PMID- 19211266
OWN - NLM
STAT- MEDLINE
DCOM- 20100108
LR  - 20091102
IS  - 1879-1336 (Electronic)
IS  - 1054-8807 (Linking)
VI  - 18
IP  - 6
DP  - 2009 Nov-Dec
TI  - Relationship between circulating levels of monocyte chemoattractant protein-1 and 
      systolic dysfunction in patients with hypertrophic cardiomyopathy.
PG  - 317-22
LID - 10.1016/j.carpath.2008.12.004 [doi]
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.
FAU - Iwasaki, Jun
AU  - Iwasaki J
AD  - Department of Cardiovascular Medicine, Okayama University Graduate School of 
      Medicine, Dentistry and Pharmaceutical Sciences, Shikata-cho, Okayama, Japan.
FAU - Nakamura, Kazufumi
AU  - Nakamura K
FAU - Matsubara, Hiromi
AU  - Matsubara H
FAU - Nakamura, Yoichi
AU  - Nakamura Y
FAU - Nishii, Nobuhiro
AU  - Nishii N
FAU - Banba, Kimikazu
AU  - Banba K
FAU - Murakami, Masato
AU  - Murakami M
FAU - Ohta-Ogo, Keiko
AU  - Ohta-Ogo K
FAU - Kimura, Hideo
AU  - Kimura H
FAU - Toh, Norihisa
AU  - Toh N
FAU - Nagase, Satoshi
AU  - Nagase S
FAU - Oka, Takefumi
AU  - Oka T
FAU - Morita, Hiroshi
AU  - Morita H
FAU - Kusano, Kengo Fukushima
AU  - Kusano KF
FAU - Ohe, Tohru
AU  - Ohe T
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20090211
PL  - United States
TA  - Cardiovasc Pathol
JT  - Cardiovascular pathology : the official journal of the Society for Cardiovascular 
      Pathology
JID - 9212060
RN  - 0 (CCL2 protein, human)
RN  - 0 (Chemokine CCL2)
SB  - IM
MH  - Cardiomyopathy, Hypertrophic/*blood/*complications
MH  - Chemokine CCL2/biosynthesis/*blood
MH  - Disease Progression
MH  - Enzyme-Linked Immunosorbent Assay
MH  - Female
MH  - Humans
MH  - Immunohistochemistry
MH  - Male
MH  - Middle Aged
MH  - Myocardium/metabolism
MH  - Ventricular Dysfunction, Left/*blood/*complications
EDAT- 2009/02/13 09:00
MHDA- 2010/01/09 06:00
CRDT- 2009/02/13 09:00
PHST- 2008/01/15 00:00 [received]
PHST- 2008/10/29 00:00 [revised]
PHST- 2008/12/03 00:00 [accepted]
PHST- 2009/02/13 09:00 [entrez]
PHST- 2009/02/13 09:00 [pubmed]
PHST- 2010/01/09 06:00 [medline]
AID - S1054-8807(08)00185-3 [pii]
AID - 10.1016/j.carpath.2008.12.004 [doi]
PST - ppublish
SO  - Cardiovasc Pathol. 2009 Nov-Dec;18(6):317-22. doi: 10.1016/j.carpath.2008.12.004. 
      Epub 2009 Feb 11.