TY - JOUR
T1 - Relationship between circulating levels of monocyte chemoattractant protein-1 and systolic dysfunction in patients with hypertrophic cardiomyopathy
AU - Iwasaki, Jun
AU - Nakamura, Kazufumi
AU - Matsubara, Hiromi
AU - Nakamura, Yoichi
AU - Nishii, Nobuhiro
AU - Banba, Kimikazu
AU - Murakami, Masato
AU - Ohta-Ogo, Keiko
AU - Kimura, Hideo
AU - Toh, Norihisa
AU - Nagase, Satoshi
AU - Oka, Takefumi
AU - Morita, Hiroshi
AU - Kusano, Kengo Fukushima
AU - Ohe, Tohru
N1 - Funding Information:
Dr. Nakamura was supported by a grant from the Japan Foundation of Cardiovascular Research; in part by a Grant-in-Aid for Young Scientists (A) from the Ministry of Education, Culture, Sports, Science and Technology (No.17689026); in part by a Grant from Mitsui Life Social Welfare Foundation; and in part by Japan Heart Foundation/Pfizer Japan Inc. Grant for Research on Cardiovascular Disease, Japan.
PY - 2009/11
Y1 - 2009/11
N2 - 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.
AB - 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.
KW - Cardiomyopathy
KW - Heart failure
KW - Monocyte
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U2 - 10.1016/j.carpath.2008.12.004
DO - 10.1016/j.carpath.2008.12.004
M3 - Article
C2 - 19211266
AN - SCOPUS:70350574104
VL - 18
SP - 317
EP - 322
JO - Cardiovascular Pathology
JF - Cardiovascular Pathology
SN - 1054-8807
IS - 6
ER -