title: Relationship between circulating levels of monocyte chemoattractant protein-1 and systolic dysfunction in patients with hypertrophic cardiomyopathy.
abstract: 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).
  
  
  CONCLUSIONS
  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.
authors.affiliation: Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Shikata-cho, Okayama, Japan.
authors.forename: Jun
authors.initials: J
authors.lastname: Iwasaki
authors.forename: Kazufumi
authors.initials: K
authors.lastname: Nakamura
authors.forename: Hiromi
authors.initials: H
authors.lastname: Matsubara
authors.forename: Yoichi
authors.initials: Y
authors.lastname: Nakamura
authors.forename: Nobuhiro
authors.initials: N
authors.lastname: Nishii
authors.forename: Kimikazu
authors.initials: K
authors.lastname: Banba
authors.forename: Masato
authors.initials: M
authors.lastname: Murakami
authors.forename: Keiko
authors.initials: K
authors.lastname: Ohta-Ogo
authors.forename: Hideo
authors.initials: H
authors.lastname: Kimura
authors.forename: Norihisa
authors.initials: N
authors.lastname: Toh
authors.forename: Satoshi
authors.initials: S
authors.lastname: Nagase
authors.forename: Takefumi
authors.initials: T
authors.lastname: Oka
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Morita
authors.forename: Kengo Fukushima
authors.initials: KF
authors.lastname: Kusano
authors.forename: Tohru
authors.initials: T
authors.lastname: Ohe
mesh_terms: D002312:Cardiomyopathy, Hypertrophic / Q000097:blood* / Q000150:complications*; D018932:Chemokine CCL2 / Q000096:biosynthesis / Q000097:blood*; D018450:Disease Progression; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D008297:Male; D008875:Middle Aged; D009206:Myocardium / Q000378:metabolism; D018487:Ventricular Dysfunction, Left / Q000097:blood* / Q000150:complications*
chemical_list: C111835:CCL2 protein, human; D018932:Chemokine CCL2