| Relationship between circulating levels of monocyte chemoattractant protein-1 and systolic dysfunction in patients with hypertrophic cardiomyopathy. | |
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MedLine Citation:
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PMID: 19211266 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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BACKGROUND: Progression of hypertrophic cardiomyopathy (HCM) to left ventricular dilatation and systolic dysfunction sometimes occurs. However, the mechanism of the transition from hypertrophy to dysfunction has not been elucidated. It has been reported that circulating levels of monocyte chemoattractant protein-1 (MCP-1), which is a major factor promoting the accumulation of macrophages, are increased in patients with congestive heart failure. We measured circulating levels of MCP-1 in patients with HCM and examined whether MCP-1 was expressed in the myocardium of HCM patients. We also examined whether circulating levels of MCP-1 were correlated with left ventricular dysfunction. METHODS: Circulating levels of MCP-1 were measured by an enzyme immunoassay in 26 patients with HCM (60+/-2 years old) and 20 control subjects (57+/-2 years old). Cardiac function was evaluated by two-dimensional echocardiography and cardiac catheterization. RESULTS: HCM patients had significantly elevated levels of MCP-1 (HCM: 309+/-30 vs. control: 178+/-8 pg/ml, P<.001). MCP-1 levels in patients with systolic dysfunction were significantly higher than those in patients without systolic dysfunction (P<.05) and were also significantly higher than those in patients with outflow obstruction (P<.05). Immunohistochemical analysis revealed that MCP-1 was expressed in endomyocardial biopsy samples obtained from HCM patients with systolic dysfunction. Furthermore, MCP-1 levels were inversely correlated with fractional shortening (r=-.401, P<.05) and correlated with left ventricular end-diastolic pressure (r=-.579, P<.01). CONCLUSION: These results show that MCP-1 is associated with, and might be involved in the pathogenesis of, left ventricular systolic dysfunction in patients with HCM. |
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Authors:
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Jun Iwasaki; Kazufumi Nakamura; Hiromi Matsubara; Yoichi Nakamura; Nobuhiro Nishii; Kimikazu Banba; Masato Murakami; Keiko Ohta-Ogo; Hideo Kimura; Norihisa Toh; Satoshi Nagase; Takefumi Oka; Hiroshi Morita; Kengo Fukushima Kusano; Tohru Ohe |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2009-02-11 |
Journal Detail:
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Title: Cardiovascular pathology : the official journal of the Society for Cardiovascular Pathology Volume: 18 ISSN: 1879-1336 ISO Abbreviation: Cardiovasc. Pathol. Publication Date: 2009 Nov-Dec |
Date Detail:
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Created Date: 2009-11-02 Completed Date: 2010-01-08 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 9212060 Medline TA: Cardiovasc Pathol Country: United States |
Other Details:
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Languages: eng Pagination: 317-22 Citation Subset: IM |
Affiliation:
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Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Shikata-cho, Okayama, Japan. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Cardiomyopathy, Hypertrophic
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blood*,
complications* Chemokine CCL2 / biosynthesis, blood* Disease Progression Enzyme-Linked Immunosorbent Assay Female Humans Immunohistochemistry Male Middle Aged Myocardium / metabolism Ventricular Dysfunction, Left / blood*, complications* |
| Chemical | |
Reg. No./Substance:
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0/CCL2 protein, human; 0/Chemokine CCL2 |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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