Difference between revisions of "Cardiovascular System - Ventricular Septal Defects"
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Revision as of 08:40, 12 February 2012
The Ventricular Septal Defect (VSD) is the most common form of congenital cardiovascular anomaly, occurring in nearly 50% of all infants with a congenital heart defect. Usually occurs in the membranous (perimembranous) rather than muscular interventricular septum, and is more frequent in males that females.
Perimembranous defects are located close to the aortic and tricuspid valves and adjacent to atrioventricular conduction bundle.
Some Recent Findings
The first western clinical description of ventricular septal defects was made by Henri Roger in 1879, which later became known as ‘’maladie de Roger’’. His description was based upon 6 acyanotic patients and autopsy finding of a child with ventricular septal defect.
- (Heath-Edward grade) A pathological grading system for pulmonary artery structural changes that occur with congenital cardiac septal defects. The classification is named after the two original paper authors Donald HEATH and Jessee EDWARDS (PMID 13573570) and grades from I to VI with increasing severity of arterial changes.
- Grade I - hypertrophy of the media of small muscular arteries and arterioles.
- Grade II - intimal cellular proliferation in addition to medial hypertrophy.
- Grade III - advanced medial thickening with hypertrophy and hyperplasia including progressive intimal proliferation and concentric fibrosis. Results in an obliteration of the arterioles and small arteries.
- Grade IV - "plexiform lesions" of the muscular pulmonary arteries and arterioles with a plexiform network of capillary-like channels within a dilated segment.
- Grade V - complex plexiform, angiomatous and cavernous lesions and hyalinization of intimal fibrosis.
- Grade VI - necrotizing arteritis
- Links: Cardiovascular Abnormalities Ventricular Septal Defects | Atrial Septal Defects | PMID 13573570 Circulation)
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)
"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." 
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.
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Search Pubmed: Ventricular Septal Defect
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Cite this page: Hill, M.A. (2021, February 27) Embryology Cardiovascular System - Ventricular Septal Defects. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Cardiovascular_System_-_Ventricular_Septal_Defects
- © Dr Mark Hill 2021, UNSW Embryology ISBN: 978 0 7334 2609 4 - UNSW CRICOS Provider Code No. 00098G