Familial Wolff-Parkinson-White syndrome

Chia, B.L.; Yew, F.C.; Chay, Suhwoo; Tan, Augustine H. H.

doi:10.1016/s0022-0736(82)80016-2

Cited by 24 publications

(12 citation statements)

References 6 publications

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“…While most affected individuals appear to be sporadic, screening studies have suggested that at least 3% of probands have a symptomatic affected first degree relative ( 1). Reports of familial WPW have demonstrated an autosomal dominant mode of inheritance (2)(3)(4)(5)(6)(7)(8).…”

Section: Introductionmentioning

confidence: 99%

Familial Hypertrophic cardiomyopathy with Wolff-Parkinson-White syndrome maps to a locus on chromosome 7q3.

MacRae¹,

Ghaisas²,

Kass³

et al. 1995

J. Clin. Invest.

192

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We have mapped a disease locus for Wolff-Parkinson-White syndrome (WPW) and familial hypertrophic cardiomyopathy (FHC) segregating in a large kindred to chromosome 7 band q3. Although WPW syndrome and FHC have been observed in members of the same family in prior studies, the relationship between these two diseases has remained enigmatic. A large family with 25 surviving individuals who are affected by one or both of these conditions was studied. The disease locus is closely linked to loci D7S688, D7S505, and D7S483 (maximum two point LOD score at D7S505 was 7.80 at 0 = 0). While four different FHC loci have been described this is the first locus that can be mutated to cause both WPW and/or FHC. (J. Clin. Invest. 1995. 96:1216-1220

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Section: Introductionmentioning

confidence: 99%

Familial Hypertrophic cardiomyopathy with Wolff-Parkinson-White syndrome maps to a locus on chromosome 7q3.

MacRae¹,

Ghaisas²,

Kass³

et al. 1995

J. Clin. Invest.

192

View full text Add to dashboard Cite

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“…A genetic basis for this condition was initially inferred by Vidaillet et al 2 who found familial occurrence of accessory atrioventricular (AV) pathways in 3.4% of WPW probands. Typically, WPW syndrome occurs sporadically; however, in a minority of cases it is inherited either as an autosomal dominant simple pre-excitation trait,3 or as part of a more complex phenotype, such as Ebstein’s anomaly,4 mitochondrial disease,5 or hypertrophic cardiomyopathy (HCM) 6. The first description of a molecular basis of WPW syndrome was provided by Blair et al 7 and Gollob et al 8 who reported mutations in the γ-2 regulatory subunit of AMP activated protein kinase ( PRKAG2) in patients with familial HCM and WPW syndrome.…”

mentioning

confidence: 99%

20p12.3 microdeletion predisposes to Wolff-Parkinson-White syndrome with variable neurocognitive deficits

Lalani

Thakuria

Cox

et al. 2008

Journal of Medical Genetics

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Background-Wolff-Parkinson-White syndrome (WPW) is a bypass reentrant tachycardia that results from an abnormal connection between the atria and ventricles. Mutations in PRKAG2 have been described in patients with familial WPW syndrome and hypertrophic cardiomyopathy. Based on the role of bone morphogenetic protein (BMP) signaling in the development of annulus fibrosus in mice, it has been proposed that BMP signaling through the type 1a receptor and other downstream components may play a role in preexcitation.

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“…In 10% atrial ectopic tachycardia and junctional ectopic tachycardia can be found. There are reports about a familial and autosomal recessive inheritance of Wolf-Parkinson-White syndrome [5,16]. In Wolf-Parkinson-White syndrome there is a positive family history in 20% of cases.…”

Section: Discussionmentioning

confidence: 99%

Familial Association of Congenital Left Heart Abnormalities and Sustained Fetal Arrhythmia

et al. 1999

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Hypoplastic left heart syndrome (HLHS) is the most common cause of death from heart disease in the first week of life. There are reports about familial concordance by presumed morphogenetic mechanisms of abnormal embryonic blood flow with phenotypes of varying severity. The risk of having a child with a left heart lesion after a previously affected child may be as high as 5% to 12%. We present case reports from four families in which sustained fetal arrhythmia (three ectopic atrial tachycardias and one severe bradycardia due to excessive ectopic atrial beats) was demonstrated. Within these four families a close relative of the mother (a previous child, a brother, or a nephew) had severe left heart abnormality (three with HLHS and one with severe aortic valve stenosis). The association of sustained fetal arrhythmia of ectopic atrial origin and severe left heart abnormalities could be expected to occur by chance in a very low percentage of cases. We conclude that sustained fetal atrial ectopic arrhythmia is a congenital abnormality and should be considered as a risk factor for inherited congenital heart abnormalities.

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Familial Wolff-Parkinson-White syndrome

Cited by 24 publications

References 6 publications

Familial Hypertrophic cardiomyopathy with Wolff-Parkinson-White syndrome maps to a locus on chromosome 7q3.

Familial Hypertrophic cardiomyopathy with Wolff-Parkinson-White syndrome maps to a locus on chromosome 7q3.

20p12.3 microdeletion predisposes to Wolff-Parkinson-White syndrome with variable neurocognitive deficits

Familial Association of Congenital Left Heart Abnormalities and Sustained Fetal Arrhythmia

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