PMID- 10520779
OWN - NLM
STAT- MEDLINE
DCOM- 19991027
LR  - 20190708
IS  - 0735-1097 (Print)
IS  - 0735-1097 (Linking)
VI  - 34
IP  - 4
DP  - 1999 Oct
TI  - Angiotensin-converting enzyme inhibition reduces monocyte chemoattractant 
      protein-1 and tissue factor levels in patients with myocardial infarction.
PG  - 983-8
AB  - OBJECTIVES: 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.
FAU - Soejima, H
AU  - Soejima H
AD  - Department of Cardiovascular Medicine, Kumamoto University School of Medicine, 
      Kumamoto City, Japan.
FAU - Ogawa, H
AU  - Ogawa H
FAU - Yasue, H
AU  - Yasue H
FAU - Kaikita, K
AU  - Kaikita K
FAU - Takazoe, K
AU  - Takazoe K
FAU - Nishiyama, K
AU  - Nishiyama K
FAU - Misumi, K
AU  - Misumi K
FAU - Miyamoto, S
AU  - Miyamoto S
FAU - Yoshimura, M
AU  - Yoshimura M
FAU - Kugiyama, K
AU  - Kugiyama K
FAU - Nakamura, S
AU  - Nakamura S
FAU - Tsuji, I
AU  - Tsuji I
LA  - eng
PT  - Clinical Trial
PT  - Journal Article
PT  - Randomized Controlled Trial
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Am Coll Cardiol
JT  - Journal of the American College of Cardiology
JID - 8301365
RN  - 0 (Angiotensin-Converting Enzyme Inhibitors)
RN  - 0 (Anticoagulants)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Lipoproteins)
RN  - 0 (lipoprotein-associated coagulation inhibitor)
RN  - 69PN84IO1A (Enalapril)
RN  - 9035-58-9 (Thromboplastin)
SB  - IM
MH  - Aged
MH  - Aged, 80 and over
MH  - Angiotensin-Converting Enzyme Inhibitors/adverse effects/*therapeutic use
MH  - Anticoagulants/blood
MH  - Chemokine CCL2/*blood
MH  - Double-Blind Method
MH  - Enalapril/adverse effects/*therapeutic use
MH  - Enzyme-Linked Immunosorbent Assay
MH  - Female
MH  - Humans
MH  - Lipoproteins/blood
MH  - Macrophages/drug effects/immunology
MH  - Male
MH  - Middle Aged
MH  - Monocytes/*drug effects/immunology
MH  - Myocardial Infarction/*drug therapy/immunology
MH  - Thromboplastin/*metabolism
EDAT- 1999/10/16 00:00
MHDA- 1999/10/16 00:01
CRDT- 1999/10/16 00:00
PHST- 1999/10/16 00:00 [pubmed]
PHST- 1999/10/16 00:01 [medline]
PHST- 1999/10/16 00:00 [entrez]
AID - S0735-1097(99)00318-6 [pii]
AID - 10.1016/s0735-1097(99)00318-6 [doi]
PST - ppublish
SO  - J Am Coll Cardiol. 1999 Oct;34(4):983-8. doi: 10.1016/s0735-1097(99)00318-6.