Heart Development Flashcards by Connor Faust

Primitive hematopoietic stem cells

Make erythrocytes, megakaryocytes and macrophages

Meet immediate needs of the early embryo

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Definitive hematopoietic stem cells

Programmed from hemogenic endothelial cells found in the aortic-gonadal-mesonephric (AGM) region
Appear at day 27, seed the liver at day 30
Generate full spectrum of myeloid and lymphoid cell lineages
Without AGM, you never get definitive hematopoietic stem cells

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Sites of hematopoiesis

Yolk sac mesoderm- day 17-60: source of early RBCs and macrophages
Liver primordia: beginning day 23, continues to birth
AGM dorsal aorta: colonizes liver
Lymph organs
Bone marrow

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AGM region vasculogenesis

Hematopoiesis is coupled to vasculogenesis, which is different from the rest of the embryo
Mesodermal cells directly turn into endothelial cells and form blood vessels in most other areas

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Angiogenesis vs vasculogenesis

Vasculogenesis is de novo formation of blood vessels, while angiogenesis is the sprouting of new vessels from existing ones

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Intussusception

Taking an existing blood vessel and splitting it in half

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Angioma

Abnormal blood vessel and lymphatic capillary growth via vasculogenesis
Capillary hemangioma- excessive formation of capillaries
Cavernous hemangioma- excessive formation of venous sinuses

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Primary heart field

Splanchnic mesoderm- precardiomyocytes
Endoderm
Endothelial precursor cells form angiogenic clusters (all though this is a vasculogenic process) which form cardiac crescent and two endocardial tubes

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Endocardial tube formation

Splanchnic mesoderm consisting of precardomyocytes continue with the process of body folding and bring the two tubes towards the midline
Fuse into one single tube formed from endocardium and myocardium, and the tube dangles from dorsal mesocardium
Dorsal mesocardium must rupture so the tube can loop

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Proepicardial organ

Remnants of dorsal mesocardium that are responsible for forming the epicardium- cardiovasculature, CT and visceral layer of pericardium

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Primitive ventricle and proximal portion of outflow

Primitive ventricle forms left ventricle

Proximal portion of outflow forms the right ventricle

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Sinus horns

Two horns come together to form sinus venosus, which expands into atrium

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Lengthening of the heart tube is due to

Growth of the second heart field

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Neural crest cells

Do not add to heart
Regulate GF that comes from endoderm to drive proliferation of precardiac mesenchyme/mesoderm
If NCCs do not migrate to correct place there will be problems with cardiac looping

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Heterotaxia

Any symmetry anomaly
Situs inversus- total side reversal of organs
Situs ambiguous- partial reversal of organs
Visceroatrial heterotaxia - right sided heart, normal GI
Ventricular inversion- reverse cardiac looping, right sided left ventricle

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Right vitelline vein and Right common cardinal vein

Right vitelline becomes inferior vena cava, right common cardinal becomes superior vena cava

Cushion tissue and separating atria and ventricles

Myocardial cells produce more extracellular matrix which pushes endocardial cells from both sides towards eachother
Endocardial cells are signaled by myocardium to undergo epithelial–>mesenchymal/mesodermal cell transition so the two sides can fuse
This is how AV septum is formed

Valves derived from what tissue

Endocardium which is derived from intraembryonic splanchnic mesoderm

Cushion tissue in outflow tract is derived from

Both endocardium (intraembryonic splanchnic mesoderm) and neural crest cells (ectoderm)

Persistent AV canal

Failure of AV septum fusion
Results in atrial septal defect and ventricular septal defect
Abnormal or agenesis of AV valves
Pulmonary hypertension, exercise intolerance, shortness of breath
Linked with downs syndrome

How does O2 rich blood entering right atrium bypass the pulmonary circuit and get into the systemic side

One-way flutter valve between atria formed by dorsal mesenchymal protrusion
Ductus arteriosus allows blood entering right atrium to travel to left atrium

Early blood flow into right atrium flows through

Goes through foramen ovale, then displaces septum primum from septum secundum and through foramen secundum

Fibrous CT of AV septum is derived from

Endocardium

Foramen primum is filled in by

Cushion tissue

AV septal defects

Excessive erosion of septum primum or inadequate development of septum secundum Causes high atrial septal defect Low hole septal defect caused by foramen primum defect

Septation of outflow tract

To form complete interventricular septum, there must be spiraling of the conotruncal swellings that align with the muscular portion of the IV septum as well as the AV septum

Shifting of AV canal

AV canal must shift towards the midline during development If it does not, both the aorta and pulmonary artery exit via the right ventricle, accompanied by a ventricular septal defect Can be caused by insufficient cardiac looping Symptoms include cyanosis, breathlessness, murmur, poor weight gain

Cardiac NC cells

Important for sprouting of secondary heart field, lengthening/looping of the heart tube, septation of the outflow tract

Ventricular septal defects

Most common congenital heart defect Initially there will be blood flow from left to right side, increasing blood flow to pulmonary circuit Later after development there will be blood flow from right to left side

Persistent truncus arteriosus

There will be a ventricular septal defect involved Cyanosis Look into this more- not well described

Tetralogy of fallout

Small pulmonary artery VSD Right ventricle must work harder and hypertrophies Over-riding aorta (those are the four symptoms- tetra) Causes right to left shunt at birth, causing cyanosis

Transposition of great vessels

Conotruncal ridges formed and fused but did not spiral Right ventricle connected to the aorta, left connected to the pulmonary artery Ductus arteriosus allows oxygenated blood to get to embryo

Pulmonary valvular atresia

Blood comes into right atria but cannot be pumped out pulmonary artery Left ventricle does all the work and hypertrophies Only way to get oxygenated blood is to have blood flow through foramen ovale and back through the ductus arteriosus

Aortic valvular stenosis

Left ventricle has to work harder causing hypertrophy

Aortic valvular atresia

Left ventricle has no workload so it is much smaller | Right ventricle does all the work so it hypertrophies

Bicuspid aortic valve

Initially asymptomatic but can develop left ventricular hypertrophy over time Associated with development of aortic aneurysms

Tricuspid atresia

Tricuspid valve has no opening No blood can enter right ventricle, so it is hypoplastic There is a patent foramen ovale that persists and ductus arteriosus so that oxygenated blood can be distributed Usually involves a VSD

Hypoplastic left ventricle

Mitral valve is not formed or very small Aortic valve is not formed or very small Ascending portion of aorta is underdeveloped Patent ductus arteriosus and foramen ovale (or ASD) Heart works as a uni-ventricular heart with right ventricle doing all the work