Difference between revisions of "Talk:Cardiovascular System - Abnormalities"

From Embryology
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Liang J, Gui Y, Wang W, Gao S, Li J, Song H.
 
Liang J, Gui Y, Wang W, Gao S, Li J, Song H.
 
Birth Defects Res A Clin Mol Teratol. 2010 Jun;88(6):480-6.
 
Birth Defects Res A Clin Mol Teratol. 2010 Jun;88(6):480-6.
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BACKGROUND: Maternal diabetes increases the risk of congenital heart defects in infants, and hyperglycemia acts as a major teratogen. Multiple steps of cardiac development, including endocardial cushion morphogenesis and development of neural crest cells, are challenged under elevated glucose conditions. However, the direct effect of hyperglycemia on embryo heart organogenesis remains to be investigated.
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METHODS: Zebrafish embryos in different stages were exposed to D-glucose for 12 or 24 hr to determine the sensitive window during early heart development. In the subsequent study, 6 hr post-fertilization embryos were treated with either 25 mmol/liter D-glucose or L-glucose for 24 hr. The expression of genes was analyzed by whole-mount in situ hybridization.
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RESULTS: The highest incidence of cardiac malformations was found during 6-30 hpf exposure periods. After 24 hr exposure, D-glucose-treated embryos exhibited significant developmental delay and diverse cardiac malformations, but embryos exposed to L-glucose showed no apparent phenotype. Further investigation of the origin of heart defects showed that cardiac looping was affected earliest, while the specification of cardiac progenitors and heart tube assembly were complete. Moreover, the expression patterns of tbx5, tbx20, and has2 were altered in the defective hearts.
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CONCLUSIONS: Our data demonstrate that elevated glucose alone induces cardiac defects in zebrafish embryos by altering the expression pattern of tbx5, tbx20, and has2 in the heart. We also show the first evidence that cardiac looping is affected earliest during heart organogenesis. These research results are important for devising preventive and therapeutic strategies aimed at reducing the occurrence of congenital heart defects in diabetic pregnancy.
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PMID: 20306498
 
PMID: 20306498
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http://www.ncbi.nlm.nih.gov/pubmed/20306498
  
 
===Incidence of congenital heart defects in the Czech Republic--current data===
 
===Incidence of congenital heart defects in the Czech Republic--current data===

Revision as of 07:20, 10 November 2010

2010

Elevated glucose induces congenital heart defects by altering the expression of tbx5, tbx20, and has2 in developing zebrafish embryos

Liang J, Gui Y, Wang W, Gao S, Li J, Song H. Birth Defects Res A Clin Mol Teratol. 2010 Jun;88(6):480-6.

BACKGROUND: Maternal diabetes increases the risk of congenital heart defects in infants, and hyperglycemia acts as a major teratogen. Multiple steps of cardiac development, including endocardial cushion morphogenesis and development of neural crest cells, are challenged under elevated glucose conditions. However, the direct effect of hyperglycemia on embryo heart organogenesis remains to be investigated.

METHODS: Zebrafish embryos in different stages were exposed to D-glucose for 12 or 24 hr to determine the sensitive window during early heart development. In the subsequent study, 6 hr post-fertilization embryos were treated with either 25 mmol/liter D-glucose or L-glucose for 24 hr. The expression of genes was analyzed by whole-mount in situ hybridization.

RESULTS: The highest incidence of cardiac malformations was found during 6-30 hpf exposure periods. After 24 hr exposure, D-glucose-treated embryos exhibited significant developmental delay and diverse cardiac malformations, but embryos exposed to L-glucose showed no apparent phenotype. Further investigation of the origin of heart defects showed that cardiac looping was affected earliest, while the specification of cardiac progenitors and heart tube assembly were complete. Moreover, the expression patterns of tbx5, tbx20, and has2 were altered in the defective hearts.

CONCLUSIONS: Our data demonstrate that elevated glucose alone induces cardiac defects in zebrafish embryos by altering the expression pattern of tbx5, tbx20, and has2 in the heart. We also show the first evidence that cardiac looping is affected earliest during heart organogenesis. These research results are important for devising preventive and therapeutic strategies aimed at reducing the occurrence of congenital heart defects in diabetic pregnancy.

PMID: 20306498 http://www.ncbi.nlm.nih.gov/pubmed/20306498

Incidence of congenital heart defects in the Czech Republic--current data

Ceska Gynekol. 2010 May;75(3):221-42.

(Article in Czech)

The study presents current results of analysis of CHD incidences in the Czech Republic in the 1994 - 2008 period. Children born with a CHD make more than 36% out of all children born with a congenital anomaly. CHD themselves represents an important part (more than 40%) of all diagnosed congenital anomalies in the Czech Republic. Over the period of the study there was a slight increase of diagnosed CHD during 1994 - 1999 followed by a slight decrease from 2000 with an exception of 2007 year. The most frequent of diagnosed CHD were ventricular septal defect (Q21.0) and atrial septal defect (Q21.1). Both defects incidences changes influence not only a total CHD but also a total congenital anomalies incidence. An influence of prenatal diagnostics among the five selected CHD was most important in hypoplastic left heart syndrome (Q23.4), less so in others. In prenatal diagnostics group, it is necessary to distinguish between those anomalies, which led to pregnancy termination (parts of both chromosomal and non-chromosomal syndromes and/or association with other severe anomalies) and those in which pregnancy leads to a delivery (late diagnostics, operabile defects, parental decision). CHD can be a part of chromosomal syndromes. In our study, in prenatally diagnosed CHD it was more than 42%. A presence of other associated diagnoses of congenital anomalies in births will significantly influence infant mortality and morbidity.

http://www.ncbi.nlm.nih.gov/pubmed/20731304


Clinical outcome in Down syndrome patients with congenital heart disease

Cir Cir. 2010 May-Jun;78(3):245-50.

[Article in English, Spanish]

Martínez-Quintana E, Rodríguez-González F, Medina-Gil JM, Agredo-Muñoz J, Nieto-Lago V.

Complejo Hospitalario Universitario Insular-Materno Infantil, Las Palmas de Gran Canaria, Spain. efrenmartinezquintana@yahoo.es Abstract BACKGROUND: Long-term complications of Down syndrome patients with congenital heart disease are poorly known.

METHODS: We carried out a retrospective study of Down syndrome patients with congenital heart disease and patients with atrioventricular septal defect with and without Down syndrome.

RESULTS: Between 2004 and 2008, 317 patients with congenital heart disease were followed-up in the Adult Congenital Heart Disease Unit. Of these patients, 19 (6%) with a mean age of 26.8 +/- 8.1 years had Down syndrome. Atrioventricular septal defect was the most frequent congenital heart disease(63%) followed by ventricular septal defect (26%). Ten patients (53%) were operated on during childhood. Three of these patients required reoperation during adulthood (two patients due to left ventricle outflow tract obstruction and one patient due to left atrioventricular valve insufficiency). Four patients (21%) had Eisenmenger syndrome with improvement of functional class in those treated with bosentan, two patients (10.5%) had bacterial endocarditis and two patients (10.5%) died. No significant differences were seen in left atrioventricular valve insufficiency between atrioventricular septal defect in patients with and without Down syndrome (1.5 +/- 0.9 vs. 1.7 +/- 0.8, p = 0.689).

CONCLUSIONS: Left atrioventricular valve insufficiency and left ventricle outflow tract obstruction were the most frequent long-term complications requiring surgical reintervention in patients with atrioventricular septal defect.

PMID: 20642908 http://www.ncbi.nlm.nih.gov/pubmed/20642908