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Congenital Complete Heart Block (congenital + complete_heart_block)

Distribution by Scientific Domains
Medical Sciences100%

Selected Abstracts

Assessment of Fetal Rhythm in Complete Congenital Heart Block by Magnetocardiography

PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 6 2000
RONALD T. WAKAI
We report high precision assessment of fetal rhythm in utero in a case of isolated congenital complete heart block using fetal magnetocardiography. The recordings reveal a remarkably strong tendency for the atria and ventricles to synchronize, which is manifested by the continual presence of ventriculophasic sinus arrhythmia and frequent episodes of accrochage and isorhythmic AV dissociation. [source]

Anesthetic management of an infant with lupus and congenital complete heart block

PEDIATRIC ANESTHESIA, Issue 2 2006
Deepak Kumar Sreevastava
No abstract is available for this article. [source]

Transforming growth factor ,1 in the pathogenesis of autoimmune congenital complete heart block: Lesson from twins and triplets discordant for the disease

ARTHRITIS & RHEUMATISM, Issue 1 2006
Rolando Cimaz
Objective Clinical evidence and experimental evidence suggest that anti-Ro/La autoantibodies are necessary but not sufficient for the development of congenital complete heart block (CCHB). Maternal, fetal, and environmental factors may also contribute to heart damage in CCHB. The aim of our study was to investigate polymorphisms of transforming growth factor ,1 (TGF,1) and tumor necrosis factor , (TNF,) genes in twins and triplets discordant for CCHB whose mothers are anti-Ro/La positive. Methods We studied 2 families in which 1 of the mothers gave birth to triplets and the other gave birth to twins. Only 1 child in each family was affected by CCHB, although 1 of the triplets had incomplete heart block. We analyzed TNF, and TGF,1 polymorphisms in the 2 babies with CCHB and their siblings. TNF, polymorphisms at the promoter region and TGF,1 polymorphisms at codons 10 and 25 were determined using polymerase chain reaction,restriction fragment length polymorphism analysis. In addition, the production of TGF,1 and TNF, by resting or mitogen-stimulated peripheral blood mononuclear cells in cell culture supernatants was evaluated by enzyme-linked immunosorbent assay. Results The profibrotic TGF,1 genotype was detected in the twin with CCHB but not in the healthy twin, while all of the triplets displayed the same TGF,1 genotype at codon 10. Peripheral blood mononuclear cells from the children with CCHB displayed higher spontaneous and mitogen-stimulated TGF,1 secretion than was observed in their siblings. No differences regarding TNF, polymorphisms and secretion of TNF, were observed. Conclusion The results of this study suggest that, besides anti-Ro/La autoantibodies, a fetal profibrotic response might contribute to the development of CCHB, but additional pathogenic mechanism(s) are also likely to play a role. [source]