Source:http://linkedlifedata.com/resource/pubmed/id/21572004
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
2
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| pubmed:dateCreated |
2011-8-2
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| pubmed:abstractText |
Frequency potentiation of contractile function is a major mechanism of the increase in myocardial performance during exercise. In heart failure (HF), this positive force-frequency relation is impaired, and the abnormal left ventricular (LV)-arterial coupling is exacerbated by tachycardia. A myofilament Ca(2+) sensitizer, levosimendan, has been shown to improve exercise tolerance in HF. This may be due to its beneficial actions on the force-frequency relation and LV-arterial coupling (end-systolic elastance/arterial elastance, E(ES)/E(A)). We assessed the effects of therapeutic doses of levosimendan on the force-frequency relation and E(ES)/E(A) in nine conscious dogs after pacing-induced HF using pressure-volume analysis. Before HF, pacing tachycardia increased E(ES), shortened ?, and did not impair E(ES)/E(A) and mechanical efficiency (stroke work/pressure-volume area, SW/PVA). In contrast, after HF, pacing at 140, 160, 180, and 200 beat/min (bpm) produced smaller a increase of E(ES) or less shortening of ?, whereas E(ES)/E(A) (from 0.56 at baseline to 0.42 at 200 bpm) and SW/PVA (from 0.52 at baseline to 0.43 at 200 bpm) progressively decreased. With levosimendan, basal E(ES) increased 27% (6.2 mmHg/ml), ? decreased 11% (40.8 ms), E(ES)/E(A) increased 34% (0.75), and SW/PVA improved by 15% (0.60). During tachycardia, E(ES) further increased by 23%, 37%, 68%, and 89%; ? decreased by 9%, 12%, 15%, and 17%; and E(ES)/E(A) was augmented by 11%, 16%, 31%, and 33%, incrementally, with pacing rate. SW/PVA was improved (0.61 to 0.64). In conclusion, in HF, treatment with levosimendan restores the normal positive LV systolic and diastolic force-frequency relation and prevents tachycardia-induced adverse effect on LV-arterial coupling and mechanical efficiency.
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| pubmed:grant | |
| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical | |
| pubmed:status |
MEDLINE
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| pubmed:month |
Aug
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| pubmed:issn |
1522-1539
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| pubmed:author | |
| pubmed:issnType |
Electronic
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| pubmed:volume |
301
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
H488-96
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| pubmed:meshHeading |
pubmed-meshheading:21572004-Analysis of Variance,
pubmed-meshheading:21572004-Animals,
pubmed-meshheading:21572004-Cardiac Pacing, Artificial,
pubmed-meshheading:21572004-Cardiotonic Agents,
pubmed-meshheading:21572004-Disease Models, Animal,
pubmed-meshheading:21572004-Dogs,
pubmed-meshheading:21572004-Excitation Contraction Coupling,
pubmed-meshheading:21572004-Heart Failure,
pubmed-meshheading:21572004-Heart Rate,
pubmed-meshheading:21572004-Hydrazones,
pubmed-meshheading:21572004-Male,
pubmed-meshheading:21572004-Myocardial Contraction,
pubmed-meshheading:21572004-Pyridazines,
pubmed-meshheading:21572004-Stroke Volume,
pubmed-meshheading:21572004-Tachycardia,
pubmed-meshheading:21572004-Time Factors,
pubmed-meshheading:21572004-Ventricular Dysfunction, Left,
pubmed-meshheading:21572004-Ventricular Function, Left,
pubmed-meshheading:21572004-Ventricular Pressure
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| pubmed:year |
2011
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| pubmed:articleTitle |
Levosimendan restores the positive force-frequency relation in heart failure.
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| pubmed:affiliation |
Cardiology Section, Wake Forest University School of Medicine, Winston-Salem, North Carolina, USA.
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| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
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