PMID- 14574083
OWN - NLM
STAT- MEDLINE
DCOM- 20040420
LR  - 20220409
IS  - 0920-3206 (Print)
IS  - 0920-3206 (Linking)
VI  - 17
IP  - 3
DP  - 2003 May
TI  - Serum MCP-1 and VEGF levels are not affected by inhibition of the 
      renin-angiotensin system in patients with acute myocardial infarction.
PG  - 249-55
AB  - Monocyte chemoattractant protein-1 (MCP-1) and vascular endothelial growth factor 
      (VEGF) stimulate angiogenesis in ischemic tissues, and both of their expression 
      are stimulated by angiotensin II. We measured the serum concentrations of MCP-1 
      and VEGF in patients with acute myocardial infarction (AMI) and investigated the 
      effects of an early administration of angiotensin-converting enzyme inhibitor 
      (ACEI) and angiotensin II type 1 receptor blocker (ARB) on their levels. 
      Thirty-six patients with AMI were divided randomly into 3 therapeutic groups; the 
      ACEI perindopril, the ARB candesartan and control (without perindopril and 
      candesartan), and the drugs were administered within 36 hours after the onset of 
      AMI. Peripheral blood mononuclear cells (PBMC) obtained from the patients were 
      incubated for 24 hours. The levels of MCP-1 and VEGF in the serum and the 
      supernatant of PBMC were measured by ELISA. The serum MCP-1 and VEGF levels in 
      AMI patients at the time of admission were not significantly different from those 
      in healthy control subjects, but both MCP-1 and VEGF levels in the patients were 
      increased significantly after 7 days. There was no significant difference in the 
      serum MCP-1 and VEGF levels among the 3 therapeutic groups. The production of 
      MCP-1 and VEGF by PBMC was also increased in AMI patients compared with healthy 
      control subjects, and there was also no difference in their production among the 
      3 therapeutic groups. In conclusion, circulating MCP-1 and VEGF levels and their 
      production by PBMC are elevated during the course of AMI, and early 
      administration of ACEI and ARB does not affect their levels.
FAU - Murakami, Yoshiaki
AU  - Murakami Y
AD  - Division of Cardiovascular Medicine, Jichi Medical School, Tochigi, Japan.
FAU - Kurosaki, Kenji
AU  - Kurosaki K
FAU - Matsui, Keiji
AU  - Matsui K
FAU - Shimada, Kazuyuki
AU  - Shimada K
FAU - Ikeda, Uichi
AU  - Ikeda U
LA  - eng
PT  - Clinical Trial
PT  - Journal Article
PT  - Randomized Controlled Trial
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Cardiovasc Drugs Ther
JT  - Cardiovascular drugs and therapy
JID - 8712220
RN  - 0 (Angiotensin II Type 1 Receptor Blockers)
RN  - 0 (Angiotensin-Converting Enzyme Inhibitors)
RN  - 0 (Benzimidazoles)
RN  - 0 (Biphenyl Compounds)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Tetrazoles)
RN  - 0 (Vascular Endothelial Growth Factor A)
RN  - S8Q36MD2XX (candesartan)
RN  - Y5GMK36KGY (Perindopril)
SB  - IM
MH  - Aged
MH  - Aged, 80 and over
MH  - Angiotensin II Type 1 Receptor Blockers
MH  - Angiotensin-Converting Enzyme Inhibitors/pharmacology
MH  - Benzimidazoles/pharmacology
MH  - Biphenyl Compounds
MH  - Chemokine CCL2/biosynthesis/*blood
MH  - Enzyme-Linked Immunosorbent Assay
MH  - Female
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - Monocytes/metabolism
MH  - Myocardial Infarction/*metabolism/*physiopathology
MH  - Perindopril/pharmacology
MH  - Renin-Angiotensin System/*drug effects/physiology
MH  - Tetrazoles/pharmacology
MH  - Vascular Endothelial Growth Factor A/biosynthesis/*blood
EDAT- 2003/10/24 05:00
MHDA- 2004/04/21 05:00
CRDT- 2003/10/24 05:00
PHST- 2003/10/24 05:00 [pubmed]
PHST- 2004/04/21 05:00 [medline]
PHST- 2003/10/24 05:00 [entrez]
AID - 5145958 [pii]
AID - 10.1023/a:1026128308440 [doi]
PST - ppublish
SO  - Cardiovasc Drugs Ther. 2003 May;17(3):249-55. doi: 10.1023/a:1026128308440.