title: Coronary collaterals: the role of MCP-1 during the early phase of acute myocardial infarction.
abstract: BACKGROUND
  The collateral growth (arteriogenesis) of an individual may vary from complete to absent during the early phase of acute myocardial infarction (AMI). However, the mechanisms underlying the large differences in the extent and adequacy of collateralization remain unclear. We hypothesized that shear stress-induced activation of monocyte chemoattractant protein-1 could potently contribute to the development of coronary collaterals during the early phase of AMI.
  
  
  METHODS
  We enrolled forty patients with AMI who did not receive reperfusion therapy within 24 h after the onset of chest pain and who also underwent coronary angiography (CAG) from 1 to 7 days after admission (mean duration: 3.6+/-2.2 days). The grades of the collateral development were angiographically defined and grouped according to the grade of collaterals as absent (score 0, n=20) or well-developed (score 2, n=20) collateral circulation. The plasma concentrations of vascular endothelial growth factor (VEGF), endostatin, monocyte chemoattractant protein-1 (MCP-1), and stromal cell-derived factor-1 (SDF-1) were assessed by enzyme-linked immunosorbent assay and then these values were compared between the two groups.
  
  
  RESULTS
  There were no differences in the demographic and angiographic characteristics except for the number of total occlusion in culprit lesion. The plasma MCP-1 levels were significantly higher in the group with well-developed collateral circulation compared to the group with absent collateral circulation (262+/-216 vs. 151+/-88 pg/ml, respectively, p=0.043). However, the plasma levels of VEGF, endostatin and SDF-1 were not different on comparisons between the groups (VEGF; 369+/-377 vs. 324+/-363 pg/ml, endostatin; 1.74+/-1.71 vs. 1.49+/-1.15 ng/ml, SDF-1; 1806+/-508 vs. 2091+/-772 pg/ml, respectively).
  
  
  CONCLUSIONS
  During the early phase of AMI, the plasma levels of MCP-1 were significantly increased in the patients with well-developed collateral circulation as compared to those patients with absent collateral circulation. These findings suggested that the shear stress-induced overexpression of MCP-1 contributes significantly to the development of coronary collaterals during the early phase of AMI.
authors.affiliation: Division of Cardiology, Department of Internal Medicine, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea.
authors.forename: Hun-Jun
authors.initials: HJ
authors.lastname: Park
authors.forename: Kiyuk
authors.initials: K
authors.lastname: Chang
authors.forename: Chan Seok
authors.initials: CS
authors.lastname: Park
authors.forename: Sung Won
authors.initials: SW
authors.lastname: Jang
authors.forename: Sang-Hyun
authors.initials: SH
authors.lastname: Ihm
authors.forename: Pum Joon
authors.initials: PJ
authors.lastname: Kim
authors.forename: Sang-Hong
authors.initials: SH
authors.lastname: Baek
authors.forename: Ki-Bae
authors.initials: KB
authors.lastname: Seung
authors.forename: Kyu-Bo
authors.initials: KB
authors.lastname: Choi
mesh_terms: D000368:Aged; D018932:Chemokine CCL2 / Q000502:physiology*; D054377:Chemokine CXCL12 / Q000097:blood; D003097:Collateral Circulation / Q000502:physiology*; D017023:Coronary Angiography; D003324:Coronary Artery Disease / Q000000981:diagnostic imaging / Q000503:physiopathology; D003326:Coronary Circulation / Q000502:physiology*; D052279:Creatine Kinase, MB Form / Q000097:blood; D043169:Endostatins / Q000097:blood; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000000981:diagnostic imaging / Q000503:physiopathology*; D019210:Troponin I / Q000097:blood; D042461:Vascular Endothelial Growth Factor A / Q000097:blood
chemical_list: C111835:CCL2 protein, human; C515255:CXCL12 protein, human; D018932:Chemokine CCL2; D054377:Chemokine CXCL12; D043169:Endostatins; D019210:Troponin I; C467484:VEGFA protein, human; D042461:Vascular Endothelial Growth Factor A; D052279:Creatine Kinase, MB Form