Source:http://linkedlifedata.com/resource/pubmed/id/16728224
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
11
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pubmed:dateCreated |
2006-5-26
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pubmed:abstractText |
It was hypothesized that restricted diastolic leaflet motion is implicated not only in the mechanism of systolic mitral regurgitation (MR) but also in the mechanism of diastolic MR observed in patients with severe heart failure. Cardiac resynchronization therapy (CRT) can oppose increased mitral leaflet tethering by increasing transmitral pressure, thereby providing an opportunity to explore this hypothesis. A total of 26 consecutive candidates for CRT with diastolic MR were compared with 26 candidates without diastolic MR. Maximal diastolic mitral leaflet opening and inflow direction and measures of mitral valve apparatus (i.e., mitral annular diameters, calculated mitral annular area, and tethering distance) were assessed from the apical 4-chamber view before and during CRT. There were no significant differences in New York Heart Association functional class, ejection fraction, QRS duration, PR interval, systolic MR grade, or 2-dimensional geometry of the mitral valve apparatus between the groups. Patients with diastolic MR had more restricted maximal diastolic leaflet openings (54 degrees +/- 17 degrees vs 71 degrees +/- 11 degrees , p = 0.003) and substantially smaller inflow angles (66 degrees +/- 7 degrees vs 79 degrees +/- 9 degrees , p = 0.0003) compared with patients without diastolic MR. After the institution of CRT, diastolic MR was eliminated in all patients, although there were no significant changes in any of the parameters of mitral valve apparatus. In conclusion, abnormal mitral valve tethering is a constitutive element of the mechanism of diastolic MR in patients with left ventricular dysfunction. Its acute resolution after CRT does not seem to be caused by changes in mitral valve geometry but rather by an increase in transmitral closing forces.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:status |
MEDLINE
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pubmed:month |
Jun
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pubmed:issn |
0002-9149
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
1
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pubmed:volume |
97
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1611-4
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pubmed:dateRevised |
2007-11-15
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pubmed:meshHeading |
pubmed-meshheading:16728224-Cardiac Pacing, Artificial,
pubmed-meshheading:16728224-Diastole,
pubmed-meshheading:16728224-Echocardiography,
pubmed-meshheading:16728224-Electrocardiography,
pubmed-meshheading:16728224-Heart Failure,
pubmed-meshheading:16728224-Humans,
pubmed-meshheading:16728224-Mitral Valve Insufficiency,
pubmed-meshheading:16728224-Myocardial Contraction,
pubmed-meshheading:16728224-Prognosis,
pubmed-meshheading:16728224-Severity of Illness Index
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pubmed:year |
2006
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pubmed:articleTitle |
Mechanism of diastolic mitral regurgitation in candidates for cardiac resynchronization therapy.
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pubmed:affiliation |
Heart Institute, Chaim Sheba Medical Center, Tel Hashomer, Israel.
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pubmed:publicationType |
Journal Article,
Comparative Study
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