Source:http://linkedlifedata.com/resource/pubmed/id/17851694
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
5
|
| pubmed:dateCreated |
2007-11-21
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| pubmed:abstractText |
Hypertrophic Cardiomyopathy (HCM) is a disease with variable rate of progression. Young age is an independent risk factor for poor outcome in HCM. The influence of renin-angiotensin-aldosterone (RAAS) genotype on the progression of HCM in children is unknown. Children with HCM (n = 65) were enrolled prospectively across two centers (2001-2005). All subjects were genotyped for five RAAS gene polymorphisms previously associated with LV hypertrophy (pro-LVH): AGT M235T, ACE DD, CMA-1903 A/G, AGTR1 1666 A/C and CYP11B2-344 C/T. Linear regression models, based on maximum likelihood estimates, were created to assess the independent effect of RAAS genotype on LV hypertrophy (LVH). Forty-six subjects were homozygous for <2 and 19 were homozygous for > or =2 pro-LVH RAAS polymorphisms. Mean age at presentation was 9.6 +/- 6 years. Forty children had follow-up echocardiograms after a median of 1.5 years. Indexed LV mass (LVMI) and LV mass z-scores were higher at presentation and follow-up in subjects with > or =2 pro-LVH genotypes compared to those with <2 (P < 0.05). Subjects with > or =2 pro-LVH genotypes also demonstrated a greater increase in septal thickness (IVST) and in LV outflow tract (LVOT) obstruction on follow-up (P < 0.05). On multivariate analysis, a higher number of pro-LVH genotypes was associated with a larger effect size (P < 0.05). Pro-LVH RAAS gene polymorphisms are associated with progressive septal hypertrophy and LVOT obstruction in children with HCM. Identification of RAAS modifier genes may help to risk-stratify patients with HCM.
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| pubmed:grant | |
| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical | |
| pubmed:status |
MEDLINE
|
| pubmed:month |
Dec
|
| pubmed:issn |
1432-1203
|
| pubmed:author |
pubmed-author:AuerbachScottS,
pubmed-author:ChungWendy KWK,
pubmed-author:DengLiyongL,
pubmed-author:GruberDorotaD,
pubmed-author:HsuDaphne TDT,
pubmed-author:KaufmanBeth DBD,
pubmed-author:ManlhiotCedricC,
pubmed-author:MitalSeemaS,
pubmed-author:PapavassiliouDimitrios PDP,
pubmed-author:PrakashAshwinA,
pubmed-author:PrintzBeth FBF,
pubmed-author:ReddySushmaS,
pubmed-author:SehnertAmy JAJ
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| pubmed:issnType |
Electronic
|
| pubmed:volume |
122
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
515-23
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| pubmed:dateRevised |
2008-9-3
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| pubmed:meshHeading |
pubmed-meshheading:17851694-Adolescent,
pubmed-meshheading:17851694-Adult,
pubmed-meshheading:17851694-Alleles,
pubmed-meshheading:17851694-Base Sequence,
pubmed-meshheading:17851694-Cardiomyopathy, Hypertrophic, Familial,
pubmed-meshheading:17851694-Child,
pubmed-meshheading:17851694-Child, Preschool,
pubmed-meshheading:17851694-DNA Primers,
pubmed-meshheading:17851694-Echocardiography, Doppler,
pubmed-meshheading:17851694-Female,
pubmed-meshheading:17851694-Gene Frequency,
pubmed-meshheading:17851694-Genotype,
pubmed-meshheading:17851694-Humans,
pubmed-meshheading:17851694-Hypertrophy, Left Ventricular,
pubmed-meshheading:17851694-Infant,
pubmed-meshheading:17851694-Infant, Newborn,
pubmed-meshheading:17851694-Male,
pubmed-meshheading:17851694-Phenotype,
pubmed-meshheading:17851694-Polymorphism, Genetic,
pubmed-meshheading:17851694-Prospective Studies,
pubmed-meshheading:17851694-Renin-Angiotensin System
|
| pubmed:year |
2007
|
| pubmed:articleTitle |
RAAS gene polymorphisms influence progression of pediatric hypertrophic cardiomyopathy.
|
| pubmed:affiliation |
Department of Pediatrics, Columbia University, New York, NY, 10032, USA.
|
| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't,
Multicenter Study,
Research Support, N.I.H., Extramural
|