Cardiovascular System - Heart Valve Development: Difference between revisions

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===Historic===
===Historic===
{{Historic Disclaimer}}
{{Historic Disclaimer}}
Odgers PNB. [[Paper - The Development of the Atrio-Ventricular Valves in Man|The Development of the Atrio-Ventricular Valves in Man]] (1939) J Anat. 73:643-57. PMID 17104787
 
{{Ref-Odgers1939}}
 


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Revision as of 02:10, 2 June 2016

Embryology - 28 Mar 2024    Facebook link Pinterest link Twitter link  Expand to Translate  
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Introduction

Human embryo heart right atrio-ventricular valve (stage 22)
Human embryo heart valve (stage 22)

The heart valves form between the atria and ventricles (mitral valve, tricuspid valve) and between the atria and blood vessels (aortic valve, pulmonary valve). The cardiac cushions in the atrioventricular (AV) canal contain cells that are the primordia of the cardiac valves. The atrioventricular valves are attached to papillary muscles by chordae tendineae.

Scleraxis (SCX) is a transcription factor involved in tendon and ligament development and has been identified as also expressed in early heart valve development.[1]

Mitral valve also called the "bicuspid valve".

Cardiac Tutorial: Intermediate - Heart Valves | Advanced - Valve Development


Cardiovascular Links: cardiovascular | Heart Tutorial | Lecture - Early Vascular | Lecture - Heart | Movies | 2016 Cardiac Review | heart | coronary circulation | heart valve | heart rate | Circulation | blood | blood vessel | blood vessel histology | heart histology | Lymphatic | ductus venosus | spleen | Stage 22 | cardiovascular abnormalities | OMIM | 2012 ECHO Meeting | Category:Cardiovascular
Historic Embryology - Cardiovascular 
1902 Vena cava inferior | 1905 Brain Blood Vessels | 1909 Cervical Veins | 1909 Dorsal aorta and umbilical veins | 1912 Heart | 1912 Human Heart | 1914 Earliest Blood-Vessels | 1915 Congenital Cardiac Disease | 1915 Dura Venous Sinuses | 1916 Blood cell origin | 1916 Pars Membranacea Septi | 1919 Lower Limb Arteries | 1921 Human Brain Vascular | 1921 Spleen | 1922 Aortic-Arch System | 1922 Pig Forelimb Arteries | 1922 Chicken Pulmonary | 1923 Head Subcutaneous Plexus | 1923 Ductus Venosus | 1925 Venous Development | 1927 Stage 11 Heart | 1928 Heart Blood Flow | 1935 Aorta | 1935 Venous valves | 1938 Pars Membranacea Septi | 1938 Foramen Ovale | 1939 Atrio-Ventricular Valves | 1940 Vena cava inferior | 1940 Early Hematopoiesis | 1941 Blood Formation | 1942 Truncus and Conus Partitioning | Ziegler Heart Models | 1951 Heart Movie | 1954 Week 9 Heart | 1957 Cranial venous system | 1959 Brain Arterial Anastomoses | Historic Embryology Papers | 2012 ECHO Meeting | 2016 Cardiac Review | Historic Disclaimer

Some Recent Findings

  • Twist1 directly regulates genes that promote cell proliferation and migration in developing heart valves[2] "Twist1, a basic helix-loop-helix transcription factor, is expressed in mesenchymal precursor populations during embryogenesis and in metastatic cancer cells. In the developing heart, Twist1 is highly expressed in endocardial cushion (ECC) valve mesenchymal cells and is down regulated during valve differentiation and remodeling. Previous studies demonstrated that Twist1 promotes cell proliferation, migration, and expression of primitive extracellular matrix (ECM) molecules in ECC mesenchymal cells. Furthermore, Twist1 expression is induced in human pediatric and adult diseased heart valves."
  • Hemodynamic patterning of the avian atrioventricular valve [3] "In this study, we develop an innovative approach to rigorously quantify the evolving hemodynamic environment of the atrioventricular (AV) canal of avian embryos. Ultrasound generated velocity profiles were imported into Micro-Computed Tomography generated anatomically precise cardiac geometries between Hamburger-Hamilton (HH) stages 17 and 30. Computational fluid dynamic simulations were then conducted and iterated until results mimicked in vivo observations. Blood flow in tubular hearts (HH17) was laminar with parallel streamlines, but strong vortices developed simultaneous with expansion of the cushions and septal walls. For all investigated stages, highest wall shear stresses (WSS) are localized to AV canal valve-forming regions. Peak WSS increased from 19.34 dynes/cm(2) at HH17 to 287.18 dynes/cm(2) at HH30, but spatiotemporally averaged WSS became 3.62 dynes/cm(2) for HH17 to 9.11 dynes/cm(2) for HH30. Hemodynamic changes often preceded and correlated with morphological changes. These results establish a quantitative baseline supporting future hemodynamic analyses and interpretations."
More recent papers
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Search term: Heart Valve Embryology

