Relationship between circulating levels of monocyte chemoattractant protein-1 and systolic dysfunction in patients with hypertrophic cardiomyopathy.
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.
Iwasaki
Jun
J
Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Shikata-cho, Okayama, Japan.
Nakamura
Kazufumi
K
Matsubara
Hiromi
H
Nakamura
Yoichi
Y
Nishii
Nobuhiro
N
Banba
Kimikazu
K
Murakami
Masato
M
Ohta-Ogo
Keiko
K
Kimura
Hideo
H
Toh
Norihisa
N
Nagase
Satoshi
S
Oka
Takefumi
T
Morita
Hiroshi
H
Kusano
Kengo Fukushima
KF
Ohe
Tohru
T
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*
C111835:CCL2 protein, human; D018932:Chemokine CCL2