Kinetics of chemokines in acute myocardial infarction.
BACKGROUND
Chemokines are supposed to play an important role in the activation of monocytes and in the development of atherosclerosis. There are also suggestions that chemokine-mediated enhanced coagulability may be related to the pathogenesis of acute coronary syndromes.Aim. To assess the kinetics of 3 chemokines: Monocyte Chemoattractant Protein-1 (MCP-1), Macrophage Inflammatory Protein-1alfa (MIP-1alpha) and Regulated on Activation Normal T cell Expressed and Secreted (RANTES) in patients with ST-elevation myocardial infarction (STEMI).


METHODS
The study group consisted of 40 patients (pts) with STEMI who were divided into 2 groups -- 16 pts with anterior MI (AMI) and 24 pts with inferior or lateral MI (IMI). According to the type of received therapy, the pts were divided into 2 other groups: group A -- 30 pts treated with thrombolytic agents or primary angioplasty and group B -- 10 pts without recanalisation therapy. The control group consisted of 10 healthy volunteers. Blood samples for MCP-1, MIP-1alpha and RANTES serum levels was taken on admission and 3 h, 24 h, 48 h, 72 h and 7 days afterwards.


RESULTS
The baseline MCP-1 and RANTES levels were significantly higher in pts with STEMI than in controls (1068.9 vs 880.9 pg/ml, p<0.05; 50.8 vs 33.9 pg/ml, p<0.005). In pts with STEMI, peak levels of MCP-1 and MIP-1alpha were significantly higher 3h than 24h from admission (MCP-1 1274.4 vs 1097.4 pg/ml, p<0.02; MIP-1alpha 39.2 vs 22.0 pg/ml, p<0.01). In all STEMI pts there was a positive correlation between MIP-1alpha 3h and left ventricular ejection fraction (LVEF) (r=0.455, p<0.05) and a negative correlation between MIP-1alpha 3h and LV end-diastolic diameter (LVEED) (r=-0.453, p<0.05). A significant positive correlation between TnI level and chemokines in both AMI and IMI patients was detected, being the highest in AMI and IMI groups when MIP-1alpha 24 h and TnI were compared (R=0.852, p<0.003 and R=0.646, p<0.0001). In pts with IMI, a positive correlation between RANTES, MIP-1alpha 3h and LVEF was found (R=0.322, p<0.03 and R=0.399, p<0.008). In group A, all MIP-1alpha values were significantly higher than in group B. Also, peak MIP-1alpha levels significantly differed between groups A and B (44.8 vs 8.3 pg/ml, p<0.006). In pts from group B, a negative correlation between MCP-1 measured an admission and LVEF was found (R=-0.690, p<0.05).


CONCLUSIONS
We found a significant elevation of chemokines in the early period of acute MI. The correlations between different parameters suggest, that chemokines may serve as new parameters of immune activation in STEMI and also may play the dominant role in the cardiac inflammatory response and subsequent repair processes.
Kobusiak-Prokopowicz
Małgorzata
M
Department of Cardiology, Medical Academy, Wrocław, Poland.
Orzeszko
Jacek
J
Mazur
Grzegorz
G
Mysiak
Andrzej
A
Orda
Alina
A
Mazurek
Walentyna
W
D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D015906:Angioplasty, Balloon, Coronary; D016022:Case-Control Studies; D018932:Chemokine CCL2 / Q000097:blood*; D054405:Chemokine CCL3; D054407:Chemokine CCL4; D018946:Chemokine CCL5 / Q000097:blood*; D005260:Female; D006801:Humans; D019402:Macrophage Inflammatory Proteins / Q000097:blood*; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood* / Q000188:drug therapy / Q000503:physiopathology / Q000628:therapy*; D015912:Thrombolytic Therapy; D013997:Time Factors
C111835:CCL2 protein, human; D018932:Chemokine CCL2; D054405:Chemokine CCL3; D054407:Chemokine CCL4; D018946:Chemokine CCL5; D019402:Macrophage Inflammatory Proteins