Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2009-10-26
pubmed:abstractText
Between 30% and 60% of clinical cases of hypertrophic cardiomyopathy (HC) can be attributed to mutations in the genes encoding cardiac myofilament proteins. Interestingly, it appears that the likelihood of an underlying myofilament mutation can be predicted by echocardiographic assessment of left ventricular morphology. However, it is not known whether genotypically characterized HC exists as a separate entity with discrete phenotypic morphology and histology or to what extent recognized polymorphisms of the renin-angiotensin-aldosterone system (RAAS) influence this relationship. The presence of cardiac myofilament and mutations and RAAS polymorphisms will have a strong association with the severity of histologic features of HC and characteristic septal shape.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
1097-6744
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
158
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
799-805
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed:year
2009
pubmed:articleTitle
Histologic characterization of hypertrophic cardiomyopathy with and without myofilament mutations.
pubmed:affiliation
Department of Internal Medicine, Mayo Clinic, Rochester, MN 55905, USA.
pubmed:publicationType
Journal Article