Document Detail


Cardiac retention of [11C]HED in genotyped long QT patients: a potential amplifier role for severity of the disease.
MedLine Citation:
PMID:  12775564     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Although mutations in cardiac sodium and potassium channel genes are associated with congenital long QT syndrome (LQTS), a "modifier" role of the sympathetic nervous system was proposed to explain the distinct severity of the disease. We evaluated cardiac sympathetic innervation using [11C]hydroxyephedrine ([11C]HED) and positron emission tomography (PET) in genotyped LQTS patients. H215O and [11C]HED PET studies were performed in 11 patients (5 symptomatic) and 8 controls. Perfusion and [11C]HED images were depicted as 36-sector polar maps. Sectorial values of perfusion (H2O%), absolute (HEDRet) and relative retention (HED%Ret) of [11C]HED, and the ratio of HED%Ret to H2O% (HED%Ret/H2O%) were calculated. Normal databases were obtained from controls. Sectorial values below 2SD database values were defined as "outside sectors." Controls and patients showed similar sectorial perfusion. Sectorial HEDRet did not differ between groups, but means of HED%Ret were lower in three sectors for patients (P < 0.05). Three sectors from 3 controls had HED%Ret below 2SD, whereas 36 sectors in 9 patients were outside sectors (P < 0.01). In patients, average HED%Ret/H2O% was lower in 9 sectors (P < 0.05 vs. controls); 2 outside sectors were found in controls, but 43 outside sectors were found in patients (P < 0.01), 77% of them in the 5 symptomatic patients. Heterogeneous [11C]HED retention was localized in the septal, anterior, and lateral walls. Most LQTS patients showed a localized and decreased pattern of [11C]HED retention. The larger number of heterogeneous sectors in symptomatic patients suggests that sympathetic function could play an amplifier role for severity of the disease.
Authors:
Alejandro N Mazzadi; Xavier André-Fouët; Jérôme Duisit; Véronique Gebuhrer; Nicolas Costes; Philippe Chevalier; Claire Rodriguez; Jean-Jacques Schott; Hervé Le Marec; Pascale Guicheney; Didier Le Bars; Marc Janier
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Publication Detail:
Type:  Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't     Date:  2003-05-29
Journal Detail:
Title:  American journal of physiology. Heart and circulatory physiology     Volume:  285     ISSN:  0363-6135     ISO Abbreviation:  Am. J. Physiol. Heart Circ. Physiol.     Publication Date:  2003 Sep 
Date Detail:
Created Date:  2003-08-13     Completed Date:  2003-09-26     Revised Date:  2008-10-28    
Medline Journal Info:
Nlm Unique ID:  100901228     Medline TA:  Am J Physiol Heart Circ Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  H1286-93     Citation Subset:  IM    
Affiliation:
Centre d'Exploration et de Recherche Médicales par Emission de Positons, 69003 Lyon, France.
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MeSH Terms
Descriptor/Qualifier:
Adolescent
Adult
Carbon Radioisotopes / diagnostic use
Cation Transport Proteins*
Contrast Media
DNA-Binding Proteins*
Ephedrine / analogs & derivatives*,  diagnostic use*
Ether-A-Go-Go Potassium Channels
Female
Genotype
Heart / innervation,  radionuclide imaging
Humans
KCNQ Potassium Channels
KCNQ1 Potassium Channel
Long QT Syndrome / genetics*,  radionuclide imaging*
Male
Middle Aged
Phenotype
Potassium Channels / genetics
Potassium Channels, Voltage-Gated*
Severity of Illness Index
Sympathetic Nervous System / physiology
Tomography, Emission-Computed / methods*
Trans-Activators*
Chemical
Reg. No./Substance:
0/Carbon Radioisotopes; 0/Cation Transport Proteins; 0/Contrast Media; 0/DNA-Binding Proteins; 0/ERG protein, human; 0/ERG1 potassium channel; 0/Ether-A-Go-Go Potassium Channels; 0/KCNH6 protein, human; 0/KCNQ Potassium Channels; 0/KCNQ1 Potassium Channel; 0/KCNQ1 protein, human; 0/Potassium Channels; 0/Potassium Channels, Voltage-Gated; 0/Trans-Activators; 299-42-3/Ephedrine; 3002-40-2/3-hydroxyephedrine

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