ovale. Blood
cannot flow in the opposite direction, as the
muscular strength of the septum secundum
prevents prolapse of the septum primum
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Minor trabeculations appear during early development of
the primordial ventricle. Following growth of the ventricles
further trabeculations appear and grow as larger, muscular
structures. Some researchers believe that as the
trabeculations grow they coalesce resulting in the formation
of the ventricular septum. However, the more commonly
described theory of septation begins with the appearance of
a primordial muscular interventricular (IV) ridge
developing in the floor of the ventricle near the apex. As
either side of the ventricle grows and dilates, their medial
walls fuse forming the prominent IV septum. The foramen
located between the cranial portion of the IV septum and the
endocardial cushions: the IV foramen, closes by the end of
the seventh week as the bulbar ridges (see next section) fuse
with the endocardial cushions.
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Active proliferation of neural crest mesenchymal cells in
the bulbus cordis during the fifth week creates bulbar
ridges which are continuous in thetruncus arteriosus. The
neural crest cells migrate through the
primordial pharynx and over the aortic arch arteries to
reach the outflow tract. The bulbar ridges undergo a 180°
spiral to create the helical aorticopulmonary septum. As the
ridges grow and develop myocardium they fuse in a distalto-proximal direction. Fusion occurs during the sixth week,
allowing for cleavage of the aorta and pulmonary trunk.
The spiralling nature of the ridges causes the pulmonary
trunk to twist around the aorta. Note that the bulbus cordis
accounts for the smooth conus
arteriosus (or infundibulum) in the right ventricle and
the aortic vestibule in the left ventricle.
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There are four valves in the adult heart,
depicted below. There are two AV valves which
comprise leaflets as well as the structures that
tether these leaflets to the ventricular walls.
The aortic and pulmonary valves, termed
the semilunar valves, are located in the aorta
and pulmonary trunk respectively. They are
each made of three cusps.
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The AV valves begin to form between the fifth and eighth
weeks of development. The left AV valve
has anterior andposterior leaflets and is termed
thebicuspid or mitralvalve. The right AV valve has a third,
small, septalcusp and thus is called thetricuspid valve.
The valve leafletsare attached to the ventricular walls by
thin fibrous chords: the chordae tendineae, which insert
into small muscles attached to the ventricle wall:
the papillary muscles. These structures are sculpted from
the ventricular wall
The semilunar valves are formed from the bulbar
ridges and subendocardial valve tissue. The primordial
semilunar valve consists of a mesenchymal core covered by
endocardium. Excavation occurs, thinning the valve tissue
thus creating its final shape.
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Upon folding of the embryo the paired dorsal aortae
connecting to the cranial end of the heart tube are
brought ventrally to form the first aortic arches.
Additional aortic arches develop over the next few
weeks which are later remodelled to form the arteries
of the upper body. Caudal to the arches, the paired
dorsal aortae fuse to form a single median dorsal aorta
which develops the following branches:
Ventral (gut) branches - derived from the vitelline
arteries
Lateral branches - supply retroperitoneal structures
Dorsolateral branches (intersegmental arteries) supply the head, neck, body wall, limbs and vertebral
column
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The vitelline venous system gives rise to the liver
sinusoids and portal system and forms the ductus
venosus which acts as a shunt from the umbilical vein
to the IVC. The IVC is formed during a left-to-right
shift in the embryonic veins and is composed of:
A hepatic segment - from the hepatic vein and
sinusoids
A prerenal segment - from the right subcardinal vein
A renal segment - from subcardinal and supracardinal
anastomosis
A postrenal segment - from right supracardinal vein
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The main function of these shunts is to redirect oxygenated blood
away from the lungs, liver and kidney (whose functions are
performed by the placenta).
Oxygenated blood is carried from the placenta to the foetus in the
umbilical vein, most of which then passes through the ductus
venosus to the IVC while some blood supplies the liver via the
portal vein. Blood from the liver drains into the IVC through the
hepatic veins. The blood in the IVC is a mixture of oxygenated
blood from the umbilical vein and desaturated blood from the
lower limbs and abdominal organs (e.g. the liver). This blood
enters the right atrium where most of it is directed to the left
atrium through the foramen ovale and from here to the left
ventricle and aorta. The remainder of the blood in the right atrium
passes with blood from the SVC (from the head and upper limbs)
to the right ventricle and pulmonary artery where most of it
passes to the aorta via the ductus arteriosus. The blood passes
from the aorta to the hypogastric arteries, umbilical arteries and
then back to the placenta.
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A variety of developmental defects occur as a
result of prenatal exposure to alcohol (ethanol) in
utero. In humans, those defects are collectively
classified as Fetal Alcohol Spectrum Disorders,
with Fetal Alcohol Syndrome (FAS) representing
the more severe defects. FAS is defined by pre- and
post-natal growth retardation, minor facial
abnormalities, and deficiencies in the central
nervous system (CNS). In addition to those defects,
prenatal exposure to alcohol impacts
cardiogenesis, the developmental stage of heart
formation.
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Prenatal exposure to alcohol induces a variety of
abnormalities in the developing heart which include:
atrial and ventricular abnormalities, issues with valve
formation, and a potential increase in the risk of heart
disease later in adulthood. The specific defects that
have been observed from prenatal alcohol exposure
include defects to the atrioventricular valves (tricuspid
and mitral) that allow blood to flow backward into the
atria; ventricular septal defects, commonly known as a
“hole in the heart” between the left and right
ventricles; enlargement of the left ventricle, the
primary pumping chamber in the heart; and an
increased risk of developing heart disease later in adult
life.
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http://search.medicinenet.com/search/search
_results/default.aspx?Searchwhat=1&query=m
esoderm&I1=Search
http://www.ncbi.nlm.nih.gov/pmc/articles/P
MC1767109/
http://php.med.unsw.edu.au/embryology/in
dex.php?title=Cardiovascular_System_Develo
pment

Langman's Medical Embryology 11th ed., Sadler, T
W, (Thomas W.); Langman, Jan. Philadelphia :
Wolters Kluwer Lippincott Williams & Wilkins
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Developmental Biology, 6th ed., Gilbert, Scott F;
Sunderland (MA): Sinauer Associates; 2000
Larsen's human embryology 4th ed. Schoenwolf, Gary
C; Larsen, William J, (William James). Philadelphia,
PA : Elsevier/Churchill Livingstone
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O'Neil, Erica, "Effects of Prenatal Alcohol
Exposure on Cardiac Development". Embryo
Project Encyclopedia (2011-04-30). ISSN: 19405030
http://embryo.asu.edu/handle/10776/2097.