rdf:type |
|
lifeskim:mentions |
|
pubmed:issue |
10
|
pubmed:dateCreated |
2002-3-12
|
pubmed:abstractText |
Specific ion channel mutations underlie the congenital long-QT syndrome (LQTS). However, the mechanisms by which dysfunction at the molecular level translates into functional electrical instability leading to torsade de pointes (TdP) in LQTS are poorly understood.
|
pubmed:grant |
|
pubmed:language |
eng
|
pubmed:journal |
|
pubmed:citationSubset |
AIM
|
pubmed:chemical |
|
pubmed:status |
MEDLINE
|
pubmed:month |
Mar
|
pubmed:issn |
1524-4539
|
pubmed:author |
|
pubmed:issnType |
Electronic
|
pubmed:day |
12
|
pubmed:volume |
105
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
1247-53
|
pubmed:dateRevised |
2007-11-14
|
pubmed:meshHeading |
pubmed-meshheading:11889021-Action Potentials,
pubmed-meshheading:11889021-Animals,
pubmed-meshheading:11889021-Body Surface Potential Mapping,
pubmed-meshheading:11889021-Disease Models, Animal,
pubmed-meshheading:11889021-Dogs,
pubmed-meshheading:11889021-Electric Stimulation,
pubmed-meshheading:11889021-Electrocardiography,
pubmed-meshheading:11889021-Electrophysiologic Techniques, Cardiac,
pubmed-meshheading:11889021-Heart Conduction System,
pubmed-meshheading:11889021-Long QT Syndrome,
pubmed-meshheading:11889021-Myocardium,
pubmed-meshheading:11889021-Sotalol,
pubmed-meshheading:11889021-Torsades de Pointes
|
pubmed:year |
2002
|
pubmed:articleTitle |
Unique topographical distribution of M cells underlies reentrant mechanism of torsade de pointes in the long-QT syndrome.
|
pubmed:affiliation |
Heart and Vascular Research Center and Departments of Medicine and Biomedical Engineering, Case Western Reserve University, Cleveland, Ohio 44109-1998, USA.
|
pubmed:publicationType |
Journal Article,
In Vitro,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
|