title: Angiotensin-converting enzyme inhibition reduces monocyte chemoattractant protein-1 and tissue factor levels in patients with myocardial infarction.
abstract: OBJECTIVE
  We investigated the effects of enalapril therapy on plasma tissue factor (TF), tissue factor pathway inhibitor (TFPI) and monocyte chemoattractant protein-1 (MCP-1) levels in patients with acute myocardial infarction.
  
  
  BACKGROUND
  Macrophages express TF in human coronary atherosclerotic plaques. Both TF and TFPI are major regulators of coagulation and thrombosis. Monocyte chemoattractant protein-1 is a monocyte and macrophage chemotactic and activating factor.
  
  
  METHODS
  In a randomized, double-blind, placebo-controlled study beginning about two weeks after myocardial infarction, 16 patients received four weeks of placebo (placebo group) and another 16 patients received four weeks of enalapril 5 mg daily therapy (enalapril group). We performed blood sampling after administration of the doses.
  
  
  RESULTS
  There were no significant differences in the serum angiotensin-converting enzyme (ACE) activity, plasma TF, free TFPI or MCP-1 levels before administration between the enalapril and placebo groups. In the enalapril group, ACE activity (IU/liter) (14.0 before, 5.2 on day 3, 5.8 on day 7, 6.3 on day 28), TF levels (pg/ml) (223, 203, 182, 178) and MCP-1 levels (pg/ml) (919, 789, 790, 803) significantly decreased by day 28. However, the free TFPI levels (ng/ml) (28.2, 26.5, 26.8, 28.4) did not change. These four variables were unchanged during the study period in the placebo group.
  
  
  CONCLUSIONS
  This study demonstrated that administration of enalapril reduces the increased procoagulant activity in patients with myocardial infarction associated with inhibition of the activation and accumulation of macrophages and monocytes.
authors.affiliation: Department of Cardiovascular Medicine, Kumamoto University School of Medicine, Kumamoto City, Japan.
authors.forename: H
authors.initials: H
authors.lastname: Soejima
authors.forename: H
authors.initials: H
authors.lastname: Ogawa
authors.forename: H
authors.initials: H
authors.lastname: Yasue
authors.forename: K
authors.initials: K
authors.lastname: Kaikita
authors.forename: K
authors.initials: K
authors.lastname: Takazoe
authors.forename: K
authors.initials: K
authors.lastname: Nishiyama
authors.forename: K
authors.initials: K
authors.lastname: Misumi
authors.forename: S
authors.initials: S
authors.lastname: Miyamoto
authors.forename: M
authors.initials: M
authors.lastname: Yoshimura
authors.forename: K
authors.initials: K
authors.lastname: Kugiyama
authors.forename: S
authors.initials: S
authors.lastname: Nakamura
authors.forename: I
authors.initials: I
authors.lastname: Tsuji
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000009:adverse effects / Q000627:therapeutic use*; D000925:Anticoagulants / Q000097:blood; D018932:Chemokine CCL2 / Q000097:blood*; D004311:Double-Blind Method; D004656:Enalapril / Q000009:adverse effects / Q000627:therapeutic use*; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D006801:Humans; D008074:Lipoproteins / Q000097:blood; D008264:Macrophages / Q000187:drug effects / Q000276:immunology; D008297:Male; D008875:Middle Aged; D009000:Monocytes / Q000187:drug effects* / Q000276:immunology; D009203:Myocardial Infarction / Q000188:drug therapy* / Q000276:immunology; D013925:Thromboplastin / Q000378:metabolism*
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D000925:Anticoagulants; D018932:Chemokine CCL2; D008074:Lipoproteins; C051928:lipoprotein-associated coagulation inhibitor; D004656:Enalapril; D013925:Thromboplastin