PMID- 9040055 OWN - NLM STAT- MEDLINE DCOM- 19970527 LR - 20061115 IS - 0022-2828 (Print) IS - 0022-2828 (Linking) VI - 29 IP - 1 DP - 1997 Jan TI - Plasma levels of the monocyte chemotactic and activating factor/monocyte chemoattractant protein-1 are elevated in patients with acute myocardial infarction. PG - 419-23 AB - 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. FAU - Matsumori, A AU - Matsumori A AD - Department of Cardiovascular Medicine, Kyoto University, Sakyo-ku, Japan. FAU - Furukawa, Y AU - Furukawa Y FAU - Hashimoto, T AU - Hashimoto T FAU - Yoshida, A AU - Yoshida A FAU - Ono, K AU - Ono K FAU - Shioi, T AU - Shioi T FAU - Okada, M AU - Okada M FAU - Iwasaki, A AU - Iwasaki A FAU - Nishio, R AU - Nishio R FAU - Matsushima, K AU - Matsushima K FAU - Sasayama, S AU - Sasayama S LA - eng PT - Clinical Trial PT - Comparative Study PT - Controlled Clinical Trial PT - Journal Article PT - Research Support, Non-U.S. Gov't PL - England TA - J Mol Cell Cardiol JT - Journal of molecular and cellular cardiology JID - 0262322 RN - 0 (Chemokine CCL2) RN - 0 (Cytokines) RN - 0 (Interleukin-8) SB - IM MH - Adult MH - Aged MH - Aged, 80 and over MH - Angina Pectoris/blood MH - Chemokine CCL2/*blood MH - Cytokines/blood MH - Female MH - Humans MH - Interleukin-8/*blood MH - Linear Models MH - Male MH - Middle Aged MH - Myocardial Infarction/*blood EDAT- 1997/01/01 00:00 MHDA- 1997/01/01 00:01 CRDT- 1997/01/01 00:00 PHST- 1997/01/01 00:00 [pubmed] PHST- 1997/01/01 00:01 [medline] PHST- 1997/01/01 00:00 [entrez] AID - S0022-2828(96)90285-0 [pii] AID - 10.1006/jmcc.1996.0285 [doi] PST - ppublish SO - J Mol Cell Cardiol. 1997 Jan;29(1):419-23. doi: 10.1006/jmcc.1996.0285.