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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
3
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pubmed:dateCreated |
2004-2-25
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pubmed:abstractText |
Genetic defects in the plasma membrane-associated sarcoglycan complex produce cardiomyopathy characterized by focal degeneration. The infarct-like pattern of cardiac degeneration has led to the hypothesis that coronary artery vasospasm underlies cardiomyopathy in this disorder. We evaluated the coronary vasculature of gamma-sarcoglycan mutant mice and found microvascular filling defects consistent with arterial vasospasm. However, the vascular smooth muscle sarcoglycan complex was intact in the coronary arteries of gamma-sarcoglycan hearts with perturbation of the sarcoglycan complex only within the adjacent myocytes. Thus, in this model, coronary artery vasospasm derives from a vascular smooth muscle-cell extrinsic process. To reduce this secondary vasospasm, we treated gamma-sarcoglycan-deficient mice with the calcium channel antagonist verapamil. Verapamil treatment eliminated evidence of vasospasm and ameliorated histological and functional evidence of cardiomyopathic progression. Echocardiography of verapamil-treated, gamma-sarcoglycan-null mice showed an improvement in left ventricular fractional shortening (44.3 +/- 13.3% treated versus 37.4 +/- 15.3% untreated), maximal velocity at the aortic outflow tract (114.9 +/- 27.9 cm/second versus 92.8 +/- 22.7 cm/second), and cardiac index (1.06 +/- 0.30 ml/minute/g versus 0.67 +/- 0.16 ml/minute/g, P < 0.05). These data indicate that secondary vasospasm contributes to the development of cardiomyopathy and is an important therapeutic target to limit cardiomyopathy progression.
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pubmed:grant |
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/14982859-10481911,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14982859-10485893,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14982859-10488149,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14982859-10629222,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14982859-10678176,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14982859-10679963,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14982859-10679964,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14982859-10862711,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14982859-10974018,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14982859-10993904,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14982859-11160141,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14982859-11257475,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14982859-11322951,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14982859-11357018,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14982859-12122112,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14982859-12189167,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14982859-1741056,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14982859-1986002,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14982859-2259381,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14982859-2671096,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14982859-2973484,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14982859-6215853,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14982859-7094244,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14982859-8188626,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14982859-8923014,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14982859-8968749,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14982859-9018440,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14982859-9243091,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14982859-9475163,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14982859-9732288,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14982859-9874799
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
AIM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Mar
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pubmed:issn |
0002-9440
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
164
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1063-71
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:14982859-Animals,
pubmed-meshheading:14982859-Calcium Channel Blockers,
pubmed-meshheading:14982859-Cardiomyopathies,
pubmed-meshheading:14982859-Coronary Vasospasm,
pubmed-meshheading:14982859-Cytoskeletal Proteins,
pubmed-meshheading:14982859-Disease Models, Animal,
pubmed-meshheading:14982859-Disease Progression,
pubmed-meshheading:14982859-Echocardiography,
pubmed-meshheading:14982859-Fluorescent Antibody Technique,
pubmed-meshheading:14982859-Heart,
pubmed-meshheading:14982859-Heart Function Tests,
pubmed-meshheading:14982859-Immunoblotting,
pubmed-meshheading:14982859-Membrane Glycoproteins,
pubmed-meshheading:14982859-Mice,
pubmed-meshheading:14982859-Mice, Mutant Strains,
pubmed-meshheading:14982859-Muscle, Smooth, Vascular,
pubmed-meshheading:14982859-Myocardium,
pubmed-meshheading:14982859-Sarcoglycans,
pubmed-meshheading:14982859-Verapamil
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pubmed:year |
2004
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pubmed:articleTitle |
Secondary coronary artery vasospasm promotes cardiomyopathy progression.
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pubmed:affiliation |
Department of Molecular Genetics and Cell Biology, Section of Cardiology, University of Chicago, Chicago, Illinois, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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