title: Plasma levels of the monocyte chemotactic and activating factor/monocyte chemoattractant protein-1 are elevated in patients with acute myocardial infarction.
abstract: Cardiac inflammatory responses appear to play a pivotal role in scar formation after acute myocardial infarction. Monocyte chemotactic and activating factor (MCAF) monocyte chemoattractant protein-1 (MCP-1) is a cytokine with chemotactic activity for mononuclear phagocytes, but also for NK cells, T cells, mast cells, and basophils. To investigate the possible involvement of MCAF/MCP-1 in the pathogenesis, its course was studied in patients with acute myocardial infarction. Twenty-three consecutive patients with acute myocardial infarction and 18 patients with angina pectoris were studied. Cytokines were measured by enzyme-linked immunosorbent assay. Plasma levels of interleukin IL-1alpha, IL-1beta, and IL-2 were below the detection limit of our method. IL-6 and interferon-gamma were detected in 17.4%, and tumor necrosis factor-alpha in 13.0% of patients with acute myocardial infarction, but the frequency was not statistically significantly different from that in angina pectoris. The plasma level of MCAF/MCP-1 in myocardial infarction tended to increase at 3 h after the onset of chest pain (133 +/- 19 pg/ml, P= 0.06) and was significantly elevated at 9 h (143 +/- 20 pg/ml) when compared with that in angina pectoris (87 +/- 6 pg/ml, P<0.05). The MCAF/MCP-1 level remained increased during the 24-hours observation period (P<0.01), and maximum level (168 +/- 13 pg/ml) was seen at 24 hour. The level of MCAF/ MCP-1 correlated significantly with the plasma level of another chemokine, IL-8, at 12 h after the onset of chest pain (r=0.51, P<0.05), suggesting that common stimuli mediate the release of both cytokines in myocardial infarction. The identification of MCAF/MCP-1 as an inflammatory mediator in acute myocardial infarction suggests that mononuclear phagocytes may play an important role in the early stage of the disease.
authors.affiliation: Department of Cardiovascular Medicine, Kyoto University, Sakyo-ku, Japan.
authors.forename: A
authors.initials: A
authors.lastname: Matsumori
authors.forename: Y
authors.initials: Y
authors.lastname: Furukawa
authors.forename: T
authors.initials: T
authors.lastname: Hashimoto
authors.forename: A
authors.initials: A
authors.lastname: Yoshida
authors.forename: K
authors.initials: K
authors.lastname: Ono
authors.forename: T
authors.initials: T
authors.lastname: Shioi
authors.forename: M
authors.initials: M
authors.lastname: Okada
authors.forename: A
authors.initials: A
authors.lastname: Iwasaki
authors.forename: R
authors.initials: R
authors.lastname: Nishio
authors.forename: K
authors.initials: K
authors.lastname: Matsushima
authors.forename: S
authors.initials: S
authors.lastname: Sasayama
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000787:Angina Pectoris / Q000097:blood; D018932:Chemokine CCL2 / Q000097:blood*; D016207:Cytokines / Q000097:blood; D005260:Female; D006801:Humans; D016209:Interleukin-8 / Q000097:blood*; D016014:Linear Models; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood*
chemical_list: D018932:Chemokine CCL2; D016207:Cytokines; D016209:Interleukin-8