Cardiovascular System - Atrial Septal Defects: Difference between revisions

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'''Search Pubmed:''' http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=search&term=Atrial%20Septal%20Defect Atrial Septal Defect]
'''Search Pubmed:''' [http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=search&term=Atrial%20Septal%20Defect Atrial Septal Defect]


==External Links==
==External Links==

Revision as of 06:46, 29 January 2012

Introduction

Atrial Septal Defect

Atrial Septal Defects (ASD) are a group of common (1% of cardiac) congenital anomolies defects occuring in a number of different forms and more often in females.

  • patent foramen ovale- allows a continuation of the atrial shunting of blood, in 25% of people a probe patent foramen ovale (allowing a probe to bepassed from one atria to the other) exists.
  • ostium secundum defect
  • endocardial cushion defect involving ostium primum
  • sinus venosus defect - contributes about 10% of all ASDs and occurs mainly in a common and less common form. Common ("usual type") - in upper atrial septum which is contiguous with the superior vena cava. Less common - at junction of the right atrium and inferior vena cava.
  • common atrium

Treatment: The surgical repair requires a cardiopulmonary bypass and is recommended in most cases of ostium secundum ASD, even though there is a significant risk involved. Ostium primum defects tend to present earlier and are often associated with endocardial cushion defects and defective mitral or tricuspid valves. In such cases, valve replacement may be necessary and the extended operation has a considerable chance of mortality.

  • Increasingly closure by a transcatheter device closure has been applied.
  • Repair of atrial septal defects on the perfused beating heart (atrial septal defect size 2 cm - 4.5 cm) [1]


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

  • Spontaneous Closure of Muscular Trabecular Ventricular Septal Defect: Comparison of Defect Positions PMID 21517965 "We performed a historical cohort study for which 150 patients <3 months of age (median age, 9 days) diagnosed as having a muscular trabecular VSD were selected. ...We infer that midventricular muscular trabecular VSD tends to close spontaneously earlier and more frequently than either anterior or apical muscular trabecular VSD."

Cardiovascular Abnormalities

Data shown as a percentage of all major abnormalities based upon published statistics using the same groupings as Congenital Malformations Australia 1981-1992 P. Lancaster and E. Pedisich ISSN 1321-8352.

Heart defects and preterm birth are the most common causes of neonatal and infant death. The long-term development of the heart combined with extensive remodelling and post-natal changes in circulation lead to an abundance of abnormalities associated with this system.

A UK study literature showed that preterm infants have more than twice as many cardiovascular malformations (5.1 / 1000 term infants and 12.5 / 1000 preterm infants) as do infants born at term and that 16% of all infants with cardiovascular malformations are preterm. (0.4% of live births occur at greater than 28 weeks of gestation, 0.9% at 28 to 31 weeks, and 6% at 32 to 36 weeks. Overall, 7.3% of live-born infants are preterm)[2]

"Baltimore-Washington Infant Study data on live-born cases and controls (1981-1989) was reanalyzed for potential environmental and genetic risk-factor associations in complete atrioventricular septal defects AVSD (n = 213), with separate comparisons to the atrial (n = 75) and the ventricular (n = 32) forms of partial AVSD. ...Maternal diabetes constituted a potentially preventable risk factor for the most severe, complete form of AVSD." [3]

In addition, there are in several congenital abnormalities that exist in adults (bicuspid aortic valve, mitral valve prolapse, and partial anomalous pulmonary venous connection) which may not be clinically recognized.


References

  1. <pubmed>19876418</pubmed>
  2. <pubmed>16322141</pubmed>
  3. <pubmed>11241431</pubmed>

Articles

<pubmed>17967198</pubmed>


Search Pubmed

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Cite this page: Hill, M.A. (2024, April 26) Embryology Cardiovascular System - Atrial Septal Defects. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Cardiovascular_System_-_Atrial_Septal_Defects

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