<pubmed limit=5>Heart Valve Embryology</pubmed>

Textbooks

  • Human Embryology (2nd ed.) Larson Ch7 p151-188 Heart
  • The Developing Human: Clinically Oriented Embryology (6th ed.) Moore and Persaud Ch14: p304-349
  • Before we Are Born (5th ed.) Moore and Persaud Ch12; p241-254
  • Essentials of Human Embryology Larson Ch7 p97-122 Heart
  • Human Embryology Fitzgerald and Fitzgerald Ch13-17: p77-111

Tutorial Images

Cardiac Tutorial: Intermediate - Heart Valves | Advanced - Valve Development

Fetal Heart Valve Sounds

<mp3player>File:Week17 fetal heart rate.mp3</mp3player>

Audio recording of the Second Trimester fetal heart (GA week 17).

The characteristic "lub-dup" sounds are associated with closing of heart valves.

  • First sound (lub) occurs as atrioventricular valves close and signifies beginning of systole (contraction)
  • Second sound (dup) occurs when semilunar valves close at the beginning of ventricular diastole (relaxation)
Links: Fetal Heart Sounds Audio

Molecular

Scleraxis (Scx) - basic helix–loop–helix transcription factor expressed in the progenitors and cells of all tendon tissues (mouse).[4]

Periostin - regulates lineage commitment of valve precursor cells (chicken).[5]

Gata4 and Gata6

Tbx5

Images

Historic

Historic Disclaimer - information about historic embryology pages 
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Pages where the terms "Historic" (textbooks, papers, people, recommendations) appear on this site, and sections within pages where this disclaimer appears, indicate that the content and scientific understanding are specific to the time of publication. This means that while some scientific descriptions are still accurate, the terminology and interpretation of the developmental mechanisms reflect the understanding at the time of original publication and those of the preceding periods, these terms, interpretations and recommendations may not reflect our current scientific understanding.     (More? Embryology History | Historic Embryology Papers)

Odgers PNB. The development of the atrio-ventricular valves in man. (1939) J Anat. 73: 643-57. PMID 17104787


Abnormalities

Noonan syndrome

An autosomal dominant single-gene cause of congenital heart disease. Patients also have proportionate short stature, facial abnormalities, and an increased risk of myeloproliferative disease. About half the patients have mutations in PTPN11, encoding the protein tyrosine phosphatase SHP2. A recent study in mice has identified PTPN11 acting in endocardium to enhance endocardial-mesenchymal transformation.[6]

References

  1. <pubmed>24983472</pubmed>
  2. <pubmed>22242143</pubmed>
  3. <pubmed>21181939</pubmed>
  4. <pubmed>18802027</pubmed>
  5. <pubmed>19334280</pubmed>
  6. <pubmed>19251646</pubmed>

Reviews

<pubmed>20809794</pubmed> <pubmed>20201901</pubmed> <pubmed>14567955</pubmed> <pubmed>12768658</pubmed>

Articles

<pubmed>17549728</pubmed> <pubmed>16914500</pubmed> <pubmed>17104787</pubmed>

Search PubMed

Search Pubmed: heart valve development | heart valve morphogenesis | Valvulogenesis

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Cite this page: Hill, M.A. (2024, March 28) Embryology Cardiovascular System - Heart Valve Development. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Cardiovascular_System_-_Heart_Valve_Development

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© Dr Mark Hill 2024, UNSW Embryology ISBN: 978 0 7334 2609 4 - UNSW CRICOS Provider Code No. 00098G