Document Detail


Transmural differences in myocardial contraction in long-QT syndrome: mechanical consequences of ion channel dysfunction.
MedLine Citation:
PMID:  20855658     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: Long-QT syndrome (LQTS) is characterized by prolonged myocardial action potential duration. The longest action potential duration is reported in the endomyocardium and midmyocardium. Prolonged action potential duration in LQTS may cause prolonged cardiac contraction, which can be assessed by strain echocardiography. We hypothesized that myocardial contraction is most prolonged in subendocardial myofibers in LQTS patients and that inhomogeneous transmural contraction is related to the risk of spontaneous arrhythmia. METHODS AND RESULTS: We included 101 genotyped LQTS mutation carriers and 35 healthy individuals. A history of cardiac arrhythmias was present in 48 mutations carriers, and 53 were asymptomatic. Myocardial contraction duration was assessed by strain echocardiography as time from the ECG Q wave to peak strain in 16 LV segments. Strain was assessed along the longitudinal axis, predominantly representing subendocardial fibers, and along the circumferential axis, representing midmyocardial fibers. Mean contraction duration was longer in LQTS mutation carriers compared with healthy individuals (445 ± 45 versus 390 ± 40 milliseconds; P<0.001) and longer in symptomatic compared with asymptomatic LQTS mutation carriers (460 ± 40 versus 425 ± 45 milliseconds; P<0.001). Contraction duration by longitudinal strain was longer than by circumferential strain in symptomatic LQTS patients (460 ± 45 versus 445±45 milliseconds; P=0.008) but not in asymptomatic patients and healthy individuals, indicating transmural mechanical dispersion. This time difference was present in a majority of LV segments and was most evident in patients with LQT2 and the Jervell and Lange-Nielsen syndrome. CONCLUSION: Contraction duration in symptomatic LQTS mutation carriers was longer in the subendocardium than in the midmyocardium, indicating transmural mechanical dispersion, which was not present in asymptomatic and healthy individuals.
Authors:
Kristina Hermann Haugaa; Jan P Amlie; Knut Erik Berge; Trond P Leren; Otto A Smiseth; Thor Edvardsen
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-09-20
Journal Detail:
Title:  Circulation     Volume:  122     ISSN:  1524-4539     ISO Abbreviation:  Circulation     Publication Date:  2010 Oct 
Date Detail:
Created Date:  2010-10-05     Completed Date:  2010-10-29     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0147763     Medline TA:  Circulation     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1355-63     Citation Subset:  AIM; IM    
Affiliation:
Department of Cardiology, Oslo University Hospital, Oslo, Norway.
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MeSH Terms
Descriptor/Qualifier:
Action Potentials
Arrhythmias, Cardiac / etiology,  physiopathology
Carrier State
Echocardiography
Electrocardiography
Genotype
Heart / physiopathology
Homozygote
Humans
Ion Channels / physiology*
Long QT Syndrome / genetics,  physiopathology*,  ultrasonography
Myocardial Contraction / physiology*
Reference Values
Stress, Mechanical
Ventricular Function, Left / physiology
Chemical
Reg. No./Substance:
0/Ion Channels
Comments/Corrections
Comment In:
Circulation. 2010 Oct 5;122(14):1353-4   [PMID:  20855657 ]

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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